逃离胃微循环血管收缩。

P. Guth, E. Smith
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引用次数: 22

摘要

由于肾上腺素能刺激引起的血管收缩导致内脏阻力血管逃逸,这归因于粘膜下动静脉吻合器(分流)扩张引起的粘膜下血流量增加。将这一假设应用于大鼠胃微循环,用体内显微镜进行了研究。采用图像分裂电视显微镜记录系统,测定胃粘膜下小动脉(13-33妈)对3 min左内脏神经刺激、去甲肾上腺素增殖和加压素超裂变的反应。所有刺激都产生最初的血管收缩。所有使用去甲肾上腺素和神经刺激的大鼠都出现了逃逸现象,但使用加压素的5只大鼠中只有1只出现了逃逸现象。没有发现分流。研究表明胃粘膜下小动脉表现出逃逸现象,提示其他内脏床的“自我调节逃逸”也可能是由于收缩血管的松弛而不是分流的打开。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Escape from vasoconstriction in the gastric microcirculation.
Escape of splanchic resistance vessels from vasconstriction due to adrenergic stimulation has been attributed to increasing submucosal blood flow due to dilation of submucosal arteriovenous anastomes (shunts). This postulate, as applied to the rat gastric microcirculation, was studied by in vivo microscopy. Using an image-splittingTV microscope recording system, response of gastric submucosal arterioles (13-33 mum)to 3 min of left splanchnic nerve stimulation, norepinephrine superfision, and vasopressin superfission was measured. All stimuli produced initial vasoconstriction. Escape occurred in all rats with nerve stimulation and norepinephrine, but in onlyone of five with vasopressin. No shunts were seen. The study demonstrates that thegastric submucosal arterioles exhibit an escape phenomenon, suggesting that "autoregulatory escape" in other splanchic beds also may be due to relaxation of constricted vessels and not to opening of shunts.
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