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

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 I D1G提示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 I D 1G I D 1-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.

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.