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门静脉高压大鼠中血液消化诱导的内脏充血和门静脉血流以及奥曲肽的作用

Blood digestion-induced splanchnic hyperemia and portal blood flow in portal hypertensive rats and the role of octreotide.

作者信息

Kotzampassi K, Eleftheriadis E

机构信息

Department of Surgery, University of Thessaloniki, Greece.

出版信息

J Gastroenterol. 1998 Oct;33(5):678-83. doi: 10.1007/s005350050155.

Abstract

We aimed to investigate whether the presence of blood within the intestinal lumen after variceal bleeding would lead to reactive intestinal hyperemia, which in turn could result in the worsening of portal hemodynamics, and thus bleeding recurrence. Two models of portal hypertensive Wistar rats were used: 32 CCl4-cirrhotics with a low index of portal-systemic shunting and 32 that had been previously subjected to portal vein stenosis, with a high index of portal-systemic shunting; 32 Wistar rats served as controls. The rats were divided into four groups, each comprising 8 cirrhotics, 8 portal vein stenosis rats, and 8 controls. Intestinal microcirculation and portal blood flow were assessed by laser-Doppler and transit-time ultrasonic flow probes, respectively, before and 60 min after the injection of 2 ml of blood (groups 1 and 2) or an equal volume of NaCl 0.9% (placebo; groups 3 and 4) into the intestinal lumen. Octreotide (0.2 microg/100 g body weight [BW]) (groups 1 and 3) or NaCl 0.9% (groups 2 and 4) was then given subcutaneously, and 30 min later the final measurements were performed. The presence of blood within the intestinal lumen resulted in an increase in intestinal microcirculation in rats in all groups, while portal blood flow was increased in portal vein stenosis rats and controls, and decreased in cirrhotics. The presence of NaCl 0.9% had no effect. Octreotide, but not NaCl 0.9%, led to a decrease in both intestinal microcirculation and portal blood flow. The findings of this study suggest that intestinal hyperemia induced by digestion of blood in the enteric lumen increases or decreases portal blood flow, the result being strongly related to the portal hypertension model used. Since the main difference between the models was the extent of portal-systemic shunting, this may suggest a relationship between portal blood flow and portal-systemic shunting. This relationship could explain why variceal bleeding stops in some patients but recurs in others.

摘要

我们旨在研究静脉曲张破裂出血后肠腔内血液的存在是否会导致反应性肠充血,进而导致门静脉血流动力学恶化,从而导致出血复发。使用了两种门静脉高压Wistar大鼠模型:32只四氯化碳诱导的肝硬化大鼠,其门静脉-体循环分流指数较低;32只先前接受过门静脉狭窄手术的大鼠,其门静脉-体循环分流指数较高;32只Wistar大鼠作为对照。将大鼠分为四组,每组包括8只肝硬化大鼠、8只门静脉狭窄大鼠和8只对照大鼠。在向肠腔内注入2 ml血液(第1组和第2组)或等体积的0.9%氯化钠(安慰剂;第3组和第4组)之前和之后60分钟,分别用激光多普勒和渡越时间超声血流探头评估肠道微循环和门静脉血流。然后皮下注射奥曲肽(0.2 μg/100 g体重[BW])(第1组和第3组)或0.9%氯化钠(第2组和第4组),30分钟后进行最终测量。肠腔内血液的存在导致所有组大鼠的肠道微循环增加,而门静脉狭窄大鼠和对照大鼠的门静脉血流增加,肝硬化大鼠的门静脉血流减少。0.9%氯化钠的存在没有影响。奥曲肽而非0.9%氯化钠导致肠道微循环和门静脉血流均减少。本研究结果表明,肠腔内血液消化引起的肠充血会增加或减少门静脉血流,其结果与所使用的门静脉高压模型密切相关。由于模型之间的主要差异在于门静脉-体循环分流的程度,这可能表明门静脉血流与门静脉-体循环分流之间存在关联。这种关联可以解释为什么静脉曲张破裂出血在一些患者中停止而在另一些患者中复发。

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