Medicolegal study on alcohol-induced sudden death. (Effect of ethanol on vascular responses)

血管壁上的周向神经的存在，包括对称性、异位性和感官神经是众所周知的。使用不含内酯的孤立大鼠超级中间式artery，我们研究了尼古丁-和电刺激（ES）-诱导的vasorelaxation，其中一些是由vasodilator神经介导的。在消毒剂的神经中，这是众所周知的，因为那里有一种敏感的、敏感的神经。尼古丁诱导的放松并不被血管活性内源性多肽（VIP）抑制剂、basilen blue或N-y D1 G-y D1-nitro-L-arginine抑制。物质P并没有诱导放松。ES-诱导的放松是由四氯毒素的预处理抑制的，建议放松是由消毒剂神经介导的。在用辣椒素、尼古丁-和ES诱导的放松装置被抑制的植物中。However，N-I D1 G-I-D1-nitro-L-arginine tended to depress ES-induced relaxation，但没有显示出显著的差异。这些、尼古丁和ES诱导的放松似乎由钙素基因相关肽（CGRP）或其他放松因子（s）比硝酸氧化物介导。乙醇抑制的尼古丁-和ES-放松，但明显管理的CGRP并没有被乙醇抑制。因此，乙醇对神经介导的放松的影响似乎主要是由于对CGRP介导的放松的抑制作用。“抑制作用似乎在一个前体水平上出现。”

The presence of perivascular nerve including sympathetic, parasympathetic and sensory nerves in blood vessel wall is known. Using isolated rat superior mesenteric artery without endothelium, we investigated the effect of ethanol on nicotine- and electric stimulation (ES)-induced vasorelaxations which are mediated by vasodilator nerve. In vasodilator nerves, it is known that there are nitrergic and capsaicin-sensitive nerves. Nicotine-induced relaxations were not inhibited by vasoactive intestinal polypeptide (VIP) inhibitor, basilen blue or NィイD1GィエD1-nitro-L-arginine. Substance P did not induced relaxation. ES-induced relaxation was inhibited by the pretreatment with tetrodotoxin, suggesting that the relaxation is mediated by vasodilator nerve. In the arteries pretreated with capsaicin, nicotine- and ES-induced relaxations were inhibited. However, NィイD1GィエD1-nitro-L-arginine tended to depress ES-induced relaxation but did not show a significant difference. Thus, nicotine- and ES-induced relaxations seem to be mediated by calcitonin gene-related peptide (CGRP) or other relaxing factor(s) rather than nitric oxide. Ethanol inhibited nicotine- and ES-relaxations but the exogenously administered CGRP was not inhibited by ethanol. Therefore, effect of ethanol on nerve-mediated relaxations seem to be mainly due to inhibitory action on CGRP-mediated relaxation. The inhibitory action seems to occur at a presynaptic level.