猫小肠缺血/再灌注过程中一氧化氮生成和上皮功能障碍的时间过程。

Circulatory shock Pub Date : 1994-03-01
S Kanwar, B L Tepperman, D Payne, L R Sutherland, P Kubes
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引用次数: 0

摘要

本研究的目的是将一氧化氮的产生与缺血后猫小肠再灌注时间联系起来。小肠缺血1小时和再灌注4小时后,上皮通透性(以51Cr-EDTA的血腔清除率来量化)增加了约10倍。在60至120分钟内,L-NAME输注进一步增强了这种增加,但在240分钟时则没有。Ca(2+)依赖性一氧化氮合酶活性在再灌注3和4小时时降低了约50%,而在整个实验中未检测到Ca(2+)非依赖性一氧化氮合酶活性。在再灌注开始时给予l -精氨酸可在前120分钟减弱再灌注诱导的上皮屏障功能障碍,但在180或240分钟时则没有。在再灌注1小时后持续输注一氧化氮供体(CAS 754)可在再灌注4小时时降低上皮通透性。总之,随着再灌注时间的延长,一氧化氮的产生减少,可能是由于一氧化氮合酶水平的降低。
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Time course of nitric oxide production and epithelial dysfunction during ischemia/reperfusion of the feline small intestine.

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.

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