Patel V B, Why H J, Richardson P J, Preedy V R
Department of Clinical Biochemistry, King's College School of Medicine & Dentistry, London, UK.
Adverse Drug React Toxicol Rev. 1997 Mar;16(1):15-43.
We have discussed in this review many features and possible mechanisms responsible for the development of alcoholic cardiomyopathy. The evidence suggests that defects in myofibrillar protein turnover occur in both acute and chronic alcohol studies. Possible mechanisms to explain poor contractile function include alterations in cellular calcium, magnesium or phosphate homeostasis. The toxic effects of acetaldehyde or the formation of fatty acid ethyl esters may cause impairment of mitochondrial oxidative phosphorylation. Alternatively, reduced amounts of heat shock proteins may result in poor assembly and protection of proteins. In acute ethanol toxicity ischaemia may occur, possibly due to increased xanthine oxidase activity or beta-adrenergic stimulation. Chronic alcohol consumption can also lead to the development of hypertension via magnesium loss and consequent alterations in peripheral vascular calcium regulation. However, these are only a few facets of a complex relationship between alcohol and the cardiovascular system.
在本综述中，我们讨论了酒精性心肌病发展过程中的许多特征和可能机制。证据表明，在急性和慢性酒精研究中均出现肌原纤维蛋白周转缺陷。解释收缩功能不良的可能机制包括细胞钙、镁或磷酸盐稳态的改变。乙醛的毒性作用或脂肪酸乙酯的形成可能导致线粒体氧化磷酸化受损。另外，热休克蛋白数量减少可能导致蛋白质组装不良和保护不足。在急性乙醇中毒时，可能由于黄嘌呤氧化酶活性增加或β-肾上腺素能刺激而发生缺血。长期饮酒还可通过镁流失以及外周血管钙调节的相应改变导致高血压。然而，这些只是酒精与心血管系统之间复杂关系的几个方面。
