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作 者:盛树力[1] 张万江[1] 伍洁[1] 孙波[1] 刘延津[1] 高凤琴[1] 季鹰[1] 吴建中[1] 王天佑[1] 战其民 杨如珊 徐东[3]
机构地区:[1]北京市神经外科研究所 [2]北京天坛医院 [3]北京医科大学
出 处:《首都医学院学报》1990年第4期259-265,共7页
摘 要:观察了降钙素基因相关肽(calcitonin gene related peptide,CGRP)对人脑血管的扩张作用以及对动物和人脑血流量的影响.结果表明:1.CGRP可使由内皮素(endo thelin),神经肽Y(neuropeptide Y)、去甲肾上腺素、5-羟色胺或胆囊收缩素(CCK)等引起的收缩的人离体血管舒张。2.颈内动脉注入CGRP后,可使脑血流量增加60%。3.经侧脑室给药,CGRP可拮抗内皮素减少脑血流的作用,而使脑血流暂时恢复正常。4.3例患有脑梗塞病人静脉滴注CGRP后,可使病人血压下降,单光子CT扫描(single photon emission computedtomography,SPECT)显示脑量流血增加30%~80%。提示CGRP可能作为缺血性脑血管病治疗的一种药物。CGRP is present in nerve fibres in central and peripheral arteries, where it is a potent vasodilator. The purpose of our research is to examine the effect of CGRP on human cerebral arteries and cerebral blood flow (CBF). Our results show that 1) CGRP can significnatly blunt the vasoconstriction caused by ebdothelin, neuropeptide Y (NPY), serotonin, noradrenaline, and CCK; 2) 50μg CGRP injected iv for 10 minutes into three patients who had cerebral embolisms increased CBF 32%~80% as measured by single photon emission computed tomography (SPECT), the levels of NPY, renin and angiotensin II in the patients' blood did not change after administration of CGRP; 3) an increase in CBF was seen in rabbits following injections of CGRP (4μg) into the internal carotid artery; 4) the intracerebroventricular (i. c. v. ) administration of endothelin (5ng) caused a decrease in CBF in rats, but it was reversed by CGRP (5ng, i. c. v. ); and 5) endothelin (5ng, i. c. v.) also induced an elevation of plasma alsosterone, but it was not antagonized by CGRP (5ng, i. c. v.). We conclude that CGRP can counteract the constriction of human arteries by various agents and increase CBF significantly. We deduce that the effect of CGRP is mediated by the increased calcium influx through dihydropyridine-sensitive calcium channels.
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