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正常大鼠和门静脉高压大鼠肠道内源性血管收缩张力

Endogenous vasoconstrictor tone in intestine of normal and portal hypertensive rats.

作者信息

Joh T, Granger D N, Benoit J N

机构信息

Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130.

出版信息

Am J Physiol. 1993 Jan;264(1 Pt 2):H171-7. doi: 10.1152/ajpheart.1993.264.1.H171.

Abstract

The purpose of the present study was to determine the effects of endogenous norepinephrine, vasopressin (AVP), and angiotensin II (ANG II) on normal intestinal microvascular dimensions and to determine whether endogenous vasoconstrictor tone was altered in chronic portal hypertension. The intestine of normal and portal hypertensive rats was prepared for in vivo microscopic observation, and an arteriole (1A, 2A, or 3A) was selected for study. Arteriolar diameter and erythrocyte velocity were continuously monitored and used in the calculation of arteriolar blood flow. Once steady-state conditions were established, specific antagonists to alpha-adrenergic, AVP, or ANG II receptors were applied locally to remove the influences of each of these systems. In normal animals, blockade of alpha-adrenergic receptors produced a 1.3, 1.5, and 14.7% increase in the diameter of 1A, 2A, and 3A, respectively. AVP blockade in normal animals produced an 8.7, 1.6, and 1.5% increase in the diameter of 1A, 2A, and 3A, respectively; ANG II blockade only produced an increase in 3A diameter (5.8%). alpha-Adrenergic blockade produced a smaller increase in portal hypertensive 3A diameter (2.3%) compared with normal rats. AVP and ANG II blockade produced a significantly larger dilation of 3A (AVP, 4.8%) and 1A (ANG II, 3.8%), respectively, compared with control. Plasma AVP and ANG II levels were higher in portal hypertensive (AVP, 9.1 pg/ml; ANG II, 8.6 pg/ml) than in normal rats (AVP, 5.5 pg/ml; ANG II, 6.6 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究的目的是确定内源性去甲肾上腺素、血管加压素(AVP)和血管紧张素II(ANG II)对正常肠微血管尺寸的影响,并确定慢性门静脉高压时内源性血管收缩张力是否改变。将正常和门静脉高压大鼠的肠道制备用于体内显微镜观察,并选择一条小动脉(1A、2A或3A)进行研究。连续监测小动脉直径和红细胞速度,并用于计算小动脉血流量。一旦建立稳态条件,局部应用α-肾上腺素能、AVP或ANG II受体的特异性拮抗剂以消除这些系统各自的影响。在正常动物中,阻断α-肾上腺素能受体分别使1A、2A和3A的直径增加1.3%、1.5%和14.7%。正常动物中阻断AVP分别使1A、2A和3A的直径增加8.7%、1.6%和1.5%;阻断ANG II仅使3A直径增加(5.8%)。与正常大鼠相比,α-肾上腺素能阻断使门静脉高压3A直径增加较小(2.3%)。与对照组相比,阻断AVP和ANG II分别使3A(AVP,4.8%)和1A(ANG II,3.8%)显著扩张。门静脉高压大鼠(AVP,9.1 pg/ml;ANG II,8.6 pg/ml)的血浆AVP和ANG II水平高于正常大鼠(AVP,5.5 pg/ml;ANG II,6.6 pg/ml)。(摘要截断于250字)

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