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组胺释放以及超氧化物歧化酶、别嘌呤醇和雷尼替丁对大鼠失血性休克的预处理

Histamine release and SOD, allopurinol and ranitidine pretreatment in haemorrhagic shock in the rat.

作者信息

Zöllei I, Asakawa H, Karácsonyi S

机构信息

Department of Surgery of Szent-Györgyi Albert Medical University, Szeged, Hungary.

出版信息

Acta Physiol Hung. 1992;80(1-4):303-9.

PMID:1285366
Abstract

Histamine release have been demonstrated in haemorrhagic shock. There are some observations that oxygen free radicals can cause histamine release. Oxygen free radicals play a role in the pathogenesis of gastric mucosal lesions. The goal of this study was to determine whether ranitidine or SOD and allopurinol pretreatment modify the histamine release during and after the haemorrhagic shock in the rat. In the anaesthetized rat 0.1 N HCl was instilled into the stomach and the rat was bled to reduce the blood pressure to 30 mmHg for 20 min. The shed blood was reinfused. Twenty min later the stomach was removed. The area of gastric mucosal lesions were measured, histological grading was made. Blood samples taken from the carotid artery were examined by radioimmunoassay (IMMUNOTECH) to determine the plasma histamine level. Plasma histamine level did not change significantly during the preparative surgery, but there was a significant increase of histamine level by the end of shock period. After the reinfusion of the blood the plasma histamine remained essentially at the same level for five min. Oxygen free radicals did not cause an important histamine release. By the end of the experiment the histamine level decreased dramatically. Ranitidine, allopurinol and SOD pretreatment provided significant protection against the gastric mucosal lesions. Allopurinol and SOD did not influence significantly the histamine level. Ranitidine caused significant histamine release immediately after the injection and every histamine value was significantly higher in this group except for the final value which was lower than the control one. The oxygen free radicals were not found as endogenous histamine releasers in this study.

摘要

在失血性休克中已证实有组胺释放。有一些观察结果表明氧自由基可导致组胺释放。氧自由基在胃黏膜损伤的发病机制中起作用。本研究的目的是确定雷尼替丁或超氧化物歧化酶(SOD)及别嘌呤醇预处理是否能改变大鼠失血性休克期间及之后的组胺释放。在麻醉的大鼠中,将0.1N盐酸注入胃内,然后放血使血压降至30mmHg并维持20分钟。将放出的血液回输。20分钟后取出胃。测量胃黏膜损伤面积并进行组织学分级。通过放射免疫分析法(免疫技术公司)检测从颈动脉采集的血样,以测定血浆组胺水平。在准备手术期间血浆组胺水平无明显变化,但在休克期末组胺水平显著升高。血液回输后,血浆组胺在5分钟内基本保持在同一水平。氧自由基未引起重要的组胺释放。在实验结束时组胺水平急剧下降。雷尼替丁、别嘌呤醇和SOD预处理对胃黏膜损伤有显著的保护作用。别嘌呤醇和SOD对组胺水平无显著影响。雷尼替丁在注射后立即引起显著的组胺释放,除了最终值低于对照组外,该组的每个组胺值均显著高于对照组。在本研究中未发现氧自由基是内源性组胺释放剂。

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