首页 > 最新文献

Circulatory shock最新文献

英文 中文
Comparison of effects of margarite extract and recombinant human superoxide dismutase on paraquat-induced superoxide anion radicals in rat lung. 人造玛格丽特提取物和重组人超氧化物歧化酶对百草枯诱导的大鼠肺超氧阴离子自由基影响的比较。
Pub Date : 1994-08-01
H Ogata, X X Luo, X Xu

The effects of medicinal margarite extract and recombinant human superoxide dismutase (r-h SOD) on acute paraquat intoxication were examined in the rat lung. Forty-eight Sprague-Dawley rats under pentobarbital anesthesia were randomly assigned to one of four groups receiving i.v. injection of physiological saline (control), i.v. injection of 70 mg/kg paraquat, or i.v. injection of either 50 mg/kg of margarite extract or 50,000 unit/kg of r-h SOD 10 minutes before and 1 and 2 hours after an equivalent paraquat administration. Examination of lung superoxide anion radicals (O2-.), lipid peroxides, and histopathological changes showed that paraquat significantly increased superoxide anion radicals (383% of control) reacted with CLA-phenyl. Both margarite extract and r-h SOD decreased superoxide anion radicals to 119% and 83% of control, respectively. Margarite extract, rather than r-h SOD, significantly alleviated the paraquat-induced infiltration of polymorphonuclear leukocytes and macrophages into the alveolar walls. There were no significant inter-group differences in lipid peroxides in the lung. Component analysis showed that margarite extract was rich in L- and D-arginine. The scavenging mechanism of margarite extract may be related to L-arginine but needs to be further verified in the future study.

研究了中药提取物和重组人超氧化物歧化酶(r-h SOD)对急性百草枯中毒大鼠肺组织的影响。48只经戊巴比妥麻醉的Sprague-Dawley大鼠被随机分为四组,分别在给药前10分钟和给药后1、2小时静脉注射生理盐水(对照)、静脉注射70 mg/kg百草枯、静脉注射50 mg/kg人造黄油提取物或50,000单位/kg r-h SOD。肺超氧阴离子自由基(O2-)、脂质过氧化物和组织病理学变化的检测显示,百草枯显著增加了与cla -苯基反应的超氧阴离子自由基(对照组的383%)。人造黄油提取物和r-h SOD均可使超氧阴离子自由基减少119%和83%。玛格丽特提取物,而不是r-h SOD,显著减轻百草枯诱导的多形核白细胞和巨噬细胞向肺泡壁的浸润。各组间肺组织脂质过氧化物含量差异无统计学意义。成分分析表明,人造黄油提取物中含有丰富的L-精氨酸和d -精氨酸。玛格丽特提取物的清除机制可能与l -精氨酸有关,但需要在未来的研究中进一步验证。
{"title":"Comparison of effects of margarite extract and recombinant human superoxide dismutase on paraquat-induced superoxide anion radicals in rat lung.","authors":"H Ogata,&nbsp;X X Luo,&nbsp;X Xu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The effects of medicinal margarite extract and recombinant human superoxide dismutase (r-h SOD) on acute paraquat intoxication were examined in the rat lung. Forty-eight Sprague-Dawley rats under pentobarbital anesthesia were randomly assigned to one of four groups receiving i.v. injection of physiological saline (control), i.v. injection of 70 mg/kg paraquat, or i.v. injection of either 50 mg/kg of margarite extract or 50,000 unit/kg of r-h SOD 10 minutes before and 1 and 2 hours after an equivalent paraquat administration. Examination of lung superoxide anion radicals (O2-.), lipid peroxides, and histopathological changes showed that paraquat significantly increased superoxide anion radicals (383% of control) reacted with CLA-phenyl. Both margarite extract and r-h SOD decreased superoxide anion radicals to 119% and 83% of control, respectively. Margarite extract, rather than r-h SOD, significantly alleviated the paraquat-induced infiltration of polymorphonuclear leukocytes and macrophages into the alveolar walls. There were no significant inter-group differences in lipid peroxides in the lung. Component analysis showed that margarite extract was rich in L- and D-arginine. The scavenging mechanism of margarite extract may be related to L-arginine but needs to be further verified in the future study.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"43 4","pages":"161-5"},"PeriodicalIF":0.0,"publicationDate":"1994-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18891975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sex steroid hormones in circulatory shock, sepsis syndrome, and septic shock. 性类固醇激素在循环性休克、败血症综合征和感染性休克中的作用。
Pub Date : 1994-08-01
F Fourrier, A Jallot, L Leclerc, M Jourdain, A Racadot, J L Chagnon, A Rime, C Chopin

Methods: Estrone (E1), estradiol (E2), testosterone (T), FSH, and LH levels were daily measured during a ten day period in 50 critically ill patients (38 men, 12 post-menopausal women). Patients were separated into four groups: A) no circulatory failure, no sepsis, B) sepsis syndrome without circulatory failure, C) circulatory failure without sepsis syndrome, D) septic shock. Results of hormonal measurements were compared 1) among the 4 groups, 2) between male and female patients, 3) between septic and nonseptic patients. The potential for the infusion of the vasoactive drug dobutamine to induce sex hormonal changes was documented in ten additional septic shock patients by measuring cortisol, E1, and T at base-line and after dobutamine infusion. Changes in active renin and plasma renin activity (PRA) were used as indirect witness of the dobutamine-induced beta 2-stimulation.

Results: A dramatic increase in E1 and E2 levels was observed in women of groups B and D, and only in male patients of group D. In the septic patients, estrogen levels peaked at days 1 and 2 and trended to normal from day 6 after the onset of sepsis, while FSH and LH decreased. No difference was found between survivors and non-survivors. Whatever the group, male patients had low T levels throughout the study. Dobutamine induced a significant increase in active renin levels and a decrease in the regression slope between renin and PRA. Cortisol levels remained normal. No significant change in E1 and T was observed after dobutamine.

Conclusions: High estrogen levels were specifically observed in patients with sepsis and septic shock, either males or females. Decreased LH and FSH levels were consistent with the negative feed-back effect of high estrogen levels on pituitary secretion. Circulating T levels were decreased in all male patients. We found no correlation between sequential estrogen levels and outcome. These levels were not modified by a dobutamine-induced beta-2 stimulation.

方法:对50例危重患者(男性38例,绝经后女性12例),连续10 d,每日测定雌激素(E1)、雌二醇(E2)、睾酮(T)、卵泡刺激素(FSH)、黄体生成素(LH)水平。患者分为4组:A)无循环衰竭,无脓毒症,B)脓毒症综合征,无循环衰竭,C)循环衰竭,无脓毒症综合征,D)感染性休克。比较1)4组患者、2)男女患者、3)脓毒症患者和非脓毒症患者的激素测量结果。在另外10例感染性休克患者中,通过测量基线和多巴酚丁胺输注后的皮质醇、E1和T,证实了输注血管活性药物多巴酚丁胺诱导性激素变化的可能性。活性肾素和血浆肾素活性(PRA)的变化被用作多巴酚丁胺诱导β 2刺激的间接证据。结果:B、D组女性患者E1、E2水平显著升高,仅D组男性患者出现。脓毒症患者雌激素水平在脓毒症发病后第1、2天达到峰值,6天后趋于正常,FSH、LH水平下降。幸存者和非幸存者之间没有发现差异。不管是哪一组,在整个研究过程中,男性患者的睾酮水平都很低。多巴酚丁胺诱导活性肾素水平显著升高,肾素与PRA之间的回归斜率显著降低。皮质醇水平保持正常。多巴酚丁胺后E1和T无明显变化。结论:无论是男性还是女性,在脓毒症和脓毒性休克患者中均可观察到高雌激素水平。LH和FSH水平降低与高雌激素水平对垂体分泌的负反馈作用一致。所有男性患者的循环T水平均下降。我们发现顺序雌激素水平与结果之间没有相关性。多巴酚丁胺诱导的β -2刺激并没有改变这些水平。
{"title":"Sex steroid hormones in circulatory shock, sepsis syndrome, and septic shock.","authors":"F Fourrier,&nbsp;A Jallot,&nbsp;L Leclerc,&nbsp;M Jourdain,&nbsp;A Racadot,&nbsp;J L Chagnon,&nbsp;A Rime,&nbsp;C Chopin","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Methods: </strong>Estrone (E1), estradiol (E2), testosterone (T), FSH, and LH levels were daily measured during a ten day period in 50 critically ill patients (38 men, 12 post-menopausal women). Patients were separated into four groups: A) no circulatory failure, no sepsis, B) sepsis syndrome without circulatory failure, C) circulatory failure without sepsis syndrome, D) septic shock. Results of hormonal measurements were compared 1) among the 4 groups, 2) between male and female patients, 3) between septic and nonseptic patients. The potential for the infusion of the vasoactive drug dobutamine to induce sex hormonal changes was documented in ten additional septic shock patients by measuring cortisol, E1, and T at base-line and after dobutamine infusion. Changes in active renin and plasma renin activity (PRA) were used as indirect witness of the dobutamine-induced beta 2-stimulation.</p><p><strong>Results: </strong>A dramatic increase in E1 and E2 levels was observed in women of groups B and D, and only in male patients of group D. In the septic patients, estrogen levels peaked at days 1 and 2 and trended to normal from day 6 after the onset of sepsis, while FSH and LH decreased. No difference was found between survivors and non-survivors. Whatever the group, male patients had low T levels throughout the study. Dobutamine induced a significant increase in active renin levels and a decrease in the regression slope between renin and PRA. Cortisol levels remained normal. No significant change in E1 and T was observed after dobutamine.</p><p><strong>Conclusions: </strong>High estrogen levels were specifically observed in patients with sepsis and septic shock, either males or females. Decreased LH and FSH levels were consistent with the negative feed-back effect of high estrogen levels on pituitary secretion. Circulating T levels were decreased in all male patients. We found no correlation between sequential estrogen levels and outcome. These levels were not modified by a dobutamine-induced beta-2 stimulation.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"43 4","pages":"171-8"},"PeriodicalIF":0.0,"publicationDate":"1994-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18891977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Role of TNF-alpha in the development of autoimmunity and the pathogenesis of insulin-dependent diabetes mellitus in NOD mice. tnf - α在NOD小鼠自身免疫发展和胰岛素依赖型糖尿病发病机制中的作用
Pub Date : 1994-08-01
X D Yang, H O McDevitt
{"title":"Role of TNF-alpha in the development of autoimmunity and the pathogenesis of insulin-dependent diabetes mellitus in NOD mice.","authors":"X D Yang,&nbsp;H O McDevitt","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"43 4","pages":"198-201"},"PeriodicalIF":0.0,"publicationDate":"1994-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18895626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Receptor-selective mutants of tumour necrosis factor in the therapy of cancer: preclinical studies. 肿瘤坏死因子受体选择性突变在癌症治疗中的应用:临床前研究。
Pub Date : 1994-08-01
P Brouckaert, P Ameloot, A Cauwels, B Everaerdt, C Libert, N Takahashi, W Van Molle, W Fiers

The use of TNF-mutants that are selective agonists of the TNF-R55 is one strategy that is being explored to broaden the therapeutic margin of TNF. Several problems still have to be overcome before they can be used in clinical trials. Regarding the sensitizing effect of some infections and some tumours, we identified IFN-gamma as a mediator in BCG- but not in tumour-induced sensitization. In both models, the vessel wall is most probably the key tissue as alpha-LFA-1 antibodies could protect against lethality. Studies in primates showed that an unexpected feature, namely, the longer half-life of such mutants, might interfere with this strategy. Recent observations also indicate that the mechanism of tolerance-induction, another way to separate antitumour and toxic effects of TNF, might reside in the functional ablation of the TNF-R75. Using IL-60/0 knockout mice, we could not find any causal role for IL-6 in TNF-mediated lethality, this in contrast to results obtained previously with neutralizing antibodies. Finally, we identified the acute phase protein alpha 1-acid glycoprotein as a protein with protective properties towards TNF-induced lethality and liver damage.

使用TNF突变体作为TNF- r55的选择性激动剂是一种正在探索的策略,以扩大TNF的治疗范围。在用于临床试验之前,还有几个问题需要克服。关于某些感染和某些肿瘤的致敏作用,我们发现ifn - γ在BCG中是一种介质,但在肿瘤诱导的致敏中不是。在这两种模型中,血管壁很可能是关键组织,因为α - lfa -1抗体可以防止致死性。对灵长类动物的研究表明,一种意想不到的特征,即这种突变体的半衰期较长,可能会干扰这种策略。最近的观察还表明,另一种分离TNF的抗肿瘤和毒性作用的方法-耐受性诱导的机制可能存在于TNF- r75的功能性消融中。使用IL-60/0敲除小鼠,我们没有发现IL-6在tnf介导的致死性中有任何因果作用,这与之前用中和抗体获得的结果相反。最后,我们发现急性期蛋白α 1-酸性糖蛋白是一种对tnf诱导的致死性和肝损伤具有保护作用的蛋白质。
{"title":"Receptor-selective mutants of tumour necrosis factor in the therapy of cancer: preclinical studies.","authors":"P Brouckaert,&nbsp;P Ameloot,&nbsp;A Cauwels,&nbsp;B Everaerdt,&nbsp;C Libert,&nbsp;N Takahashi,&nbsp;W Van Molle,&nbsp;W Fiers","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The use of TNF-mutants that are selective agonists of the TNF-R55 is one strategy that is being explored to broaden the therapeutic margin of TNF. Several problems still have to be overcome before they can be used in clinical trials. Regarding the sensitizing effect of some infections and some tumours, we identified IFN-gamma as a mediator in BCG- but not in tumour-induced sensitization. In both models, the vessel wall is most probably the key tissue as alpha-LFA-1 antibodies could protect against lethality. Studies in primates showed that an unexpected feature, namely, the longer half-life of such mutants, might interfere with this strategy. Recent observations also indicate that the mechanism of tolerance-induction, another way to separate antitumour and toxic effects of TNF, might reside in the functional ablation of the TNF-R75. Using IL-60/0 knockout mice, we could not find any causal role for IL-6 in TNF-mediated lethality, this in contrast to results obtained previously with neutralizing antibodies. Finally, we identified the acute phase protein alpha 1-acid glycoprotein as a protein with protective properties towards TNF-induced lethality and liver damage.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"43 4","pages":"185-90"},"PeriodicalIF":0.0,"publicationDate":"1994-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18891979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Monophosphoryl lipid A protects against endotoxic shock via inhibiting neutrophil infiltration and preventing disseminated intravascular coagulation. 单磷脂酰脂A通过抑制中性粒细胞浸润和防止弥散性血管内凝血来预防内源性休克。
Pub Date : 1994-07-01
Z Yao, P A Foster, G J Gross

The major objective of the present study was to determine the effects of a partial structure of the lipid A moiety of gram-negative lipopolysaccharide, monophosphoryl lipid A (MLA), on endotoxin-induced mortality and disseminated intravascular coagulation (DIC) in rats. A second objective was to examine the role of polymorphonuclear neutrophil invasion to visceral organs, including lung, liver, heart, and kidney in the pathogenesis of the compromised multiorgan function which occurs in endotoxic shock. Finally, a third aim was to determine if the potential protective effects of MLA might be mediated via inhibiting neutrophil invasion to various visceral organs. Male Sprague-Dawley rats (220-260 g) were fasted over night and used the following day. In control rats, endotoxin (S. abortus equi LPS, 15 mg/kg, i.v.) produced a 89% mortality at 48 hr following its administration, and gross pathological and laboratory signs of DIC at 3 hr after injection. The latter included increased serum fibrin(ogen) degradation products (FDP, 24.00 +/- 7.81 vs. 0 micrograms/ml, P < .05), prothrombin time (PT, 16.20 +/- 1.12 vs. 13.03 +/- 0.20 sec, P < .05), and activated partial thromboplastin time (APTT, 32.70 +/- 3.83 vs. 20.11 +/- 0.60 sec, P < .05), and decreased plasma fibrinogen (233.2 +/- 41.6 vs. 406.3 +/- 23.2 mg/dl, P < .05) as well as evidence of gross visceral hemorrhage. Pretreatment with MLA (5 mg/kg) for 24 hr produced a marked reduction in endotoxin-induced mortality at 48 hr (0% versus 89% in controls) and inhibited all of the manifestations of DIC produced by endotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

本研究的主要目的是确定革兰氏阴性脂多糖单磷酰脂质a (MLA)的脂质a部分结构对内毒素诱导的大鼠死亡率和弥散性血管内凝血(DIC)的影响。第二个目的是研究多形核中性粒细胞侵入内脏器官,包括肺、肝、心和肾,在内毒素休克中发生的多器官功能受损的发病机制中的作用。最后,第三个目的是确定MLA的潜在保护作用是否可能通过抑制中性粒细胞对各种内脏器官的侵袭而介导。雄性Sprague-Dawley大鼠(220-260 g)禁食一夜,第二天使用。在对照大鼠中,内毒素(S. abortus equi LPS, 15 mg/kg,静脉注射)在给药后48小时导致89%的死亡率,在注射后3小时出现DIC的大体病理和实验室症状。后者包括血清纤维蛋白(原)降解产物(FDP, 24.00 +/- 7.81 vs. 0 μ g/ ml, P < 0.05),凝血酶原时间(PT, 16.20 +/- 1.12 vs. 13.03 +/- 0.20秒,P < 0.05),激活部分凝血活素时间(APTT, 32.70 +/- 3.83 vs. 20.11 +/- 0.60秒,P < 0.05),血浆纤维蛋白原降低(233.2 +/- 41.6 vs. 406.3 +/- 23.2 mg/dl, P < 0.05),以及内脏出血的证据。MLA (5mg /kg)预处理24小时可显著降低48小时内毒素引起的死亡率(0%,而对照组为89%),并抑制内毒素引起的DIC的所有表现。(摘要删节250字)
{"title":"Monophosphoryl lipid A protects against endotoxic shock via inhibiting neutrophil infiltration and preventing disseminated intravascular coagulation.","authors":"Z Yao,&nbsp;P A Foster,&nbsp;G J Gross","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The major objective of the present study was to determine the effects of a partial structure of the lipid A moiety of gram-negative lipopolysaccharide, monophosphoryl lipid A (MLA), on endotoxin-induced mortality and disseminated intravascular coagulation (DIC) in rats. A second objective was to examine the role of polymorphonuclear neutrophil invasion to visceral organs, including lung, liver, heart, and kidney in the pathogenesis of the compromised multiorgan function which occurs in endotoxic shock. Finally, a third aim was to determine if the potential protective effects of MLA might be mediated via inhibiting neutrophil invasion to various visceral organs. Male Sprague-Dawley rats (220-260 g) were fasted over night and used the following day. In control rats, endotoxin (S. abortus equi LPS, 15 mg/kg, i.v.) produced a 89% mortality at 48 hr following its administration, and gross pathological and laboratory signs of DIC at 3 hr after injection. The latter included increased serum fibrin(ogen) degradation products (FDP, 24.00 +/- 7.81 vs. 0 micrograms/ml, P < .05), prothrombin time (PT, 16.20 +/- 1.12 vs. 13.03 +/- 0.20 sec, P < .05), and activated partial thromboplastin time (APTT, 32.70 +/- 3.83 vs. 20.11 +/- 0.60 sec, P < .05), and decreased plasma fibrinogen (233.2 +/- 41.6 vs. 406.3 +/- 23.2 mg/dl, P < .05) as well as evidence of gross visceral hemorrhage. Pretreatment with MLA (5 mg/kg) for 24 hr produced a marked reduction in endotoxin-induced mortality at 48 hr (0% versus 89% in controls) and inhibited all of the manifestations of DIC produced by endotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"43 3","pages":"107-14"},"PeriodicalIF":0.0,"publicationDate":"1994-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18850221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Human responses to bacterial endotoxin. 人体对细菌内毒素的反应。
Pub Date : 1994-07-01
R Burrell

The literature concerning human responses to bacterial endotoxin, in particular to the purified lipopolysaccharide derivative, has been critically reviewed and summarized. Papers selected for review are those that reported studies of human subjects in a normal state of health administered defined doses of either intravenous or aerosol inhaled material. Emphasis was placed on cardiovascular, pulmonary, metabolic, and inflammatory parameters. The information detailed here can be applied to understanding the pathophysiology of human consequences to spontaneous, clinical diseases induced by this highly inflammatory and ubiquitous substance.

关于人体对细菌内毒素的反应的文献,特别是对纯化的脂多糖衍生物,已经进行了严格的审查和总结。选择供审查的论文是那些报告了在正常健康状态下接受规定剂量静脉注射或气溶胶吸入物质的人类受试者的研究。重点放在心血管、肺、代谢和炎症参数上。这里详细的信息可以应用于理解由这种高度炎症和普遍存在的物质引起的自发性临床疾病的人类后果的病理生理学。
{"title":"Human responses to bacterial endotoxin.","authors":"R Burrell","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The literature concerning human responses to bacterial endotoxin, in particular to the purified lipopolysaccharide derivative, has been critically reviewed and summarized. Papers selected for review are those that reported studies of human subjects in a normal state of health administered defined doses of either intravenous or aerosol inhaled material. Emphasis was placed on cardiovascular, pulmonary, metabolic, and inflammatory parameters. The information detailed here can be applied to understanding the pathophysiology of human consequences to spontaneous, clinical diseases induced by this highly inflammatory and ubiquitous substance.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"43 3","pages":"137-53"},"PeriodicalIF":0.0,"publicationDate":"1994-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18850225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Ventricular dysfunction in norepinephrine-induced cardiomyopathy. 去甲肾上腺素诱发心肌病的心室功能障碍。
Pub Date : 1994-07-01
F M Powers, R Pifarre, J X Thomas

Cardiac dysfunction resulting from norepinephrine-induced cardiomyopathy has not been fully investigated. This study evaluates acute and chronic changes in systolic and diastolic function at three levels of norepinephrine (NE)-induced injury. Rabbits were infused with saline or 2, 4, or 6 micrograms/kg/min NE for 90 min. Ventricular function was assessed immediately after infusion or at 48 hr using the isolated non-ejecting heart preparation. Hearts were perfused at 10 ml/min/g with Krebs-Henseleit buffer. After baseline measurements, hearts were perfused with NE (10(-10) to 10(-7) M). Steady state left ventricular pressure (LVP), +dP/dt, and -dP/dt were recorded at baseline and each NE concentration. NE infusion acutely depressed baseline LV systolic function. Decreases in LVP and +dP/dt were inversely related to dose of infused NE. By 48 hr, LVP and +dP/dt improved slightly in all NE groups but improvement was significant only in hearts from rabbits infused with 4 micrograms NE. Systolic function of hearts from animals infused with 6 micrograms NE remained depressed. Diastolic (-dP/dt) function was impaired following NE infusion when compared to saline treated hearts and did not improve within 48 hr. Although baseline function is depressed, myopathic hearts increased ventricular function the same amount as normal hearts at 10(-7) M NE. These findings demonstrate a) impairment in LV systolic and diastolic function acutely after NE infusion, b) improvement in systolic function within 48 hr, c) ability to increase contractility in response to NE is not impaired, and d) recovery of systolic function precedes improvement in diastolic function.

去甲肾上腺素引起的心肌病引起的心功能障碍尚未得到充分的研究。本研究评估在三个水平的去甲肾上腺素(NE)诱导的损伤中收缩和舒张功能的急性和慢性变化。将家兔分别输注生理盐水或2、4或6微克/千克/分钟NE,持续90分钟。在输注后立即评估心室功能,或在48小时使用离体无射血心脏制剂评估心室功能。用Krebs-Henseleit缓冲液以10 ml/min/g灌注心脏。基线测量后,心脏灌注NE(10(-10)至10(-7)M),在基线和各NE浓度下记录稳态左心室压(LVP)、+dP/dt和-dP/dt。NE输注急性降低左室收缩功能基线。LVP和+dP/dt的降低与NE输注剂量呈负相关。48小时时,所有NE组的LVP和+dP/dt均略有改善,但仅在输注4微克NE的兔心脏中有显著改善。灌注6微克NE后,小鼠心脏收缩功能仍然受到抑制。与生理盐水处理的心脏相比,NE输注后心脏舒张(-dP/dt)功能受损,并且在48小时内没有改善。虽然基线功能下降,但肌病心脏在10(-7)M NE时增加的心室功能与正常心脏相同。这些结果表明:a) NE输注后左室收缩和舒张功能急性受损;b) 48小时内收缩功能改善;c) NE对收缩能力的增强不受损害;d)收缩功能恢复在舒张功能改善之前。
{"title":"Ventricular dysfunction in norepinephrine-induced cardiomyopathy.","authors":"F M Powers,&nbsp;R Pifarre,&nbsp;J X Thomas","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cardiac dysfunction resulting from norepinephrine-induced cardiomyopathy has not been fully investigated. This study evaluates acute and chronic changes in systolic and diastolic function at three levels of norepinephrine (NE)-induced injury. Rabbits were infused with saline or 2, 4, or 6 micrograms/kg/min NE for 90 min. Ventricular function was assessed immediately after infusion or at 48 hr using the isolated non-ejecting heart preparation. Hearts were perfused at 10 ml/min/g with Krebs-Henseleit buffer. After baseline measurements, hearts were perfused with NE (10(-10) to 10(-7) M). Steady state left ventricular pressure (LVP), +dP/dt, and -dP/dt were recorded at baseline and each NE concentration. NE infusion acutely depressed baseline LV systolic function. Decreases in LVP and +dP/dt were inversely related to dose of infused NE. By 48 hr, LVP and +dP/dt improved slightly in all NE groups but improvement was significant only in hearts from rabbits infused with 4 micrograms NE. Systolic function of hearts from animals infused with 6 micrograms NE remained depressed. Diastolic (-dP/dt) function was impaired following NE infusion when compared to saline treated hearts and did not improve within 48 hr. Although baseline function is depressed, myopathic hearts increased ventricular function the same amount as normal hearts at 10(-7) M NE. These findings demonstrate a) impairment in LV systolic and diastolic function acutely after NE infusion, b) improvement in systolic function within 48 hr, c) ability to increase contractility in response to NE is not impaired, and d) recovery of systolic function precedes improvement in diastolic function.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"43 3","pages":"122-9"},"PeriodicalIF":0.0,"publicationDate":"1994-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18850223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Protective effects of a cyclic nitrone antioxidant in animal models of endotoxic shock and chronic bacteremia. 环硝酮抗氧化剂对内毒素休克和慢性菌血症动物模型的保护作用。
Pub Date : 1994-07-01
J F French, C E Thomas, T R Downs, D F Ohlweiler, A A Carr, R C Dage

Evidence of a role for oxygen-derived free radicals in the pathophysiology of endotoxic shock has been found in animal models. However, the importance of free radicals in chronic models of bacterial infection has not been examined. In this study a novel nitrone radical spin trap is described and its activity in animal models of endotoxic shock and chronic bacteremia were explored. MDL 101,002 is a cyclized variant of alpha-phenyl N-tert-butyl nitrone (PBN), an established spin trap. MDL 101,002 can react with free radicals to form persistent adducts as demonstrated by electron paramagnetic resonance (EPR) spectroscopy. This agent is about 10 times more potent than PBN as an in vitro antioxidant and scavenger of hydroxyl radicals. In a rat endotoxic shock model MDL 101,002 (3-30 mg/kg, i.p.) administered 30 min prior to endotoxin (30 mg/kg, i.p.) treatment reduced mortality in a dose-dependent manner. Peroxide-enhanced chemiluminescence in hepatic homogenates from endotoxin treated rats was elevated indicating that oxidative stress and antioxidant depletion was increased. Importantly, treatment with MDL 101,002 (30 mg/kg, i.p.) 30 min prior to, and 120 min following endotoxin, minimized the increase in chemiluminescence. MDL 101,002 also reduced mortality in a model of chronic bacteremia employing implantation of infected fibrin clots into the peritoneal cavity of gentamicin-treated leukopenic rats. MDL 101,002 (2.5 mg/kg/hr) increased survival from 24% to 52% in these rats. These data are consistent with a role for free radicals in the pathophysiology of endotoxic shock and suggest free radicals are also important mediators in chronic models of sepsis.

在动物模型中发现了氧源性自由基在内源性休克病理生理中的作用的证据。然而,自由基在慢性细菌感染模型中的重要性尚未得到检验。本研究描述了一种新的硝基自旋陷阱,并探讨了其在内毒素休克和慢性菌血症动物模型中的活性。MDL 101,002是α -苯基n -叔丁基硝基(PBN)的环化变体,是一种已建立的自旋陷阱。经电子顺磁共振(EPR)谱分析证实,MDL 101002能与自由基反应生成持久性加合物。作为体外抗氧化剂和羟基自由基清除剂,该制剂的效力是PBN的10倍左右。在大鼠内毒素休克模型中,在内毒素治疗(30 mg/kg, i.p.)前30分钟给药MDL 101002 (3-30 mg/kg, i.p.)能以剂量依赖性方式降低死亡率。内毒素处理大鼠肝脏匀浆中过氧化氢增强的化学发光增加,表明氧化应激和抗氧化剂消耗增加。重要的是,内毒素治疗前30分钟和后120分钟,用MDL 101002 (30 mg/kg, i.p.)治疗,最小化了化学发光的增加。MDL 101,002也降低了慢性菌血症模型的死亡率,将感染的纤维蛋白凝块植入庆大霉素治疗的白细胞减少大鼠的腹腔。MDL 101,002 (2.5 mg/kg/hr)使这些大鼠的存活率从24%提高到52%。这些数据与自由基在内毒素休克病理生理中的作用一致,表明自由基也是慢性脓毒症模型的重要介质。
{"title":"Protective effects of a cyclic nitrone antioxidant in animal models of endotoxic shock and chronic bacteremia.","authors":"J F French,&nbsp;C E Thomas,&nbsp;T R Downs,&nbsp;D F Ohlweiler,&nbsp;A A Carr,&nbsp;R C Dage","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Evidence of a role for oxygen-derived free radicals in the pathophysiology of endotoxic shock has been found in animal models. However, the importance of free radicals in chronic models of bacterial infection has not been examined. In this study a novel nitrone radical spin trap is described and its activity in animal models of endotoxic shock and chronic bacteremia were explored. MDL 101,002 is a cyclized variant of alpha-phenyl N-tert-butyl nitrone (PBN), an established spin trap. MDL 101,002 can react with free radicals to form persistent adducts as demonstrated by electron paramagnetic resonance (EPR) spectroscopy. This agent is about 10 times more potent than PBN as an in vitro antioxidant and scavenger of hydroxyl radicals. In a rat endotoxic shock model MDL 101,002 (3-30 mg/kg, i.p.) administered 30 min prior to endotoxin (30 mg/kg, i.p.) treatment reduced mortality in a dose-dependent manner. Peroxide-enhanced chemiluminescence in hepatic homogenates from endotoxin treated rats was elevated indicating that oxidative stress and antioxidant depletion was increased. Importantly, treatment with MDL 101,002 (30 mg/kg, i.p.) 30 min prior to, and 120 min following endotoxin, minimized the increase in chemiluminescence. MDL 101,002 also reduced mortality in a model of chronic bacteremia employing implantation of infected fibrin clots into the peritoneal cavity of gentamicin-treated leukopenic rats. MDL 101,002 (2.5 mg/kg/hr) increased survival from 24% to 52% in these rats. These data are consistent with a role for free radicals in the pathophysiology of endotoxic shock and suggest free radicals are also important mediators in chronic models of sepsis.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"43 3","pages":"130-6"},"PeriodicalIF":0.0,"publicationDate":"1994-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18850224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Nitric oxide mediates the blood flow response to intravenous adenosine in the rabbit. 一氧化氮介导兔对静脉注射腺苷的血流反应。
Pub Date : 1994-07-01
L D McKie, B L Bass, B J Dunkin, J W Harmon

The objective of this study was to determine if nitric oxide mediates the effects of exogenously administered adenosine on peripheral blood flow. An intravenous infusion of adenosine (1.0 mumol/kg/min) into male New Zealand white rabbits caused an increase in blood flow, measured using radiolabeled microspheres, throughout the gastrointestinal tract, as well as in the heart and kidneys. Prior administration of nitro-L-arginine methyl ester (L-NAME) 10 mg/kg i.v. completely blocked the hyperemic effect of adenosine on all organs studied. Administration of L-arginine (300 mg/kg bolus and 50 mg/kg/min infusion) together with L-NAME restored the hyperemic effect of adenosine. This phenomenon was specified to the L-arginine/nitric oxide pathway in that a similar pressor response induced by phenylephrine (1.5 micrograms/kg/min) did not block the effects of adenosine. We conclude that the peripheral vasodilator response to intravenously administered adenosine in the rabbit is mediated by nitric oxide.

本研究的目的是确定一氧化氮是否介导外源性给药腺苷对外周血流量的影响。在雄性新西兰大白兔体内静脉注射腺苷(1.0 μ mol/kg/min),通过放射性标记微球测量整个胃肠道、心脏和肾脏的血流量,结果显示血流量增加。先前给予硝基- l -精氨酸甲酯(L-NAME) 10mg /kg静脉注射完全阻断腺苷对所有器官的充血作用。l -精氨酸(300mg /kg, 50mg /kg/min)联合L-NAME可恢复腺苷的充血作用。这种现象被指定为l -精氨酸/一氧化氮途径,因为苯肾上腺素(1.5微克/千克/分钟)诱导的类似升压反应并没有阻断腺苷的作用。我们得出结论,外周血管扩张剂对静脉滴注腺苷的反应是由一氧化氮介导的。
{"title":"Nitric oxide mediates the blood flow response to intravenous adenosine in the rabbit.","authors":"L D McKie,&nbsp;B L Bass,&nbsp;B J Dunkin,&nbsp;J W Harmon","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The objective of this study was to determine if nitric oxide mediates the effects of exogenously administered adenosine on peripheral blood flow. An intravenous infusion of adenosine (1.0 mumol/kg/min) into male New Zealand white rabbits caused an increase in blood flow, measured using radiolabeled microspheres, throughout the gastrointestinal tract, as well as in the heart and kidneys. Prior administration of nitro-L-arginine methyl ester (L-NAME) 10 mg/kg i.v. completely blocked the hyperemic effect of adenosine on all organs studied. Administration of L-arginine (300 mg/kg bolus and 50 mg/kg/min infusion) together with L-NAME restored the hyperemic effect of adenosine. This phenomenon was specified to the L-arginine/nitric oxide pathway in that a similar pressor response induced by phenylephrine (1.5 micrograms/kg/min) did not block the effects of adenosine. We conclude that the peripheral vasodilator response to intravenously administered adenosine in the rabbit is mediated by nitric oxide.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"43 3","pages":"103-6"},"PeriodicalIF":0.0,"publicationDate":"1994-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18851565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Renal interleukin-1 expression during endotoxemia and gram-negative septicemia in conscious rats. 清醒大鼠内毒素血症和革兰氏阴性败血症时肾白介素-1的表达。
Pub Date : 1994-07-01
Z Laszik, T Nadasdy, L D Johnson, M R Lerner, D Brackett, F G Silva

Endotoxin-induced cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF) are thought to contribute to the proinflammatory effects of endotoxin in gram-negative infections. Using a conscious rat model of sepsis, induced by intravenous challenge with LD95 doses of endotoxin (n = 24) or live Escherichia coli (E. coli) (n = 24), we examined frozen sections of kidney at various intervals for evidence of IL-1 alpha and TNF alpha expression. A transient glomerular endothelial IL-1 alpha expression was demonstrated at 30 and 90 min after initiation of the sepsis in both endotoxin and E. coli-treated animals using immunohistochemistry. The endothelial IL-1 alpha expression as determined by immunohistochemistry occurred at the same time as IL-1 alpha mRNA expression, as determined by Northern blot analysis. The glomerular endothelial IL-1 alpha expression coincided with a slight but significant increase in the number of the glomerular polymorphonuclear leukocytes as identified by naphthol AS-D chloroacetate esterase enzyme histochemical reaction. Glomerular endothelial IL-1 alpha expression was virtually absent by 180 and 360 min. No TNF alpha expression was detected in the renal tissues at any time interval. Neither alpha-naphthyl acetate esterase-positive nor acid phosphatase-positive monocytes/macrophages were identified in the glomeruli. Our findings provide direct in vivo evidence that the IL-1 alpha gene product is expressed locally in the kidney by glomerular endothelial cells in this septic rat model.

内毒素诱导的细胞因子,如白细胞介素-1 (IL-1)和肿瘤坏死因子(TNF)被认为有助于内毒素在革兰氏阴性感染中的促炎作用。采用LD95剂量内毒素(n = 24)或活大肠杆菌(E. coli) (n = 24)引起的脓毒症的意识大鼠模型,我们在不同时间间隔检查肾脏冷冻切片,以寻找IL-1 α和TNF α表达的证据。免疫组织化学方法显示,内毒素和大肠杆菌治疗的动物在脓毒症开始后30和90分钟,肾小球内皮细胞中有短暂的IL-1 α表达。免疫组化检测内皮细胞IL-1 α的表达与Northern blot检测IL-1 α mRNA的表达同时发生。通过萘酚as - d氯乙酸酯酶组织化学反应发现,肾小球内皮IL-1 α的表达与肾小球多形核白细胞数量的轻微但显著增加相一致。肾小球内皮IL-1 α在180分钟和360分钟内几乎没有表达。肾组织在任何时间间隔内均未检测到TNF α的表达。肾小球中未发现α -乙酸萘酯酶阳性或酸性磷酸酶阳性的单核/巨噬细胞。我们的研究结果提供了直接的体内证据,证明IL-1 α基因产物在脓毒症大鼠模型中通过肾小球内皮细胞在肾脏中局部表达。
{"title":"Renal interleukin-1 expression during endotoxemia and gram-negative septicemia in conscious rats.","authors":"Z Laszik,&nbsp;T Nadasdy,&nbsp;L D Johnson,&nbsp;M R Lerner,&nbsp;D Brackett,&nbsp;F G Silva","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Endotoxin-induced cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF) are thought to contribute to the proinflammatory effects of endotoxin in gram-negative infections. Using a conscious rat model of sepsis, induced by intravenous challenge with LD95 doses of endotoxin (n = 24) or live Escherichia coli (E. coli) (n = 24), we examined frozen sections of kidney at various intervals for evidence of IL-1 alpha and TNF alpha expression. A transient glomerular endothelial IL-1 alpha expression was demonstrated at 30 and 90 min after initiation of the sepsis in both endotoxin and E. coli-treated animals using immunohistochemistry. The endothelial IL-1 alpha expression as determined by immunohistochemistry occurred at the same time as IL-1 alpha mRNA expression, as determined by Northern blot analysis. The glomerular endothelial IL-1 alpha expression coincided with a slight but significant increase in the number of the glomerular polymorphonuclear leukocytes as identified by naphthol AS-D chloroacetate esterase enzyme histochemical reaction. Glomerular endothelial IL-1 alpha expression was virtually absent by 180 and 360 min. No TNF alpha expression was detected in the renal tissues at any time interval. Neither alpha-naphthyl acetate esterase-positive nor acid phosphatase-positive monocytes/macrophages were identified in the glomeruli. Our findings provide direct in vivo evidence that the IL-1 alpha gene product is expressed locally in the kidney by glomerular endothelial cells in this septic rat model.</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"43 3","pages":"115-21"},"PeriodicalIF":0.0,"publicationDate":"1994-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18850222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Circulatory shock
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1