Burghardt W, Müller R, Diehl K L, Wernze H
Medizinische Universitätsklinik Würzburg.
Z Kardiol. 1988;77 Suppl 2:104-10.
To assess the role of atrial natriuretic peptide (ANP) in relation to the sympathoadrenal and renin-angiotensin-aldosterone system, and sodium excretion, 88 cirrhotic patients (mean age 52 years; 28 compensated, 28 decompensated with ascites, and 32 decompensated and treated with diuretics) and 26 control subjects were investigated. Basal ANP levels were not different between any group of cirrhotics and controls. Circulating ANP was not related to elevated plasma noradrenaline and adrenaline, and enhanced plasma renin/aldosterone levels in ascitic patients. Furthermore, ANP was not related to urinary sodium excretion, blood pressure, and heart rate. In 30 cirrhotic patients (12 compensated, 18 decompensated with ascites including eight on diuretic therapy) and nine controls, a passive leg rising procedure for 1 h was performed in order to augment central blood volume and atrial pressure physiologically. Ascitic patients (with and without diuretic treatment) experienced a slight but significant increase in plasma ANP indicating preserved responsiveness of ANP release in cirrhosis. Plasma aldosterone was markedly depressed. The data support the underfilling concept of ascitic formation in advanced stages of cirrhosis. The failure of enhanced ANP release under basal conditions may be due to the diminished effective blood volume, resulting in insufficient atrial stretching.
为评估心房利钠肽(ANP)与交感肾上腺系统、肾素 - 血管紧张素 - 醛固酮系统以及钠排泄之间的关系,对88例肝硬化患者(平均年龄52岁;28例代偿期,28例失代偿期伴腹水,32例失代偿期且接受利尿剂治疗)和26例对照者进行了研究。任何一组肝硬化患者与对照者的基础ANP水平均无差异。循环ANP与腹水患者血浆去甲肾上腺素和肾上腺素升高以及血浆肾素/醛固酮水平升高无关。此外,ANP与尿钠排泄、血压和心率无关。对30例肝硬化患者(12例代偿期,18例失代偿期伴腹水,其中8例接受利尿剂治疗)和9例对照者进行了1小时的被动抬腿操作,以生理性增加中心血容量和心房压力。腹水患者(无论是否接受利尿剂治疗)血浆ANP均有轻微但显著的升高,表明肝硬化患者ANP释放的反应性保留。血浆醛固酮明显降低。这些数据支持肝硬化晚期腹水形成的血容量不足概念。基础条件下ANP释放增强失败可能是由于有效血容量减少,导致心房拉伸不足。