EFFECTS OF ETHANOL ON TERMINAL ARTERIOLES AND MUSCULAR VENULES - DIRECT OBSERVATIONS ON THE MICROCIRCULATION
EFFECTS OF ETHANOL ON TERMINAL ARTERIOLES AND MUSCULAR VENULES - DIRECT OBSERVATIONS ON THE MICROCIRCULATION
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DOI：
10.1097/00005344-197901000-00010
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发表时间：
1979-01-01
影响因子：
3
通讯作者：
ALTURA, BT
中科院分区：
文献类型：
--
作者：
ALTURA, BM;OGUNKOYA, A;ALTURA, BT
本实验使用图像分割电视显微镜记录系统，首次显示了局部、动脉内和静脉注射乙醇对内脏终末血管床中终末小动脉（内径15-23 μm）和肌性小静脉（内径28-39 μm）的原位定量影响。无论给药途径如何，乙醇（0.05-10%）均剂量依赖性扩张终末小动脉和肌性小静脉。这些乙醇诱导的扩张反应没有修改胆碱能，组胺能（既不是H 1-也不是H 2-阻滞剂），肾上腺素能，或前列腺素合成酶拮抗剂。β-肾上腺素能阻滞剂显著增强了酒精的血管扩张作用。此外，局部和全身给予乙醇剂量依赖性抑制儿茶酚胺（肾上腺素和去甲肾上腺素）、血管紧张素、加压素和氯化钡对微观阻力和电容血管的收缩作用。儿茶酚胺，血管紧张素，和加压素诱导的收缩反应对终末小动脉更敏感的抑制乙醇比激动剂诱导的收缩反应对肌肉小静脉。在两种类型的肌肉微血管中，氯化钡对乙醇抑制反应的敏感性与其他激动剂相反。的小动脉收缩反应的持续时间显着减少后，应用乙醇，而Ba 2-诱导的小静脉收缩的持续时间增加后，应用酒精。低剂量乙醇（即0.01-0.05%）不增强对去甲肾上腺素、肾上腺素、血管紧张素、加压素或Ba 2+的收缩反应。这些结果表明乙醇可（i）对微血管平滑肌产生直接作用;（ii）减弱血管活性物质诱导的微血管收缩反应;（iii）可能干扰微血管平滑肌细胞失活或儿茶酚胺和Ba 2+的处置。结果提示，对显微血管阻力和电容的直接血管舒张作用可能在酒精引起的人和动物外周血管舒张中起重要作用。
The present experiments, using an image-splitting television microscope recording system, show for the first time the quantitative effects of topical, intra-arterial, and intravenously administered ethanol on terminal arterioles (15–23 μm id) and muscular venules (28–39 μm id), in situ, in a splanchnic terminal vascular bed. Irrespective of the route of administration, ethanol (0.05–10%) dose-dependently dilated both terminal arterioles and muscular venules. These ethanol-induced dilator responses were not modified by cholinergic, histaminergic (neither H 1-nor H 2-blockers), serotonergic, or prostaglandin synthetase antagonists. β-Adrenergic blockade significantly enhanced the vasodilator effects of the alcohol. In addition, locally as well as systemically administered ethanol dose-dependently inhibited the constrictor effects of catecholamines (epinephrine and norepinephrine), angiotensin, vasopressin, and barium chloride on the microscopic resistance and capacitance vessels. Catecholamine-, angiotensin-, and vasopressin-induced constrictor responses on terminal arterioles were more sensitive to inhibition by ethanol than were the agonist-induced contractile responses on muscular venules. The sensitivity of barium chloride responses to ethanol inhibition, in the two types of muscular microvessels, was the reverse of that observed with the other agonists. The duration of the arteriolar constrictor responses to catecholamines was reduced significantly upon application of ethanol, whereas the duration of Ba 2--induced venular constrictions was increased after application of the alcohol. Low doses of ethanol (ie, 0.01–0.05%) did not potentiate constrictor responses to norepinephrine, epinephrine, angiotensin, vasopressin, or Ba 2+ These findings indicate that ethanol can (i) exert direct effects on microvascular smooth muscle:(ii) attenuate microvascular constrictor responses induced by vasoactive substances; and (iii) possibly interfere with microvascular smooth muscle cell inactivation or disposition of catecholamines and Ba 2+. It is suggested that the direct vasodepressant actions on microscopic resistance and capacitance vessels may play a significant role in alcohol-induced peripheral vasodilatation seen in man and animals.