脑缺血后血流和神经效应机制。

Blood vessels Pub Date : 1991-01-01 DOI:10.1159/000158842
R Macfarlane, M A Moskowitz, E Tasdemiroglu, E P Wei, H A Kontos
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引用次数: 25

摘要

用微球测定法研究了8只猫三叉神经节切除后慢性单侧血管神经传递障碍后神经效应机制对脑缺血后血流调节的影响。动物在4支血管闭塞和全身性低血压引起的全身缺血10分钟后进行90分钟的再灌注。三叉神经节切除侧同侧皮质灰质再灌注后30min充血最多减少48% (p < 0.01)。轴突反射机制涉及外周感觉神经纤维释放神经肽,如P物质(SP)、降钙素基因相关肽(CGRP)和神经激肽A (NKA),介导了这种反应。SP和NKA通过内皮依赖性机制(内皮依赖性放松因子)引起血管舒张,而CGRP通过直接受体相互作用使血管平滑肌舒张。因此进行了研究,以确定内皮依赖机制介导全脑缺血后充血的程度。在7只完整猫中,局部应用乙酰胆碱(ACh;10(-7) M),内皮依赖性血管扩张剂,使用封闭颅窗技术测量。虽然乙酰胆碱在静息条件下使心肌动脉直径增加17%,但在缺血10分钟后再灌注的前60分钟,相同剂量的乙酰胆碱引起血管收缩反应(再灌注后30分钟乙酰胆碱前直径的87%)。乙酰胆碱钠诱导的血管舒张在75分钟后恢复(105%),但即使在120分钟时也低于对照组(109比117%;P < 0.05)。(摘要删节250字)
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Postischemic cerebral blood flow and neuroeffector mechanisms.

The influence of neuroeffector mechanisms in the regulation of postischemic cerebral blood flow was investigated by microsphere determination in 8 cats after chronic unilateral vascular deafferentation by trigeminal ganglionectomy. The animals were subjected to 90 min of reperfusion following 10 min of global ischemia induced by 4-vessel occlusion and systemic hypotension. Cortical hyperemia 30 min after reperfusion was attenuated by up to 48% in cortical gray matter ipsilateral to the side of trigeminal ganglionectomy (p less than 0.01). Axon reflex mechanisms involving the release of neuropeptides from peripheral sensory nerve fibers, such as substance P (SP), calcitonin gene-related peptide (CGRP) and neurokinin A (NKA), mediate this response. SP and NKA cause vasodilation by endothelium-dependent mechanisms (endothelium-dependent relaxing factor), whereas CGRP relaxes vascular smooth muscle by direct receptor interactions. Studies were therefore undertaken to determine the extent to which endothelium-dependent mechanisms mediate the hyperemia following global cerebral ischemia. In 7 intact cats, the postischemic response of pial arterioles to the topical application of acetylcholine (ACh; 10(-7) M), an endothelial-dependent vasodilator, was measured using a closed cranial window technique. Although ACh increased pial arteriolar caliber by 17% under resting conditions, the same dose elicited a vasoconstrictor response (87% of pre-ACh diameter 30 min after reperfusion) for the first 60 min of reperfusion after 10 min of ischemia. ACh-induced vasodilation was restored by 75 min (105%), but was less than control even at 120 min (109 vs. 117%; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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