抗氧化剂和PAF受体拮抗剂在大鼠肠休克中的作用。

Circulatory shock Pub Date : 1994-02-01
E Haglind, G Xia, R Rylander
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引用次数: 0

摘要

在导致低血压、小肠粘膜病变和死亡的肠缺血再灌注模型中,测试了超氧化物歧化酶(SOD)和过氧化氢酶(cat)或PAF受体拮抗剂联合使用的效果。大鼠肠缺血60 min后再灌注。一组在缺血前50分钟给予PAF受体拮抗剂BN 52021,另一组在再灌注前10分钟给予SOD + cat。一组给予生理盐水治疗,另一组作为对照组。再灌注后3小时检测血压、粘膜病变、血浆容量和血浆内毒素。在4天内测定死亡率。各组均未发现内源性内毒素,但使用的第一类SOD和cat被内毒素污染,导致使用这些物质的动物出现外源性内毒素血症。随后使用无内毒素酶。SOD + cat和PAF拮抗剂对低血压或粘膜病变均无影响。两种治疗方案给药后血浆容量均维持在对照组水平。SOD + cat组死亡率下降。SOD + cat的作用表明该模型在再灌注时释放了自由基,PAF受体拮抗剂的作用表明PAF参与了膜损伤,但在所使用的休克模型中是一种中间机制。休克动物对血浆内毒素的清除效果较差,这可能是由于休克对网状内皮系统(RES)的影响。(摘要删节250字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of antioxidants and PAF receptor antagonist in intestinal shock in the rat.

In a model of intestinal ischemia-reperfusion resulting in hypotension, mucosal lesions in the small intestine and mortality, the effects of a combination of superoxide dismutase (SOD) and catalase (cat) or a PAF receptor antagonist were tested. Intestinal ischemia was induced in rats and continued for 60 min. After this, the intestine was reperfused. A PAF receptor antagonist, BN 52021, was given 50 min before ischemia in one group, and SOD + cat was given 10 min before reperfusion in one group. One group received normal saline and one group were controls. Blood pressure, mucosal lesions, plasma volume, and endotoxin in plasma were determined up to 3 hr after reperfusion. Mortality was determined over 4 days. Endogenous endotoxin was not found in any of the groups, but the first types of SOD and cat used were contaminated with endotoxin, resulting in exogenous endotoxemia in animals which received those substances. Later endotoxin-free enzymes were used. Neither SOD + cat nor PAF antagonist had any effect on the hypotension or mucosal lesions. Plasma volume remained at the level of the control group after administration of either regimen. Mortality decreased in the group that received SOD + cat. The effects of SOD + cat indicate that free radicals were released in this model at reperfusion, and the effects of the PAF receptor antagonist indicate that PAF participates in membrane damage, but is an intermediary mechanism in the shock model used. The clearance of infused endotoxin from plasma was less effective in the shocked animals, possibly due to a shock effect on reticuloendothelial system (RES).(ABSTRACT TRUNCATED AT 250 WORDS)

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