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急性脑缺血时鼠脑微血管血管活性肠肽的变化
引用本文:杨蜀莲 童章燕. 急性脑缺血时鼠脑微血管血管活性肠肽的变化[J]. 中国医学科学院学报, 1991, 13(3): 227-229
作者姓名:杨蜀莲 童章燕
作者单位:协和医院 北京(杨蜀莲,童章燕,左红,高玉红,侯雪),协和医院 北京(陈元方)
摘    要:
血管活性肠肽(vasoactive intestinal peptide,VIP)广泛存在于动物及人大脑、脊髓和周围神经中,在支配脑血管的神经中尤为丰富.本实验观察动物脑微血管中VIP的含量及其在急性脑缺血时的改变. 材料与方法 一、动物 Wistar雄性大鼠27只,200~321.5 g,沙土鼠22只,50~69.5 g,雄性,均由本院医学实验动物研究所提供. 二、脑缺血动物模型 Wistar大鼠经乌拉坦(1g/kg,ip)麻醉后,结扎双侧颈总动脉,通过小量放

关 键 词:脑缺血 血管活性肠肽

Vasoactive intestinal peptide (VIP) concentration in ischemic rat brain microvessels]
S Yang. Vasoactive intestinal peptide (VIP) concentration in ischemic rat brain microvessels][J]. Acta Academiae Medicinae Sinicae, 1991, 13(3): 227-229
Authors:S Yang
Affiliation:PUMC Hospital, Beijing.
Abstract:
VIP is extensively localized in the brain, spinal cord and peripheral neurons, and is especially rich in the nerves innervating the cerebral vasculature. VIP is a potent vasodilator of cerebral vessels. The aim of this study was to investigate VIP contents in brain microvessels and their changes during incomplete brain ischemia. Methods: (1) Bilateral carotid artery ligation was performed in Wistar rats under urethane anesthesia to produce cerebral ischemia, which was further aggravated by bleeding to hypotension with a mean arterial pressure of 50-60 mmHg. At 5, 15 and 30 min after ligation, the rats were decapitated to obtain brain tissue. A sham surgery group served as controls. In some rats cerebral ischemia was confirmed by EEG. (2) Brain microvessels were prepared by brain homogenization in HEPES-Ringer buffer and gradient centrifugation in 30% BSA, followed by filtration through a glass bead column. (3) VIP contents were determined by radioimmunoassay. The results were that VIP contents of 30 min ischemic rats were significantly higher than in the controls (P less than 0.01). VIP contents of cerebral microvessels were also measured in two groups of gerbils. It was found that VIP contents in ischemic gerbils were significantly higher than in the controls (P less than 0.01). These results indicate that: (1) VIP is present in rat and gerbil brain microvessels. (2) During brain injury by ischemia, the increase in VIP content in cerebral microvessels may induce vasodilation and cause an increase in cerebral blood flow. This may well be an autoregulatory response to protect the ischemic brain and may have important pathophysiological implications.
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