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慢性酒精性心脏抑制的可逆性:仓鼠的31P磁共振波谱分析

Reversibility of chronic alcohol cardiac depression: 31P magnetic resonance spectroscopy in hamsters.

作者信息

Auffermann W, Wu S, Parmley W W, Higgins C B, Wikman-Coffelt J

机构信息

Department of Radiology, University of California, San Francisco 94143.

出版信息

Magn Reson Med. 1989 Mar;9(3):343-52. doi: 10.1002/mrm.1910090306.

DOI:10.1002/mrm.1910090306
PMID:2709999
Abstract

In order to investigate the reversibility of chronic alcohol cardiac depression, hamsters were fed with 50% ethanol for 3 1/2 months, reaching serum alcohol levels of 0.13 +/- 0.11 g/dl (mean +/- SD). Alcohol was then withdrawn for 2 days. Isolated hearts were perfused according to a modified Langendorff method. Energy metabolites were studied using 31P magnetic resonance spectroscopy of isolated perfused hearts standardized by HPLC analysis of freeze-clamped tissue. Total intracellular calcium [Ca2+]i was measured with atomic absorption spectrophotometry, marking the extracellular space in vivo with K(CoEDTA). In alcohol-treated hamster hearts developed pressure was significantly depressed compared to controls. End-diastolic pressure was significantly increased. Coronary flow was not changed, whereas oxygen consumption and high-energy phosphate levels were significantly depressed. Intracellular pH was significantly decreased. [Ca2+]i was significantly increased. Heart weights were significantly lower. After alcohol withdrawal ventricular function, high-energy phosphate levels, and [Ca2+]i were not significantly different from control. The results indicate that chronic alcohol consumption depresses ventricular function and energy levels and also leads to myocardial acidosis. The increase in intracellular calcium likely causes mitochondrial dysfunction. Withdrawal of alcohol is associated with reversibility of functional and energetic cardiac depression.

摘要

为了研究慢性酒精性心脏抑制的可逆性,将仓鼠用50%乙醇喂养3个半月,血清酒精水平达到0.13±0.11 g/dl(平均值±标准差)。然后戒酒2天。采用改良的Langendorff方法灌注离体心脏。通过对冷冻钳夹组织进行HPLC分析标准化后,利用离体灌注心脏的31P磁共振波谱研究能量代谢物。用原子吸收分光光度法测量总细胞内钙[Ca2+]i,用K(CoEDTA)标记体内细胞外空间。与对照组相比,酒精处理的仓鼠心脏的发展压力明显降低。舒张末期压力明显升高。冠状动脉血流量未改变,而氧耗量和高能磷酸盐水平明显降低。细胞内pH值明显降低。[Ca2+]i明显升高。心脏重量明显较低。戒酒后排空功能、高能磷酸盐水平和[Ca2+]i与对照组无明显差异。结果表明,长期饮酒会降低心室功能和能量水平,并导致心肌酸中毒。细胞内钙的增加可能导致线粒体功能障碍。戒酒与心脏功能和能量抑制的可逆性有关。

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