{"title":"Effects of antioxidants and PAF receptor antagonist in intestinal shock in the rat.","authors":"E Haglind, G Xia, R Rylander","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>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)</p>","PeriodicalId":10280,"journal":{"name":"Circulatory shock","volume":"42 2","pages":"83-91"},"PeriodicalIF":0.0000,"publicationDate":"1994-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Circulatory shock","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
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)