Ischemia-reperfusion induced gastric mucosal microcirculatory alterations in the rat.

T Kitahora, P H Guth
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Abstract

The aim of this study was to determine the gastric microcirculatory alterations occurring during reperfusion after a period of ischemia and the possible role of oxyradicals in the microcirculatory disturbance. An in vivo microscopy technique was used to observe the superficial mucosal blood flow during reperfusion. After reperfusion, mucosal blood flow resumed quickly and then slowed with eventual cessation of flow. Thirty minutes of ischemia followed by reperfusion resulted in cessation of flow in 50 +/- 4% and 81 +/- 8%, of the capillaries in the microscopic field at 15 and 30 min, respectively, after reperfusion. During this mucosal microcirculatory change, numerous white thrombi were observed flowing in the mucosal microvessels. In rats pretreated with allopurinol to inhibit oxyradical formation, blood flow was maintained to a significant and markedly greater extent. Study of the submucosal microvasculature after reperfusion revealed a marked delay in transit of a fluorescein-albumin bolus from terminal submucosal arterioles through the mucosal microvasculature and back to submucosal collecting venules. Submucosal vascular diameter change could not explain the altered mucosal blood flow. These findings indicate that there is marked slowing and cessation (in many microvessels) of gastric mucosal blood flow during reperfusion after a period of ischemia, and that the obstruction to flow occurs in the mucosal microvessels. The results of the study with allopurinol suggest that oxygen-derived free radicals generated by xanthine oxidase may play a major role in the genesis of this gastric mucosal microcirculatory disturbance.

缺血再灌注诱导大鼠胃粘膜微循环改变。
本研究的目的是确定缺血一段时间后胃再灌注过程中发生的微循环改变以及氧自由基在微循环紊乱中的可能作用。采用活体显微技术观察再灌注过程中浅表粘膜血流量。再灌注后,粘膜血流迅速恢复,然后减慢,最终停止流动。30min缺血再灌注后,在再灌注后15 min和30 min,显微镜视野中分别有50 +/- 4%和81 +/- 8%的毛细血管停止流动。在粘膜微循环变化过程中,可见大量白色血栓在粘膜微血管中流动。在用别嘌呤醇预处理以抑制氧自由基形成的大鼠中,血流得到了显著且明显更大程度的维持。再灌注后粘膜下微血管的研究显示,荧光蛋白丸从粘膜下末端小动脉经粘膜微血管并返回粘膜下集合小静脉的运输明显延迟。粘膜下血管直径的改变不能解释粘膜血流的改变。这些结果表明,缺血一段时间后,胃粘膜血流在再灌注时明显减慢和停止(在许多微血管中),并且血流阻塞发生在粘膜微血管中。别嘌呤醇的研究结果提示,黄嘌呤氧化酶产生的氧源自由基可能在这种胃粘膜微循环紊乱的发生中起主要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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