[酒精对血管功能的影响]。

Risa Kudo, Katsuya Yuui, Shogo Kasuda, Katsuhiko Hatake
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引用次数: 0

摘要

血管功能是由血管收缩和血管松弛的平衡来调节的。由于饮酒导致的这种平衡紊乱会导致各种临床状况。在这篇综述中,我们讨论了急性和慢性乙醇消耗对血管反应的影响,包括血管收缩、内皮依赖性血管松弛和神经介导的血管松弛。急性乙醇给药诱导体外乙醇初始动物血管收缩。此外,乙醇可以增强和抑制激动剂诱导的Ca(2+)依赖性血管收缩。此外,乙醇通过增加Ca2+敏感性来增强Ca(2+)非依赖性血管收缩。内皮依赖性松弛是由一氧化氮(NO)途径和内皮衍生超极化因子(EDHF)途径介导的。急性乙醇处理抑制NO-和edhf介导的松弛。此外,急性乙醇摄入还可以增强和抑制降钙素基因相关肽(CGRP)诱导的神经介导的松弛。这些相反的影响可能是由于物种或维管床的差异。因此,急性乙醇治疗降低血管松弛,从而将收缩-松弛平衡转向收缩。综上所述,这些影响是急性重度饮酒导致血管痉挛或缺血性心脏病等循环障碍的一种机制。相反,慢性低剂量乙醇对血管收缩没有影响,而慢性高剂量乙醇会增加血管收缩。此外,慢性乙醇摄入对神经介导放松的影响减弱、不变,甚至增加;因此,目前还无法对这些影响做出结论。有趣的是,慢性低剂量乙醇可增强内皮依赖性松弛;然而,较高的剂量抑制了这些反应。因此,定期或轻度至中度饮酒会增加血管松弛,并可能抑制血压升高,而长期大量饮酒可能会升高血压,导致各种临床症状。
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[Effect of alcohol on vascular function].

Vascular function is regulated by a balance of vasoconstriction and vasorelaxation. Disorder in this balance due to alcohol consumption causes various clinical conditions. In this review, we discuss the effects of acute and chronic ethanol consumption on vascular responses, including vasoconstriction, endothelium-dependent vasorelaxation, and nerve-mediated vasorelaxation. Acute ethanol administration induces vasoconstriction in ethanol-naive animals in vitro. Furthermore, ethanol can both potentiate and suppress agonist-induced Ca(2+)-dependent vasoconstriction. Moreover, ethanol augments Ca(2+)-independent vasoconstriction by increasing Ca2+ sensitivity. Endothelium-dependent relaxation is mediated by the nitric oxide (NO) pathway and the endothelium-derived hyperpolarizing factor (EDHF) pathway. Acute ethanol treatment inhibits both NO- and EDHF-mediated relaxation. Furthermore, acute ethanol ingestion can also potentiate and suppress calcitonin gene-related peptide (CGRP)-induced nerve-mediated relaxation. These opposing effects may be due to differences in species or vascular beds. Thus, acute ethanol treatment decreases vasorelaxation, thereby shifting the contraction-relaxation balance towards contraction. Combined, these effects are one mechanism by which acute heavy alcohol consumption causes circulatory disturbances such as vasospasms or ischemic heart disease. In contrast, chronic low-dose ethanol has no effect on vasoconstriction, whereas chronic high-dose ethanol increases vasoconstriction. Additionally, chronic ethanol intake has diminished, unchanged, and even increased effects on nerve-mediated relaxation; therefore, conclusions on these effects are not possible at present. Interestingly, chronic low-dose ethanol administration enhanced endothelium-dependent relaxation; however, higher doses inhibited these responses. Therefore, regular or light-to-moderate alcohol intake increases vasorelaxation and may suppress elevated blood pressure, whereas chronic heavy alcohol consumption may raise blood pressure, causing various clinical conditions.

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