Cardiac and vascular changes in cirrhosis:Pathogenic mechanisms

心血管的畸形伴随门静脉高血压和肝硬化。这些由亢奋的动态循环组成，是减少定义吝啬的动脉压和全身的脉管的抵抗，和增加的心输出量。尽管有基线，到刺激的增加的心输出量，室的影响收缩力的和变时回答被弄钝，作为肝脏硬化症的心肌症知道的一个条件。两个条件可以玩一在主要外科或肝移植以后包括腹水，流血的 variceal， hepatorenal 和增加的手术后的死亡在许多开始或加重病原的角色肝失败或门静脉高血压的复杂并发症。这评论简短检验可以位于这些心血管的畸形下面的主要机制，专注于氮的氧化物，内长的 cannabinoids，中央神经激活和肾上腺素能的受体变化。未来工作应该探讨在这些系统之间的复杂相互关系。

Cardiovascular abnormalities accompany both portal hypertension and cirrhosis. These consist of hyperdynamic circulation, defined as reduced mean arterial pressure and systemic vascular resistance, and increased cardiac output. Despite the baseline increased cardiac output, ventricular inotropic and chronotropic responses to stimuli are blunted, a condition known as cirrhotic cardiomyopathy. Both conditions may play an initiating or aggravating pathogenic role in many of the complications of liver failure or portal hypertension including ascites, variceal bleeding, hepatorenal syndrome and increased postoperative mortality after major surgery or liver transplantation. This review briefly examines the major mechanisms that may underlie these cardiovascular abnormalities, concentrating on nitric oxide, endogenous cannabinoids, central neural activation and adrenergic receptor changes. Future work should address the complex interrelationships between these systems.