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猫小肠缺血/再灌注过程中一氧化氮产生及上皮功能障碍的时间进程。

Time course of nitric oxide production and epithelial dysfunction during ischemia/reperfusion of the feline small intestine.

作者信息

Kanwar S, Tepperman B L, Payne D, Sutherland L R, Kubes P

机构信息

Department of Medical Physiology, University of Calgary, Alberta, Canada.

出版信息

Circ Shock. 1994 Mar;42(3):135-40.

PMID:8025978
Abstract

The objective of this study was to correlate nitric oxide production with time of reperfusion of the post-ischemic feline small intestine. Epithelial permeability, quantitated as blood-to-lumen clearance of 51Cr-EDTA, following 1 hr of ischemia and 4 hr of reperfusion of the small intestine, increased approximately 10-fold. This increase was further augmented by L-NAME infusion between 60 and 120 min but not at 240 min. Ca(2+)-dependent nitric oxide synthase activity was reduced by approximately 50% at 3 and 4 hr of reperfusion, whereas Ca(2+)-independent nitric oxide synthase activity was undetectable throughout the experiment. Administration of L-arginine at the start of reperfusion attenuated the reperfusion-induced epithelial barrier dysfunction for the first 120 min but not at 180 or 240 min. Continuous infusion of a nitric oxide donor (CAS 754) following 1 hr of reperfusion reduced epithelial permeability at 4 hr of reperfusion. In conclusion, a reduction in nitric oxide production was observed with time of reperfusion, possibly due to reduced nitric oxide synthase levels.

摘要

本研究的目的是将一氧化氮生成与缺血后猫小肠的再灌注时间相关联。小肠缺血1小时和再灌注4小时后,上皮通透性(以51Cr - EDTA的血到腔清除率定量)增加了约10倍。在60至120分钟之间输注L - NAME可使这种增加进一步加剧,但在240分钟时则不然。再灌注3小时和4小时时,钙依赖性一氧化氮合酶活性降低了约50%,而在整个实验过程中均未检测到钙非依赖性一氧化氮合酶活性。再灌注开始时给予L - 精氨酸在最初120分钟内减轻了再灌注诱导的上皮屏障功能障碍,但在180或240分钟时则不然。再灌注1小时后持续输注一氧化氮供体(CAS 754)可降低再灌注4小时时的上皮通透性。总之,随着再灌注时间的延长,观察到一氧化氮生成减少,这可能是由于一氧化氮合酶水平降低所致。

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