Nonreceptor-mediated intestinal vasoconstriction in portal hypertensive rats.
Nonreceptor-mediated intestinal vasoconstriction in portal hypertensive rats.
复制标题
门静脉高压大鼠非受体介导的肠血管收缩。
DOI：
10.1152/ajpheart.1994.267.1.h370
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Benoit,JN
中科院分区：
文献类型：
--
作者：
Wu,ZY;Benoit,JN
以往的研究表明，受体介导的血管收缩功能在慢性门脉高压症（PH）中受损。此外，有人认为，慢性PH中血管收缩剂有效性的改变是由于与平滑肌激活相关的细胞内事件的缺陷，而不是血管收缩剂与血管平滑肌受体的偶联受损。本研究旨在确定PH肠微循环中非受体介导的血管收缩反应是否受损。具体而言，我们研究了氟化铝诱导的G蛋白激活，KCl诱导的去极化，咖啡因诱导的细胞内Ca 2+释放和l-吲哚内酰胺诱导的蛋白激酶C激活对正常（Norm，n = 39）和PH（n = 42）大鼠肠道微循环的影响。制备小肠用于微循环研究，并转移至视频显微镜。在线测量一级小动脉（1A）直径和红细胞流速。根据流速和微血管横截面积的乘积计算血流量。在对照期后，将微血管暴露于含有氯化铝加氟化钠、氯化钾、咖啡因或l-吲哚内酰胺的溶液中。氟化铝，氯化钾，咖啡因，和l-吲哚内酰胺产生的小动脉直径的最大减少显着更大的正常大鼠相比，PH大鼠。小动脉血流量的变化也较大，在正常比PH大鼠。本研究的结果提供了第一个直接的证据表明，受损的第二信使激活的PH循环。
Previous studies have demonstrated that receptor-mediated vasoconstriction is impaired in chronic portal hypertension (PH). Furthermore, it has been suggested that altered vasoconstrictor effectiveness in chronic PH is due to a defect in the intracellular events associated with smooth muscle activation and not to impaired coupling of vasoconstrictors with vascular smooth muscle receptors. The present study was designed to determine whether nonreceptor-mediated vasoconstrictor responses are impaired in the PH intestinal microcirculation. Specifically, we examined the effects of aluminum fluoride-induced activation of G proteins, KCl-induced depolarization, caffeine-induced release of intracellular Ca2+, and l-indolactam-induced activation of protein kinase C on the intestinal microcirculation of normal (Norm, n = 39) and PH (n = 42) rats. The small intestine was prepared for microcirculatory studies and transferred to a video microscope. First-order arteriolar (1A) diameter and red cell velocity were measured on-line. Blood flow was calculated from the product of velocity and microvessel cross-sectional area. After a control period, the microvasculature was exposed to a solution containing aluminum chloride plus sodium fluoride, potassium chloride, caffeine, or l-indolactam. Maximal decreases in arteriolar diameter produced by aluminum fluoride, KCl, caffeine, and l-indolactam were significantly greater in Norm rats when compared with PH rats. Changes in arteriolar blood flow were also larger in Norm than in PH rats. The results of the present study provide the first direct evidence of an impaired response to second-messenger activation in the PH circulation.