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Effects of free radical scavengers, methylprednisolone, and ulinastatin on acute xanthine and xanthine oxidase-induced lung injury in rats. 自由基清除剂、甲基强的松龙和乌司他丁对大鼠急性黄嘌呤和黄嘌呤氧化酶诱导的肺损伤的影响。
Pub Date : 1994-06-01
M Cai, R Ogawa

We investigated the role of free radicals, especially from activated neutrophils, in acute xanthine and xanthine oxidase-induced lung injury in rats. We evaluated the effects of intravenously administered intracellular and extracellular free radical scavengers (for O2-., H2O2, and .OH), methylprednisolone (MP), and Ulinastatin (UST, a protease inhibitor), on this animal model of lung injury. At 5 min prior to the intrabronchial injection of a mixture of xanthine (X, 100 nmol) and xanthine oxidase (XO, 1 unit) used to induce unilateral lung damage, rats were pretreated intravenously with superoxide dismutase (SOD, 40 mg/kg), SOD (40 mg/kg) plus catalase (CAT, 30 mg/kg), dimethylthiourea (DMTU, 500 mg/kg), N-2-mercaptopropionyl glycine (MPG, 20 mg/kg), MP, 30 mg/kg, and UST, 50,000 units/kg. Each scavenger was infused intravenously at one-half the initial dose for 20 min after intrabronchial injection; 3 hr later, we examined the wet/dry lung weight ratios and the levels of thiobarbituric acid-reactive substances (TBARS) in lung tissue. Intrabronchial injection of the X/XO mixture markedly increased wet/dry lung weight ratios and lung tissue content of TBARS. Histopathologic changes were observed in the injected lung as well. Pretreatment with SOD + CAT, DMTU, and UST significantly reduced the increases in wet/dry lung weight ratios and lung tissue content of TBARS induced by the intrabronchial injection of the X/XO mixture. Our data suggest indirectly that free radicals (H2O2, .OH) and proteases from activated neutrophils may contribute, in part, to the lung damage induced by the O2-.-generating system of xanthine and xanthine oxidase.

我们研究了自由基,特别是来自活化中性粒细胞的自由基在大鼠急性黄嘌呤和黄嘌呤氧化酶诱导的肺损伤中的作用。我们评估了静脉注射细胞内和细胞外自由基清除剂(O2-)的效果。(H2O2和。oh)、甲基强的松龙(MP)和乌司他丁(UST,一种蛋白酶抑制剂)作用于肺损伤动物模型。在支气管内注射用于诱导单侧肺损伤的黄嘌呤(X, 100 nmol)和黄嘌呤氧化酶(XO, 1单位)的混合物前5分钟,大鼠静脉注射超氧化物歧化酶(SOD, 40 mg/kg)、SOD (40 mg/kg)加过氧化氢酶(CAT, 30 mg/kg)、二甲硫脲(DMTU, 500 mg/kg)、n -2-巯基丙酰甘氨酸(MPG, 20 mg/kg)、MP, 30 mg/kg和UST, 50,000单位/kg。支气管内注射后,以初始剂量的一半静脉滴注每种清道夫20分钟;3小时后,我们检测肺干/湿重量比和肺组织中硫代巴比妥酸反应物质(TBARS)的水平。支气管内注射X/XO混合物可显著提高肺干湿重比和肺组织中TBARS含量。注射后肺组织病理改变。SOD + CAT、DMTU和UST预处理可显著降低X/XO混合物支气管内注射引起的肺干湿重比和肺组织TBARS含量的升高。我们的数据间接表明,自由基(H2O2, . oh)和活化中性粒细胞的蛋白酶可能在一定程度上导致O2-诱导的肺损伤。黄嘌呤和黄嘌呤氧化酶的生成系统。
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引用次数: 0
Beneficial effects of extracellular glutathione against endotoxin-induced liver injury during ischemia and reperfusion. 细胞外谷胱甘肽对缺血再灌注时内毒素诱导的肝损伤的有益作用。
Pub Date : 1994-06-01
P Liu, M A Fisher, A Farhood, C W Smith, H Jaeschke

The potential beneficial effect of hepatocellular glutathione against inflammatory liver damage was investigated in a model of endotoxin-enhanced ischemia-reperfusion injury. Animals were subjected to 20 min of hepatic ischemia, followed by 4 hr of reperfusion. The injection of 0.5 mg/kg Salmonella enteritidis endotoxin potentiated liver injury and the postischemic oxidant stress, as indicated by increased plasma levels of glutathione disulfide. Depletion of hepatic glutathione levels by > 90% with phorone and inhibition of glutathione synthesis with buthionine sulfoximine further increased liver injury in this model, as indicated by enhancement of plasma alanine aminotransferase activities from 2,234 +/- 122 U/L to 4,024 +/- 282 U/L. Continuous infusion of a glutathione (GSH) solution in GSH-depleted animals (22 mumol/kg/hr) attenuated reperfusion injury by 55%. In vitro experiments demonstrated the capability of GSH to react rapidly with reactive oxygen species, such as hydrogen peroxide (H2O2) and hypochlorous acid (HOCl). Only H2O2 oxidized GSH quantitatively to its disulfide; HOCl oxidized GSH to higher oxidation states. These data support the hypothesis that the enhanced release of hepatocellular GSH functions as a defense mechanism against reactive oxygen species generated by inflammatory cells during endotoxemia and reperfusion. This internal defense system of the liver may be of general importance in preventing, or at least limiting, liver damage by reactive oxygen generated in particular by Kupffer cells during their physiological function to remove gut-derived endotoxin and bacteria.

在内毒素增强的缺血再灌注损伤模型中,研究了肝细胞谷胱甘肽对炎症性肝损伤的潜在有益作用。动物肝缺血20分钟,再灌注4小时。注射0.5 mg/kg肠炎沙门氏菌内毒素可增强肝损伤和化学反应后氧化应激,结果显示血浆谷胱甘肽二硫化物水平升高。甲硫酮使肝脏谷胱甘肽水平降低90%以上,丁硫氨酸亚砜抑制谷胱甘肽合成,进一步加重了该模型的肝损伤,血浆丙氨酸转氨酶活性从2,234 +/- 122 U/L增加到4,024 +/- 282 U/L。在谷胱甘肽(GSH)耗竭的动物中持续输注谷胱甘肽(GSH)溶液(22 μ mol/kg/hr)可使再灌注损伤减轻55%。体外实验证明了谷胱甘肽与活性氧如过氧化氢(H2O2)和次氯酸(HOCl)的快速反应能力。只有H2O2能将谷胱甘肽定量氧化为二硫化物;HOCl将谷胱甘肽氧化到更高的氧化态。这些数据支持了肝细胞GSH释放增强作为内毒素血症和再灌注期间炎症细胞产生的活性氧的防御机制的假设。肝脏的这种内部防御系统在预防或至少限制活性氧对肝脏的损害方面可能具有普遍的重要性,特别是由库普弗细胞在清除肠道内毒素和细菌的生理功能过程中产生的活性氧。
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引用次数: 0
Intrinsic pumping of mesenteric lymphatics is increased after hemorrhage in awake sheep. 清醒绵羊出血后肠系膜淋巴管的内在泵送增加。
Pub Date : 1994-06-01
B R Boulanger, S J Lloyd, M Walker, M G Johnston

Lymphatic vessels have the ability to contract and transport liquid and protein from tissue spaces to the intravascular space. The purpose of this investigation was to test whether this lymph pump is stimulated following a fixed volume hemorrhage in awake sheep. To quantitate lymphatic pumping in vivo, a mesenteric lymphatic was isolated from all lymph input and provided with Krebs solution at a fixed transmural pressure. A branch of the mesenteric duct was cannulated to provide a measure of lymph flow rate. Each animal was either bled 25% of blood volume over 5 min or was observed. Systemic arterial blood pressure declined in all bled sheep (P < 0.05). Hemorrhage had no effect on lymph flow from mesenteric ducts. However, hemorrhage significantly enhanced lymphatic pumping, approximately 200% of control values 3 hr after hemorrhage (P < 0.01). Increased lymphatic pumping after hemorrhage may play an important role in blood volume and protein restitution.

淋巴管具有收缩和将液体和蛋白质从组织空间输送到血管内空间的能力。本研究的目的是测试在清醒的绵羊发生固定容量出血后,淋巴泵是否受到刺激。为了量化体内淋巴泵送,从所有淋巴输入中分离出肠系膜淋巴,并在固定的跨壁压力下提供Krebs溶液。肠系膜导管的一个分支被插管以提供淋巴流速的测量。每只动物要么在5分钟内放出25%的血容量,要么进行观察。所有出血羊的全身动脉血压均下降(P < 0.05)。出血对肠系膜导管的淋巴流动无影响。然而,出血显著增强淋巴泵送,出血后3小时约为对照组的200% (P < 0.01)。出血后淋巴泵的增加可能在血容量和蛋白质恢复中起重要作用。
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引用次数: 0
Role of oxyradicals in cardiovascular depression and cellular injury in hemorrhagic shock and reinfusion: effect of SOD and catalase. 氧自由基在失血性休克和再输液中心血管抑制和细胞损伤中的作用:SOD和过氧化氢酶的作用。
Pub Date : 1994-06-01
R Kapoor, K Prasad

We investigated the effects of hemorrhagic shock and reinfusion on the cardiac function and contractility, plasma CK and CK-MB activity and lactate concentration, oxyradical-producing activity of polymorphonuclear leukocytes (PMNL-CL), cardiac chemiluminescence (LV-CL), antioxidant enzymatic activity [superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px)], and malondialdehyde (MDA) concentration in anesthetized dogs, to determine the role of oxyradicals in cardiac depression and cellular injury in hemorrhagic shock and reinfusion. The dogs were assigned to four groups: group I (sham), 4 hrs duration; group II, 4 hr of shock; group III, 2 hr of shock, followed by reinfusion for 2 hr; and group IV, as in group III, but pretreated with SOD and catalase. Hemorrhagic shock was produced by withdrawing blood to maintain the mean arterial pressure at 50 +/- 5 mm Hg. Cardiac function and contractility were depressed during hemorrhagic shock. Plasma CK; CK-MB and lactate; and cardiac MDA, Mn-SOD, and CuZn-SOD increased, while catalase activity decreased during shock. Following reinfusion after 2 hr of shock, hemodynamic parameters and plasma lactate tended to return toward control values. Plasma CK and CK-MB, PMNL-CL and cardiac MDA, total SOD, Mn- and CuZn-SOD increased further, while LV-CL and GSH-Px decreased. In spite of the increased antioxidant reserve, oxidative damage was noted. Pretreatment with SOD and catalase attenuated the deleterious effects of shock and reinfusion on the cardiovascular function, plasma CK, CK-MB, and lactate, PMNL-CL, cardiac MDA and SOD, and LV-CL. Protection was incomplete for cardiovascular function and plasma CK and CK-MB. These results suggest that oxyradicals (O2-, H2O2) may be partly involved in the deterioration of cardiovascular function and cellular injury during hemorrhagic shock and reinfusion.

我们研究了失血性休克和再输回对麻醉犬心功能和收缩力、血浆CK、CK- mb活性和乳酸浓度、多形核白细胞(PMNL-CL)生成氧自由基活性、心脏化学发光(lvcl)、抗氧化酶活性[超氧化物歧化酶(SOD)、过氧化氢酶、谷胱甘肽过氧化物酶(GSH-Px)]和丙二醛(MDA)浓度的影响。目的:探讨氧自由基在失血性休克和再输液时心脏抑制和细胞损伤中的作用。狗被分为四组:第一组(假),持续4小时;II组,休克4小时;III组,休克2小时,再输液2小时;IV组与III组相同,但用SOD和过氧化氢酶预处理。失血性休克是通过抽血维持平均动脉压在50 +/- 5mmhg,心功能和收缩力在失血性休克期间受到抑制。血浆CK;CK-MB和乳酸;心肌MDA、Mn-SOD和CuZn-SOD升高,过氧化氢酶活性降低。休克2小时后再输注,血流动力学参数和血浆乳酸趋于恢复到控制值。血浆CK、CK- mb、PMNL-CL和心肌MDA、总SOD、Mn-和CuZn-SOD进一步升高,而LV-CL和GSH-Px进一步降低。尽管抗氧化储备有所增加,但仍存在氧化损伤。用SOD和过氧化氢酶预处理可以减轻休克和回输对心血管功能、血浆CK、CK- mb和乳酸、PMNL-CL、心肌MDA和SOD以及LV-CL的有害影响。对心血管功能和血浆CK和CK- mb的保护是不完全的。这些结果提示,氧自由基(O2-, H2O2)可能在一定程度上参与了失血性休克和再输液过程中心血管功能的恶化和细胞损伤。
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引用次数: 0
Lactate monitoring with subcutaneous microdialysis in patients with shock: a pilot study. 用皮下微透析监测休克患者的乳酸:一项初步研究。
Pub Date : 1994-06-01
J de Boer, H Potthoff, P O Mulder, A S Dofferhoff, R J van Thiel, H Plijter-Groendijk, J Korf

We describe the use of subcutaneous microdialysis for continuous sampling of lactate to monitor the plasma lactate concentration in eight patients with shock. The dialysate lactate concentrations were significantly correlated with the plasma lactate concentrations (r = 0.8229), but the linear regression lines varied between patients. Therefore, we used the individual regression line of each patient for calibration to calculate estimated plasma values from the dialysate concentrations. While the estimated values were linearly correlated to the plasma lactate values (r = 0.912), the 95% confidence interval of the estimated values was +/- 2.8 mmol/L. Thus, subcutaneous microdialysis does not allow accurate estimation of the plasma lactate concentration. In 3 of the 8 patients, there was a significant negative correlation between the dialysate/plasma lactate ratio and the plasma lactate concentration. This suggests that besides plasma lactate, other factors such as subcutaneous adipose tissue metabolism and blood flow, may influence subcutaneous sampling and dialysate lactate concentration as well. While microdialysis can be used for on-line sampling and continuous monitoring of the concentration of extracellular substances, for the purpose of plasma lactate monitoring, sampling probes should be designed that permit intravascular placement.

我们描述了使用皮下微透析连续采样乳酸监测血浆乳酸浓度在8例患者休克。透析液乳酸浓度与血浆乳酸浓度呈显著相关(r = 0.8229),但患者间线性回归线存在差异。因此,我们使用每个患者的单独回归线进行校准,以计算透析液浓度的估计血浆值。预测值与血浆乳酸值呈线性相关(r = 0.912), 95%置信区间为+/- 2.8 mmol/L。因此,皮下微透析不能准确估计血浆乳酸浓度。8例患者中有3例透析液/血浆乳酸比值与血浆乳酸浓度呈显著负相关。这表明,除了血浆乳酸,其他因素,如皮下脂肪组织代谢和血流,也可能影响皮下取样和透析液乳酸浓度。虽然微透析可用于在线采样和连续监测细胞外物质的浓度,但为了监测血浆乳酸,应设计允许血管内放置的采样探针。
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引用次数: 0
Effect of pentoxifylline and somatostatin on tumour necrosis factor production by human pulmonary macrophages. 己酮茶碱和生长抑素对人肺巨噬细胞产生肿瘤坏死因子的影响。
Pub Date : 1994-06-01
J L Balibrea, J Arias-Díaz, C García, E Vara

Cytokines seem to act predominantly in a paracrine manner when producing their deleterious effects during sepsis. Therefore, local TNF alpha release by pulmonary macrophages would have a central role in the pathogenesis of the adult respiratory distress syndrome (ARDS). By contrast, pentoxiphylline (PTXF) can reduce lung damage in septic animal models, and somatostatin (SS-14) has been shown to down-regulate TNF alpha-receptor expression in monocytes, suggesting an immunomodulatory action for this hormone. The aim of this work was to study the effect of PTXF and SS-14 on lipopolysaccharide (LPS)-induced TNF alpha release by human pulmonary macrophages. Macrophages were obtained from multiple organ donor lungs. Donors with either a recent history of tobacco smoking, more than 72 hr of mechanical ventilation, or any radiological pulmonary infiltrate were not included in this study. After 1 hr of culture, LPS stimulated TNF alpha release in a dose-dependent manner (2.34 +/- 0.20 and 11.32 +/- 1.38 pg/microgram protein, P < 0.01, in response to 2.5 and 10 micrograms/ml LPS, respectively). This response was significantly inhibited by both PTXF, 100 micrograms/ml (0.24 +/- 0.07 vs. 2.43 +/- 0.20, P < 0.01, and 1.30 +/- 0.08 vs. 11.32 +/- 1.38, P < 0.01, pg/micrograms protein, 2.5 and 10 micrograms/ml LPS, respectively) and SS-14, 0.4 ng/ml (0.26 +/- 0.07 vs. 2.43 +/- 0.20, P < 0.01, and 0.60 +/- 0.19 vs. 11.32 +/- 1.38, P < 0.01, pg/micrograms protein, 2.5 and 10 micrograms/ml LPS, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

在脓毒症期间产生有害影响时,细胞因子似乎主要以旁分泌方式起作用。因此,肺巨噬细胞的局部TNF α释放可能在成人呼吸窘迫综合征(ARDS)的发病机制中起核心作用。相比之下,penttoxiphylline (PTXF)可以减轻脓毒症动物模型中的肺损伤,而生长抑素(SS-14)已被证明可以下调单核细胞中TNF α受体的表达,表明该激素具有免疫调节作用。本实验旨在研究PTXF和SS-14对脂多糖(LPS)诱导的人肺巨噬细胞释放TNF α的影响。巨噬细胞来自多器官供体肺。近期有吸烟史、机械通气超过72小时或任何放射性肺浸润者均未纳入本研究。培养1小时后,LPS刺激TNF α释放呈剂量依赖性(2.5和10微克/毫升LPS分别为2.34 +/- 0.20和11.32 +/- 1.38 pg/微克蛋白,P < 0.01)。100微克/ml PTXF (0.24 +/- 0.07 vs. 2.43 +/- 0.20, P < 0.01, 1.30 +/- 0.08 vs. 11.32 +/- 1.38, P < 0.01, pg/微克蛋白,2.5和10微克/ml LPS)和0.4 ng/ml SS-14 (0.26 +/- 0.07 vs. 2.43 +/- 0.20, P < 0.01, 0.60 +/- 0.19 vs. 11.32 +/- 1.38, P < 0.01, pg/微克蛋白,2.5和10微克/ml LPS)显著抑制了这种反应。(摘要删节250字)
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引用次数: 0
Altered mitochondrial redox responses in gram negative septic shock in primates. 灵长类动物革兰氏阴性感染性休克时线粒体氧化还原反应的改变。
Pub Date : 1994-05-01
S G Simonson, K Welty-Wolf, Y T Huang, J A Griebel, M S Caplan, P J Fracica, C A Piantadosi

Gram negative sepsis causes changes in oxygen supply-demand relationships. We have used a primate model of hyperdynamic gram negative sepsis produced by intravenous infusion of Escherichia coli (E. coli) to evaluate sepsis-induced alterations in mitochondrial oxidation-reduction (redox) state in muscle in vivo. The redox state of cytochrome a,a3, the terminal member of the intramitochondrial respiratory chain, was assessed in the intact forearm by near-infrared (NIR) spectroscopy. The muscle NIR data were compared to routine measures of oxygen delivery (DO2) and oxygen consumption (VO2). After E. coli infusion and fluid resuscitation, DO2 and VO2 showed minimal changes through 24 hr of sepsis. In contrast, changes in cytochrome a,a3 redox state evaluated by NIR occurred within a few hours and were progressive. Mitochondrial functional responses were correlated with structural changes observed on serial muscle biopsies. Gross morphological changes in muscle mitochondria were present in some animals as early as 12 hr, and, in most animals, by 24 hr. The morphologic changes were consistent with decreases in oxidative capacity as suggested by NIR spectroscopy. The NIR data also suggest that two mechanisms are operating to explain abnormalities in oxygen metabolism and mitochondrial function in lethal sepsis. These mechanisms include an early defect in oxygen provision to mitochondria that is followed by a progressive loss in functional cytochrome a,a3 in the muscle.

革兰氏阴性败血症引起氧供需关系的改变。我们使用了一种由静脉输注大肠杆菌(E. coli)产生的高动力革兰氏阴性脓毒症灵长类动物模型来评估脓毒症诱导的线粒体氧化还原(氧化还原)状态在体内肌肉中的改变。采用近红外(NIR)光谱法测定了完整前臂线粒体内呼吸链末端细胞色素a,a3的氧化还原状态。将肌肉近红外数据与常规的氧输送(DO2)和耗氧量(VO2)进行比较。在大肠杆菌输注和液体复苏后,DO2和VO2在24小时的脓毒症中变化很小。相比之下,近红外评价的细胞色素a,a3氧化还原状态的变化发生在几小时内,并且是进行性的。线粒体功能反应与连续肌肉活检观察到的结构变化相关。一些动物早在12小时就出现了肌肉线粒体的大体形态变化,大多数动物在24小时就出现了。近红外光谱显示,形态学变化与氧化能力下降一致。近红外数据还表明,有两种机制可以解释致死性败血症中氧代谢和线粒体功能的异常。这些机制包括线粒体供氧的早期缺陷,随后是肌肉中功能性细胞色素a,a3的逐渐丧失。
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引用次数: 0
Tumor necrosis factor alpha regulation of immunoglobulin secretion in trauma patients. 肿瘤坏死因子α对创伤患者免疫球蛋白分泌的调节作用。
Pub Date : 1994-05-01
J A Teodorczyk-Injeyan, M Cembrzynska-Nowak, S Lalani, S Rizoli, G Taylor

Major trauma-related immune dysfunction is observed at the time of augmented release of immunopathologic mediators. In the present study, T cell-dependent immunoglobulin (Ig) synthesis in peripheral blood mononuclear cell (PBMC) cultures from blunt trauma patients (N = 12, injury severity score (ISS) 27-50), was reduced by 30- > 90%. This coincided with significantly (P < 0.001-0.01) elevated secretion of the biologically active tumor necrosis factor alpha (TNF alpha). Modulation of the TNF alpha activity by anti-TNF alpha antibody (anti-TNF alpha Ab) led to dose-dependent alterations in IgG synthesis. IgG production increased (up to 300%) in cultures treated with 0.5-2 micrograms/ml of the antibody, where low levels of TNF alpha activity often persisted. However, immunoglobulin synthesis was eradicated in preparations exposed to higher concentrations (10 micrograms/ml) of anti-TNF alpha Ab and devoid of TNF alpha biological activity. The treatment with anti-TNF alpha Ab had no effect on mitogen- or alloantigen-induced PBMC proliferation. Thus, in severely traumatized patients, biological activities of endogenous TNF alpha may include modulation of T cell-dependent B lymphocyte function. Immunoregulatory potential of TNF alpha should, therefore, be considered in therapeutic strategies to abrogate its activity.

主要的创伤相关免疫功能障碍是在免疫病理介质释放增强时观察到的。在本研究中,钝性创伤患者(N = 12,损伤严重程度评分(ISS) 27-50)外周血单个核细胞(PBMC)培养物中的T细胞依赖性免疫球蛋白(Ig)合成降低了30- > 90%。这与生物活性肿瘤坏死因子α (TNF α)分泌显著(P < 0.001-0.01)升高相吻合。抗TNF α抗体(抗TNF α Ab)对TNF α活性的调节导致IgG合成的剂量依赖性改变。在0.5-2微克/毫升抗体处理的培养物中,IgG的产生增加(高达300%),其中低水平的TNF α活性通常持续存在。然而,暴露于较高浓度(10微克/毫升)的抗TNF α Ab和缺乏TNF α生物活性的制剂中,免疫球蛋白合成被根除。抗tnf α Ab治疗对有丝分裂原或同种异体抗原诱导的PBMC增殖无影响。因此,在严重创伤患者中,内源性TNF α的生物活性可能包括T细胞依赖性B淋巴细胞功能的调节。因此,在治疗策略中应考虑TNF α的免疫调节潜力,以消除其活性。
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引用次数: 0
Modulation of pyrogen-induced upregulation of endothelial cell adhesion molecules (CAMs) by interleukin-4: transcriptional mechanisms and CAM-shedding. 通过白细胞介素-4调节热原诱导的内皮细胞粘附分子(CAMs)的上调:转录机制和CAMs脱落。
Pub Date : 1994-05-01
S Kapiotis, P Quehenberger, G Sengoelge, C Pärtan, R Eher, H Strobl, D Bevec, D Zapolska, I Schwarzinger, W Speiser

The pyrogens interleukin 1 (IL-1), tumor necrosis factor (TNF), and bacterial lipopolysaccharides (LPS) are known to increase endothelial cell (EC) adhesiveness for leukocytes by stimulating surface expression of various adhesion molecules. IL-4, a product of activated T-cells, was shown to affect pyrogen-mediated regulation of EC adhesion molecule surface expression. In the present study, we investigated the effect of IL-4 on pyrogen-induced upregulation of the cell adhesion molecules (CAMs) ICAM-1 (intercellular cell adhesion molecule-1), ELAM-1 (endothelial leucocyte adhesion molecule-1), and VCAM-1 (vascular cell adhesion molecule-1) in cultured human umbilical vein EC (HUVEC). Surface expression of adhesion molecules was quantified by flow cytometry, HUVEC mRNA content was estimated by Northern blot analysis, and ICAM-1 antigen in conditioned media was measured by ELISA. Incubation of HUVEC with IL-1 (100 U/ml), TNF (500 U/ml), and LPS (10 micrograms/ml) caused significant increase in ICAM-1, ELAM-1, and VCAM-1 surface expression; IL-1 caused about an eightfold increase in ICAM-1 expression, about a 13-fold increase in ELAM-1 surface expression, and about a fourfold increase in VCAM-1 expression. Coincubation of pyrogens with IL-4 (500 U/ml) differentially influenced their proadhesive effects on the HUVEC surface. In the presence of IL-4, IL-1-induced ICAM-1 upregulation was reduced, ELAM-1 upregulation was not significantly influenced by IL-4, and induction of VCAM-1 was enhanced by IL-4.(ABSTRACT TRUNCATED AT 250 WORDS)

已知热原白介素1 (IL-1)、肿瘤坏死因子(TNF)和细菌脂多糖(LPS)通过刺激各种粘附分子的表面表达来增加内皮细胞(EC)对白细胞的粘附。IL-4是活化t细胞的产物,可影响热原介导的EC粘附分子表面表达的调节。在本研究中,我们研究了IL-4对热原诱导的人脐静脉EC (HUVEC)细胞粘附分子(CAMs) ICAM-1(细胞间细胞粘附分子-1)、内皮白细胞粘附分子-1 (ELAM-1)和血管细胞粘附分子-1 (VCAM-1)上调的影响。流式细胞术检测粘附分子表面表达,Northern blot检测HUVEC mRNA含量,ELISA检测条件培养基中ICAM-1抗原。IL-1 (100 U/ml)、TNF (500 U/ml)、LPS(10微克/ml)与HUVEC孵生后,ICAM-1、ELAM-1、VCAM-1表面表达显著升高;IL-1导致ICAM-1表达增加约8倍,ELAM-1表面表达增加约13倍,VCAM-1表达增加约4倍。热原与IL-4 (500 U/ml)共孵育对HUVEC表面的促粘作用有不同程度的影响。在IL-4存在的情况下,il -1诱导的ICAM-1上调减少,ELAM-1上调不受IL-4的显著影响,IL-4增强了VCAM-1的诱导。(摘要删节250字)
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引用次数: 0
Use of gastric intramucosal pH as a monitor during hemorrhagic shock. 失血性休克时胃粘膜内pH值监测的应用。
Pub Date : 1994-05-01
J B Yee, S W McJames

During resuscitation of the patient suffering from hemorrhagic shock, it may be difficult to determine the adequacy of treatment in the acute setting. The objective of these preliminary studies was to determine if monitoring perfusion of the gastrointestinal tract as estimated by gastric intramucosal pH (pHi) is useful as a guide during the treatment of hemorrhagic shock. Dogs were bled using a modified Wigger's method to a mean arterial blood pressure of 50 mmHg, and pHi was determined 30, 60, 90, and 120 min later. Gastric intramucosal acidosis developed within 30 min of induction of hemorrhagic shock. It was also found that pHi decreases with relatively small amounts of blood loss. There was a significant fall in pHi following hemorrhage to a mean arterial pressure of 80 mmHg from a baseline pressure of 100 mmHg. Following the reinfusion of shed blood, the pHi returned to baseline values within 30 min. It is concluded that measurements of pHi may be a useful monitor in the evaluation and initial resuscitation of patients in hemorrhagic shock.

在失血性休克患者的复苏过程中,可能很难确定在急性环境中治疗的充分性。这些初步研究的目的是确定通过胃粘膜内pH值(pHi)来监测胃肠道灌注是否有助于指导失血性休克的治疗。使用改进的Wigger方法对狗进行放血,使其平均动脉血压为50 mmHg,并在30、60、90和120分钟后测定pHi。失血性休克诱发后30分钟内发生胃粘膜内酸中毒。研究还发现,pHi随着相对少量的失血而降低。出血后pHi显著下降,平均动脉压从基线100 mmHg降至80 mmHg。输血后,pHi在30分钟内恢复到基线值。因此,pHi的测量可能是失血性休克患者评估和初步复苏的有用监测指标。
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引用次数: 0
期刊
Circulatory shock
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