Nagata H, Sekizuka E, Morishita T, Tatemichi M, Kurokawa T, Mizuki A, Ishii H
Department of Internal Medicine, Saiseikai Central Hospital, Tokyo, Japan.
Am J Physiol. 1996 Dec;271(6 Pt 1):G1028-33. doi: 10.1152/ajpgi.1996.271.6.G1028.
Topical application of ethanol to the gastrointestinal mucosa induces vasodilation. Using an in vivo microscopy technique, we studied the effect of topical ethanol on the submucosal microvessels that control mucosal blood flow in the rat stomach and identified vasoactive substances and receptors that mediate the ethanol vasoaction. Topical ethanol (1-20%) dilated submucosal arterioles dose dependently, but did not change venular diameters. An inhibitor of alcohol dehydrogenase, 1 mM 4-methylpyrazole, did not alter the ethanol vasoaction. Ethanol-induced arteriolar dilation was eliminated by adenosine deaminase, but other vasodilator inhibitors such as atropine, pyrilamine, indomethacin, human calcitonin gene-related peptide-(8-37), and N omega-nitro-L-arginine methyl ester did not prevent it. Ethanol-induced arteriolar dilation was inhibited by an adenosine A2-receptor antagonist, but not by an A1-receptor antagonist, whereas an A2-agonist, but not an A1-agonist, dose dependently dilated arterioles. Exogenous adenosine (10(-5)-10(-3) M) dilated arterioles to a similar extent as ethanol. This response was inhibited by an A2-antagonist. We conclude that nonmetabolized ethanol increases gastric mucosal blood flow via A2-receptors in submucosal arterioles.
将乙醇局部应用于胃肠道黏膜可诱导血管舒张。我们使用体内显微镜技术，研究了局部应用乙醇对控制大鼠胃黏膜血流的黏膜下微血管的影响，并确定了介导乙醇血管作用的血管活性物质和受体。局部应用乙醇（1%-20%）可使黏膜下小动脉剂量依赖性地扩张，但不改变小静脉直径。乙醇脱氢酶抑制剂1 mM 4-甲基吡唑不改变乙醇的血管作用。乙醇诱导的小动脉扩张可被腺苷脱氨酶消除，但其他血管舒张剂抑制剂，如阿托品、吡苄明、吲哚美辛、人降钙素基因相关肽-（8-37）和Nω-硝基-L-精氨酸甲酯则不能阻止这种扩张。乙醇诱导的小动脉扩张可被腺苷A2受体拮抗剂抑制，但不能被A1受体拮抗剂抑制，而A2激动剂可使小动脉剂量依赖性地扩张，A1激动剂则不能。外源性腺苷（10^-5 - 10^-3 M）使小动脉扩张的程度与乙醇相似。这种反应可被A2拮抗剂抑制。我们得出结论，未代谢的乙醇通过黏膜下小动脉中的A2受体增加胃黏膜血流量。
