Ma Z, Lee S S
Liver Unit, Gastroenterology Research Group, University of Calgary, Alberta, Canada.
Hepatology. 1996 Aug;24(2):451-9. doi: 10.1002/hep.510240226.
In cirrhosis, cardiac contractile function has been extensively documented to be abnormal. At baseline, cardiac output is increased, and this is one of the characteristics of hyperdynamic circulation. However, when cirrhotic patients are challenged by pharmacological or physiological stress, ventricular hyporesponsiveness is revealed. Similar patterns have been noted in cirrhotic animal models. This phenomenon has been termed "cirrhotic cardiomyopathy." Although alcohol abuse may contribute to some cases of cirrhotic cardiomyopathy, it has been clearly documented to occur even in the absence of alcohol ingestion. Diminished myocardial beta-adrenergic receptor signal transduction function, possibly caused by a persistent elevation in norepinephrine content, has been shown to play an important role. Alternation in cardiac plasma membrane properties due to impaired lipid metabolism is also crucial. Other possible pathogenic factors are reviewed, including accumulation of cardiodepressant substances caused by hepatocellular insufficiency, and ventricular overload secondary to increased blood volume and hyperdynamic circulation. Because the cardiac reserve function is borderline in patients with cirrhosis, cardiovascular status should be carefully monitored, especially when patients undergo stresses such as liver transplantation or portosystemic shunting procedures.
在肝硬化患者中，心脏收缩功能异常已有大量文献记载。在基线状态下，心输出量增加，这是高动力循环的特征之一。然而，当肝硬化患者受到药物或生理应激挑战时，会出现心室反应性降低。在肝硬化动物模型中也观察到类似模式。这种现象被称为“肝硬化性心肌病”。虽然酒精滥用可能导致部分肝硬化性心肌病病例，但即使在无酒精摄入的情况下也明确有该疾病发生。已表明，去甲肾上腺素含量持续升高可能导致心肌β - 肾上腺素能受体信号转导功能减弱，这起了重要作用。脂质代谢受损导致心脏质膜特性改变也很关键。还综述了其他可能的致病因素，包括肝细胞功能不全导致的心脏抑制物质蓄积，以及血容量增加和高动力循环继发的心室负荷过重。由于肝硬化患者的心脏储备功能处于临界状态，应仔细监测心血管状况，尤其是在患者接受肝移植或门体分流手术等应激情况时。
