Dogulu F H, Ozogul C, Akpek S, Kurt G, Emmez H, Ercan S, Baykaner M K
Department of Neurosurgery, Gazi University School of Medicine, Ankara, Turkey.
Acta Neurochir (Wien). 2003 Jul;145(7):579-82. doi: 10.1007/s00701-003-0039-9.
Anandamide induces not only endothelium-dependent vasodilatation through cannabinoid receptors but also some endothelium- independent vasodilator effect by calcitonin gene-related peptide release through vanilloid receptors. Endothelin-1, a powerful vasoconstrictive peptide derived from endothelial cells, has been shown to be converted to its active form after cleaving by a vascular matrix metalloproteinase which is also involved in inactivation of calcitonin gene-related peptide. The purpose of this study was to investigate whether anandamide inhibits the acute vascular and morphological effects of Endothelin-1 applied intra-arterially on rabbit basilar arteries.
Fifteen albino rabbits were anaesthetised and underwent placement of a vertebral artery catheter for angiography of the basilar artery. Animals were divided, arbitrarily, into animals in which there was either intra-arterial injection of saline (Group I, n=5), Endothelin-1 (Group II, n=5) and Endothelin-1 and anandamide (Group III, n=5). The diameter of the basilar artery between the pre and post injection angiograms was measured in each of the three groups and transmission electron microscopic investigations on basilar arteries were performed.
Angiographic studies showed that simultaneous administration of anandamide significantly attenuated Endothelin-1 induced vasoconstriction. Furthermore, it was demonstrated that anandamide reversed the morphological changes induced by Endothelin-1 on the vessel wall.
These results indicated that anandamide overcomes the angiographic and morphological effects of intrarterially administered ET-1 induced vasospasm in rabbit basilar arteries probably by induction of CGRP related vasodilatation through vanilloid receptors and prevents the acute ET-1 induced ultrastructural vessel wall damage.
花生四烯乙醇胺不仅通过大麻素受体诱导内皮依赖性血管舒张，还通过香草酸受体释放降钙素基因相关肽产生一些非内皮依赖性血管舒张作用。内皮素 -1是一种源自内皮细胞的强效血管收缩肽，已证明其在被血管基质金属蛋白酶切割后转化为活性形式，而该酶也参与降钙素基因相关肽的失活。本研究的目的是探讨花生四烯乙醇胺是否能抑制动脉内注射内皮素 -1对兔基底动脉产生的急性血管和形态学影响。
15只白化兔麻醉后，置入椎动脉导管用于基底动脉血管造影。动物被随机分为三组，分别进行动脉内注射生理盐水（第一组，n = 5）、内皮素 -1（第二组，n = 5）以及内皮素 -1和花生四烯乙醇胺（第三组，n = 5）。测量三组动物注射前后血管造影图像中基底动脉的直径，并对基底动脉进行透射电子显微镜检查。
血管造影研究表明，同时给予花生四烯乙醇胺可显著减轻内皮素 -1诱导的血管收缩。此外，还证明花生四烯乙醇胺可逆转内皮素 -1诱导的血管壁形态学变化。
这些结果表明，花生四烯乙醇胺可能通过香草酸受体诱导降钙素基因相关肽介导的血管舒张，从而克服动脉内注射内皮素 -1在兔基底动脉中引起的血管造影和形态学效应，即血管痉挛，并预防内皮素 -1诱导的急性超微结构血管壁损伤。
