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Lung and systemic oxidant and antioxidant activity after graded smoke exposure in the rat. 分级烟雾暴露后大鼠肺和全身的氧化和抗氧化活性。
Pub Date : 1994-01-01
C Lalonde, L Picard, C Campbell, R Demling

We wanted to determine the effect of a graded smoke inhalation on lung and systemic oxidant stress, and its relationship to physiological and histological change. Male Wistar rats were given 12 breaths of 10 ml/kg (n = 8) (group 1) or 20 ml/kg (n = 8) (group 2) tidal volume, using cotton toweling smoke through the trachea using positive pressure. Rats were monitored, then killed at 24 hr. Data were compared to controls (n = 8). Peak group 1 and group 2 carboxyhemoglobins were 22 +/- 6 and 46 +/- 6%, with a mortality prior to 24 hr of 14% and 50%, respectively. Group 1 rats showed only moderate lung dysfunction but with severe airway inflammation and edema, alveolar inflammation and atelectasis, with a decrease in PaO2 from the control of 96 +/- 4 to 72 +/- 5 torr. No increase in lung, liver, or kidney oxidant-induced lipid peroxidation, measured as malondialdehyde lung, liver, or kidney oxidant-induced lipid peroxidation, measured as malondialdehyde (MDA), or decrease in the antioxidant defenses catalase was noted. Group 2 rats demonstrated severe airways edema, alveolar atelectasis, and alveolar edema, and a PaO2 decreasing below 60 torr, corresponding with a 3-fold increase in lung tissue MDA and 35% decrease in catalase. In addition, liver and kidney tissue MDA doubled, and catalase activity decreased by 40%. Increased oxygen consumption was also demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

我们想要确定分级烟雾吸入对肺和全身氧化应激的影响,以及它与生理和组织学变化的关系。雄性Wistar大鼠按潮气量10 ml/kg (n = 8)(1组)或20 ml/kg (n = 8)(2组)呼吸12次,用棉毛巾正压吸烟通过气管。对大鼠进行监测,并于24小时处死。将数据与对照组(n = 8)进行比较。峰值组1和组2的羧血红蛋白分别为22 +/- 6%和46 +/- 6%,24小时前死亡率分别为14%和50%。1组大鼠仅出现中度肺功能障碍,但出现严重的气道炎症和水肿、肺泡炎症和肺不张,PaO2较对照组(96 +/- 4)下降至72 +/- 5 torr。肺、肝或肾氧化剂诱导的脂质过氧化(以丙二醛测量)没有增加,肺、肝或肾氧化剂诱导的脂质过氧化(以丙二醛(MDA)测量)也没有减少抗氧化防御过氧化氢酶。2组大鼠出现严重气道水肿、肺泡不张、肺泡水肿,PaO2降至60 torr以下,肺组织MDA升高3倍,过氧化氢酶降低35%。肝脏和肾脏组织MDA增加一倍,过氧化氢酶活性降低40%。氧气消耗也增加了。(摘要删节250字)
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引用次数: 0
Systemic and regional hemodynamic changes during endotoxin or platelet activating factor (PAF)-induced shock in rats. 内毒素或血小板活化因子(PAF)引起的大鼠休克时的全身和局部血流动力学变化。
Pub Date : 1993-12-01
M F Mulder, A A van Lambalgen, A A van Kraats, P G Scheffer, A A Bouman, G C van den Bos, L G Thijs

To evaluate the role of platelet activating factor (PAF) during endotoxin shock, we compared its effects with those of endotoxin. We measured arterial pressure (MAP), heart rate (HR), cardiac output (CO; thermodilution), arterial lactate (Calact), organ blood flow (radioactive microspheres), and organ vascular resistance in four groups of anesthetized (pentobarbital) male Wistar rats (n = 7 per group), infused from t = 0 to t = 60 min with saline (group C: time matched control), endotoxin Escherichia coli O127:B8, 8 mg.kg-1 (group E), a "low PAF dose" (1 microgram.kg-1) to cause the same decrease in MAP as in group E (group PL), or a "high PAF dose" (3 micrograms.kg-1) to cause the same decrease in CO as in group E (group PH). At t = 60 min, MAP had decreased by 33% in E and PL, and by 55% in PH group. CO had decreased by 41% in the E and PH group. Calact had increased in the E and PH group by 300 and 200%, respectively. In the E, PL and PH group, coronary vascular resistance decreased. In the splanchnic organs, endotoxin caused a decrease in blood flow due to vasoconstriction, whereas PAF (both concentrations) caused vasodilation (except for spleen). Renal vascular resistance decreased (P < 0.05) in the PL group. In all groups, vascular resistance had increased (P < 0.05) in skin, and not changed in skeletal muscle (P < 0.05). Thus, hemodynamic changes after PAF infusion were partially similar to those after endotoxin infusion (coronary vasodilation and vasoconstriction in spleen and skin).(ABSTRACT TRUNCATED AT 250 WORDS)

为了评价血小板活化因子(PAF)在内毒素休克中的作用,我们将其与内毒素的作用进行了比较。我们测量了动脉压(MAP)、心率(HR)、心输出量(CO);四组(戊巴比妥)麻醉雄性Wistar大鼠(每组7只),从t = 0至t = 60 min注射生理盐水(C组:时间匹配对照),内毒素大肠杆菌O127:B8, 8 mg,观察其动脉乳酸(Calact),器官血流(放射性微球)和器官血管阻力。“低PAF剂量”(1微克。公斤。1)导致与E组(PL组)相同的MAP减少,或“高PAF剂量”(3微克。公斤。1)导致与E组(PH组)相同的CO减少。在t = 60 min时,E组和PL组MAP下降33%,PH组下降55%。E和PH组CO降低了41%。E组和PH组的Calact分别增加了300和200%。在E、PL和PH组,冠状动脉血管阻力降低。在内脏器官中,内毒素引起血管收缩导致血流减少,而PAF(两种浓度)引起血管舒张(脾脏除外)。PL组肾血管阻力降低(P < 0.05)。各组皮肤血管阻力升高(P < 0.05),骨骼肌血管阻力无明显变化(P < 0.05)。因此,PAF输注后的血流动力学变化与内毒素输注后的血流动力学变化部分相似(脾脏和皮肤的冠状动脉血管扩张和血管收缩)。(摘要删节250字)
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引用次数: 0
Inhibition of CD18-dependent adherence of polymorphonuclear leukocytes does not affect liver oxygen consumption in fecal peritonitis in pigs. 抑制cd18依赖性多形核白细胞粘附不影响猪粪便性腹膜炎的肝脏耗氧量。
Pub Date : 1993-12-01
S Wollert, I Rasmussen, C Lundberg, B Gerdin, D Arvidsson, U Haglund

We tested the hypothesis that circulating polymorphonuclear leukocytes (PMNs), adhering to endothelium of the liver vascular bed are involved in the alterations of the liver oxygen delivery (DO2) and consumption (VO2) that is a result of fecal peritonitis in pigs. Twenty-two pigs were divided into three groups. Animals in group I (n = 7) served as controls. Fecal peritonitis was induced in groups II (n = 7) and III (n = 8). Animals in group III were pretreated with IB4, a monoclonal anti-CD18 antibody inhibiting adherence of PMNs to the endothelium. Peritonitis increased liver VO2 in groups II and III in spite of decreased liver DO2. In group I, circulating PMNs increased during the experimental period. Sepsis caused a decrease in the number of circulating PMNs in group II, an effect that was fully counteracted in group III, where the number of PMNs rose to control level. Myeloperoxidase activity and morphometric determination of PMN infiltration in liver biopsies virtually paralleled the circulating PMN count. Although fecal peritonitis is followed by a CD18-dependent leukopenia that can be counteracted by pretreatment with an anti-CD18 antibodies, this treatment does not affect the alteration in liver VO2 and DO2 observed.

我们验证了一种假设,即粘附在肝脏血管床内皮上的循环多形核白细胞(PMNs)参与了猪粪性腹膜炎导致的肝脏氧输送(DO2)和耗氧量(VO2)的改变。22头猪被分为三组。第一组(n = 7)为对照组。II组(n = 7)和III组(n = 8)诱导粪性腹膜炎。III组用IB4(一种抑制PMNs粘附内皮的单克隆抗cd18抗体)预处理。腹膜炎增加了II组和III组的肝脏VO2,尽管肝脏DO2降低。在I组,循环pmn在实验期间增加。脓毒症导致II组循环pmn数量减少,在III组完全抵消了这种影响,其中pmn数量上升到控制水平。髓过氧化物酶活性和肝活检中PMN浸润的形态测定几乎与循环PMN计数平行。虽然粪便性腹膜炎之后会出现cd18依赖性白细胞减少,可以通过抗cd18抗体预处理来抵消,但这种治疗并不影响肝脏VO2和DO2的改变。
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引用次数: 0
Increase in the plasma concentration of reduced glutathione observed in rats with liver damage induced by lipopolysaccharide/D-galactosamine: effects of ulinastatin, a urinary trypsin inhibitor. 脂多糖/ d -半乳糖胺所致肝损伤大鼠血浆还原性谷胱甘肽浓度升高:尿胰蛋白酶抑制剂乌司他丁的作用
Pub Date : 1993-12-01
H Okabe, K Irita, K Kurosawa, K Tagawa, A Koga, M Yamakawa, J Yoshitake, S Takahashi

The changes in plasma concentrations of reduced glutathione were investigated in rats with endotoxin hepatitis. An increase in serum alanine aminotransferase activity and in serum total bilirubin concentration was observed 12 hr after the intraperitoneal co-administration of small doses of Escherichia coli lipopolysaccharide and D-galactosamine in starved rats. At the same time, an increase in the plasma concentration of reduced glutathione was also observed. The increase in reduced glutathione from 14 +/- 2 to 20 +/- 9 microM (n = 11, P < 0.05) correlated well with that in serum alanine aminotransferase activity. Ulinastatin, a potent inhibitor of polymorphonuclear leukocyte elastase, partially counteracted all of these changes. Ulinastatin also reduced histological liver damage induced by endotoxin. We conclude that the increase in the plasma concentration of reduced glutathione reflects hepatocellular damage associated with endotoxin hepatitis. The partial reversal of the damage by ulinastatin is consistent with the proposal that the activation of polymorphonuclear leukocytes is involved in endotoxin hepatitis.

研究了内毒素肝炎大鼠血浆还原性谷胱甘肽浓度的变化。在饥饿大鼠腹腔注射小剂量大肠杆菌脂多糖和d -半乳糖胺12小时后,观察到血清丙氨酸转氨酶活性和血清总胆红素浓度升高。同时,还观察到血浆还原性谷胱甘肽浓度升高。还原型谷胱甘肽从14 +/- 2 μ m增加到20 +/- 9 μ m (n = 11, P < 0.05),与血清丙氨酸转氨酶活性的增加密切相关。乌司他丁,一种有效的多形核白细胞弹性酶抑制剂,部分抵消了所有这些变化。乌司他丁还能减轻内毒素引起的肝组织损伤。我们得出结论,血浆还原型谷胱甘肽浓度的增加反映了内毒素肝炎相关的肝细胞损伤。乌司他丁对损伤的部分逆转与多形核白细胞的激活参与内毒素肝炎的建议是一致的。
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引用次数: 0
Dextran vs. hydroxyethylstarch in inhibition of postischemic leukocyte adherence in striated muscle. 右旋糖酐与羟乙基淀粉对横纹肌缺血后白细胞粘附的抑制作用。
Pub Date : 1993-12-01
M D Menger, C Thierjung, F Hammersen, K Messmer

Microvascular injury associated with ischemia/reperfusion (I/R) is characterized by both "no reflow" and "reflow paradox." Prophylactic isovolemic hemodilution with dextran 60 to a hematocrit of 30% has been shown to prevent I/R-induced capillary no reflow in striated muscle. The objective of the present study was to analyze whether hemodilution prior to ischemia has the potential to reduce postischemic leukocyte-endothelium interaction, which is known to be one of the major components of I/R-induced reflow paradox. Syrian golden hamsters (n = 21) were fitted with a dorsal skinfold chamber, which contains striated muscle and subcutaneous tissue and allows for repetitive analyses of the microcirculation by means of intravital fluorescence microscopy. Four hr of pressure-induced ischemia and 30 min of subsequent reperfusion (controls, n = 7) resulted in a significant (P < 0.05) increase of microvascular leukocyte accumulation (40,630 +/- 12,731 mm-3) and adherence to the endothelial lining of postcapillary venules (74.2% +/- 11.5%) when compared to preischemic baseline (7,502 +/- 1,700 mm-3 and 3.4% +/- 1.0%, respectively). Recovery was not complete after an observation period of 24 hr reperfusion [13,735 +/- 2,666 mm-3 (P < 0.05) and 18.5% +/- 6.0% (P < 0.05)]. Prophylactic isovolemic hemodilution with 6% dextran 60 (Dx60) to a hematocrit of 30% (Dx60, n = 7) significantly attenuated postischemic leukocyte accumulation (23,402 +/- 13,837 mm-3; P < 0.05 vs. controls) and adherence (22.6% +/- 6.4%; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

与缺血/再灌注(I/R)相关的微血管损伤具有“无回流”和“回流悖论”两种特征。预防性等容血液稀释用葡聚糖60至30%的血细胞比容已被证明可以防止I/ r诱导的横纹肌毛细血管无回流。本研究的目的是分析缺血前的血液稀释是否有可能减少缺血后白细胞-内皮细胞相互作用,这是已知的I/ r诱导回流悖论的主要组成部分之一。叙利亚金仓鼠(n = 21)安装了背侧皮褶腔,其中包含横切肌和皮下组织,并允许通过活体荧光显微镜重复分析微循环。与缺血前基线(7502 +/- 1700 mm-3和3.4% +/- 1.0%)相比,4小时压力性缺血和随后30分钟再灌注(对照组,n = 7)导致微血管白细胞积累(40,630 +/- 12,731 mm-3)和毛细血管后小静脉内皮内层粘附(74.2% +/- 11.5%)显著(P < 0.05)增加。24小时再灌注观察后恢复不完全[13,735 +/- 2,666 mm-3 (P < 0.05)和18.5% +/- 6.0% (P < 0.05)]。预防性等容血液稀释6%葡聚糖60 (Dx60)至30%的红细胞比容(Dx60, n = 7)可显著减少缺血后白细胞积累(23,402 +/- 13,837 mm-3;P < 0.05,对照组)和依从性(22.6% +/- 6.4%;P < 0.05)。(摘要删节250字)
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引用次数: 0
Electrophysiologic properties of isolated adult cardiomyocytes from septic rats. 脓毒症大鼠离体成年心肌细胞的电生理特性。
Pub Date : 1993-12-01
S N Wu, S I Lue, S L Yang, H K Hsu, M S Liu

In this study, we examined the effect of sepsis on the electrical properties of isolated ventricular myocytes. Sepsis was induced by cecal ligation and puncture (CLP). The control rats were sham-operated. Membrane potentials and ionic currents in isolated cardiac myocytes were measured by the tight-seal, whole-cell patch-clamp technique. The results show that the resting membrane potentials of heart cells were significantly lower in the septic group (18 hr post-CLP) than those in the control group. However, there was no significant difference in action potential duration of 50% and 90% repolarization between the two groups of cells. In voltage-clamp experiments, isoproterenol (10 nM), a beta-adrenergic agonist, caused an increase in L-type calcium current (ICa,L) in a similar magnitude in myocytes isolated from the control and septic rats. Furthermore, isoproterenol failed to modify the time constants for ICa,L inactivation and the overall shape of current-voltage relationship for both groups of cells. These results indicate that formation of a G omega seal and subsequent tight-seal whole-cell recording with patch-clamp technique can be performed in heart cells derived from CLP-induced septic rats, and that septic rat heart is capable of responding effectively to beta-adrenergic stimulation.

在这项研究中,我们检查了脓毒症对分离心室肌细胞电学特性的影响。盲肠结扎穿刺(CLP)致脓毒症。对照大鼠是假手术。采用全细胞膜片钳技术测定离体心肌细胞的膜电位和离子电流。结果显示,脓毒症组心脏细胞静息膜电位(clp后18小时)明显低于对照组。而两组细胞在50%复极和90%复极时的动作电位持续时间无显著差异。在电压钳实验中,异丙肾上腺素(10 nM),一种β -肾上腺素能激动剂,在从对照组和脓毒症大鼠分离的肌细胞中引起相似幅度的L型钙电流(ICa,L)增加。此外,异丙肾上腺素未能改变两组细胞的ICa、L失活的时间常数和电流-电压关系的整体形状。这些结果表明,在clp诱导的脓毒症大鼠心脏细胞中可以形成G - omega封闭并随后使用膜片钳技术进行全细胞封闭记录,并且脓毒症大鼠心脏能够有效地响应β -肾上腺素能刺激。
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引用次数: 0
Macrophage treatment in suckling rat endotoxic shock. 巨噬细胞治疗哺乳大鼠内毒素休克。
Pub Date : 1993-12-01
M Goto, R C Lichtenberg, M E Gottschalk, C L Anderson, H L Mathews, W P Zeller

Gram-negative sepsis/septic shock in the human newborn continues to be a severe medical problem because of significant mortality and morbidity. Since macrophages detoxify endotoxin, a decreased number of macrophages may contribute to the newborn's sensitivity to endotoxin. In this study, peritoneal macrophages were used for the treatment of endotoxic shock in 10-day-old rats, and 24-hr mortality, plasma glucose, and lactate concentrations were monitored. Peritoneal macrophages were harvested from adult or 10-day-old rats. Caseinate-stimulated macrophages from adult and 10-day-old rats significantly decreased the mortality of 10-day-old rat endotoxic shock from 90% to 37.5% and 44.4%, respectively. Resident macrophages from adult and 10-day-old rats also decreased the mortality from 90% to 12.5% and 45.4%, respectively. Peritoneal macrophages from adult rats significantly ameliorated hypoglycemia during endotoxic shock in a dose-dependent manner. Macrophage treatment decreased plasma endotoxin concentration (P < 0.05). Macrophage treatment was important for host defense.

人类新生儿的革兰氏阴性败血症/感染性休克仍然是一个严重的医学问题,因为它具有很高的死亡率和发病率。由于巨噬细胞解毒内毒素,巨噬细胞数量的减少可能有助于新生儿对内毒素的敏感性。在这项研究中,腹腔巨噬细胞用于治疗10日龄内源性休克大鼠,并监测24小时死亡率、血浆葡萄糖和乳酸浓度。取成年大鼠或10日龄大鼠的腹膜巨噬细胞。成年大鼠和10日龄大鼠的酪氨酸刺激巨噬细胞显著降低了10日龄大鼠内毒素休克的死亡率,分别从90%降至37.5%和44.4%。来自成年大鼠和10日龄大鼠的常驻巨噬细胞也使死亡率分别从90%降低到12.5%和45.4%。成年大鼠腹腔巨噬细胞以剂量依赖的方式显著改善内毒素休克期间的低血糖。巨噬细胞处理降低了血浆内毒素浓度(P < 0.05)。巨噬细胞治疗对宿主防御很重要。
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引用次数: 0
Ketoisocaproate infusion improves survival from experimental sepsis by an antioxidant mechanism. 酮异己酸输注通过抗氧化机制提高实验性败血症的生存率。
Pub Date : 1993-12-01
T Yonekura, S Matsusue, M Walser

Sepsis was induced in rats by cecal ligation and puncture. A nutrient mixture was infused that also contained either (A) sodium 2-ketoisocaproate (NaKIC) or (B) NaHCO3, at 18.75 mmol kg/day. In group A, 34 of 43 rats (79%) survived, while only 24 of 44 rats (55%) in group B survived (P < 0.02). In a second experiment, cecal ligation and puncture were performed 1 week after bilateral adrenalectomy or sham adrenalectomy. All adrenalectomized rats died within 2 days of CLP, whether corticosterone replacement level was low, normal, or high. Four of eight sham-adrenalectomized rats receiving NaHCO3 died, but none of seven receiving NaKIC died. Combining both experiments by ANOVA, the effect of KIC on survival in adrenal-intact animals is highly significant (P = 0.002). In NaKIC-infused rats, blood level of pyruvate was higher on day 5 (P < 0.01), and plasma as well as blood levels of oxidized glutathione and ratio of oxidized/reduced glutathione were significantly lower. We conclude that KIC infusion improves survival of septic rats by an antioxidant mechanism, probably involving reaction with hydrogen peroxide.

用盲肠结扎法和穿刺法诱导大鼠脓毒症。同时注入含有(A) 2-酮异己酸钠(NaKIC)或(B) NaHCO3的营养混合物,剂量为18.75 mmol kg/d。A组43只大鼠中有34只(79%)存活,B组44只大鼠中只有24只(55%)存活(P < 0.02)。在第二个实验中,在双侧肾上腺切除术或假肾上腺切除术后1周进行盲肠结扎和穿刺。无论皮质酮替代水平低、正常或高,所有肾上腺切除大鼠均在CLP后2天内死亡。接受NaHCO3治疗的8只假肾上腺切除大鼠中有4只死亡,但接受NaKIC治疗的7只没有死亡。经方差分析,KIC对肾上腺未损伤大鼠的存活率有显著影响(P = 0.002)。注射nakic的大鼠第5天血中丙酮酸水平升高(P < 0.01),血浆和血中氧化谷胱甘肽水平及氧化/还原性谷胱甘肽比值显著降低。我们得出结论,KIC输注通过抗氧化机制提高脓毒症大鼠的存活率,可能涉及与过氧化氢的反应。
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引用次数: 0
Subcutaneous and gut tissue perfusion and oxygenation changes as related to oxygen transport in experimental peritonitis. 实验性腹膜炎的皮下和肠组织灌注和氧合变化与氧转运的关系。
Pub Date : 1993-12-01
J B Antonsson, K Kuttila, J Niinikoski, U H Haglund

Peritonitis and septic shock may lead to tissue hypoxia, but this risk is not identical in all organ systems. This study was undertaken to measure changes in tissue oxygenation and perfusion in the gut wall and subcutaneous tissue, respectively, and to examine their relation to oxygen delivery and consumption. Twelve pigs were anesthesized and mechanically ventilated. An ultrasonic flow probe was placed around the superior mesenteric artery for registration of blood flow. A mesenteric vein was cannulated for blood sampling. For calculation of gut intramural pH (pHi), a Silastic balloon (Tonomitor) was placed in the lumen of the midileum. pHi was calculated from tonometrically measured PCO2 and arterial bicarbonate concentration. The subcutaneous PO2 was measured by means of an oxygen-permeable Silastic tube implanted in the subcutis of the abdominal wall. Oxygen delivery (DO2) and consumption (VO2) were determined for the gut as well as for the whole body. In six randomly allocated animals, peritonitis was induced after a stabilization period of at least 1 hr, by instillation of autologous faeces into the abdominal cavity, while the other six animals served as controls. The animals were then followed for 5 hr. pHi remained stable in the control group, whereas a drop from 7.37 to 7.02 took place in the peritonitis group. In the test group, subcutaneous oxygen tension (PscO2) already began to fall 1 hr after the induction of peritonitis, and gained the minimum at the end of the study. In peritonitis, a moderate correlation was seen between pHi and DO2 (r = 0.51 +/- 0.16); no statistical difference was noted if pHi was correlated to gut DO2 (r = 0.56 +/- 0.18).(ABSTRACT TRUNCATED AT 250 WORDS)

腹膜炎和感染性休克可导致组织缺氧,但这种风险在所有器官系统中并不相同。本研究分别测量了肠壁和皮下组织的组织氧合和灌注的变化,并研究了它们与氧气输送和消耗的关系。对12头猪进行麻醉和机械通气。超声血流探头放置在肠系膜上动脉周围以记录血流。肠系膜静脉插管取血样。为了计算肠道内pH值(pHi),在中间管腔内放置一个硅胶球囊(压力计)。pHi是根据血压计测量的二氧化碳分压和动脉碳酸氢盐浓度计算的。通过在腹壁皮下植入一根可透氧的硅胶管来测量皮下PO2。测定了肠道和全身的氧输送(DO2)和耗氧量(VO2)。在随机分配的6只动物中,通过向腹腔内注入自身粪便,在至少1小时的稳定期后诱发腹膜炎,而其他6只动物作为对照。然后对这些动物进行5小时的随访。对照组pHi保持稳定,而腹膜炎组pHi从7.37下降到7.02。实验组在腹膜炎诱导后1小时皮下氧张力(PscO2)已开始下降,并在研究结束时达到最小值。在腹膜炎中,pHi与DO2呈正相关(r = 0.51 +/- 0.16);如果pHi与肠道DO2相关,则无统计学差异(r = 0.56 +/- 0.18)。(摘要删节250字)
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引用次数: 0
Transmigration routes and a delayed systemic hypotension in rats after intraperitoneal injection of endotoxin from Escherichia coli. 腹腔注射大肠杆菌内毒素后大鼠的转运途径和迟发性全身性低血压。
Pub Date : 1993-11-01
K Sugimoto, M Kawamura, M Katori, M Shindo, T Ohwada

An intraperitoneal injection of endotoxin (ETX; 3 mg/kg) to rats caused gradual decrease in the systemic arterial blood pressure for up to 3 hr, together with decrease in heart rate, increase in hematocrit, and changes in the core temperature (an initial increase and a subsequent decrease). Pretreatment of rats with indomethacin (10 mg/kg, p.o.) prevented the decrease in the systemic blood pressure and the changes in other three parameters. The intraperitoneal injection of ETX also induced a gradual increase in exudation of plasma for up to 3 hr, with increased levels of prostaglandin (PG) E2 and 6-keto-PGF1 alpha in the peritoneal exudate. Indomethacin inhibited the exudation of plasma. The levels of ETX in the arterial and portal venous plasmas began to increase 5 min after the intraperitoneal injection of ETX, and reached levels on the order of micrograms per milliliter plasma 10-20 min after the injection. The levels of ETX in the right and left thoracic lymph nodes, but not in the mesenteric lymph nodes, increased in parallel with those in the systemic arterial plasma. In conclusion, the delayed hypotension may be attributable to the mesenteric vasodilatation induced by PGs generated in the peritoneal cavity, and the ETX injected entered the systemic circulation mainly through lymphatic vessels, but in the initial stage, a part of ETX may be transmigrated into portal vein through damaged intestine.

腹腔注射内毒素(ETX;3 mg/kg)引起大鼠全身动脉血压逐渐下降,持续3小时,同时心率下降,红细胞压积增加,核心温度变化(最初升高,随后降低)。吲哚美辛(10mg /kg, p.o.)预处理大鼠对全身血压的降低及其他3项指标的改变均有抑制作用。腹腔注射ETX也诱导血浆渗出量逐渐增加长达3小时,并增加了腹膜渗出液中前列腺素(PG) E2和6-酮- pgf1 α的水平。吲哚美辛抑制血浆渗出。腹腔注射ETX后5 min动脉和门静脉血浆中ETX水平开始升高,注射后10 ~ 20 min达到微克/毫升血浆水平。左、右胸椎淋巴结的ETX水平与全身动脉血浆水平平行升高,但肠系膜淋巴结未见ETX水平升高。综上所述,迟发性低血压可能与腹膜腔内产生的PGs引起肠系膜血管扩张有关,注射的ETX主要通过淋巴管进入体循环,但在初始阶段,部分ETX可能通过受损的肠道转移到门静脉。
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引用次数: 0
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Circulatory shock
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