Left ventricular hypertrophy in rats with biliary cirrhosis

内科学 心室 内分泌学 医学 门脉高压 肌肉肥大 肝硬化 血管阻力 血管紧张素II 心脏病学 高动力循环 血流动力学 血压
作者
Javier Inserte,Antonia Perelló,Luís Agulló,Marisol Ruiz-Meana,Klaus-Dieter Schlüter,Noèlia Escalona,Mariona Graupera,Jaume Bosch,David García‐Dorado
出处
期刊:Hepatology [Lippincott Williams & Wilkins]
卷期号:38 (3): 589-598 被引量:52
标识
DOI:10.1053/jhep.2003.50369
摘要

Portal hypertension induces neuroendocrine activation and a hyperkinetic circulation state. This study investigated the consequences of portal hypertension on heart structure and function. Intrahepatic portal hypertension was induced in male Sprague–Dawley rats by chronic bile duct ligation (CBDL). Six weeks later, CBDL rats showed higher plasma angiotensin–II and endothelin–1 ( P < .01), 56% reduction in peripheral resistance and 73% reduction in pulmonary resistance ( P < .01), 87% increase in cardiac index and 30% increase in heart weight ( P < .01), and increased myocardial nitric oxide (NO) synthesis. In CBDL rats, macroscopic analysis demonstrated a 30% ( P < .01) increase in cross–sectional area of the left ventricular (LV) wall without changes in the LV cavity or in the right ventricle (RV). Histomorphometric analysis revealed increased cell width (12%, P < .01) of cardiomyocytes from the LV of CBDL rats, but no differences in myocardial collagen content. Myocytes isolated from the LV were wider (12%) and longer (8%) than right ventricular myocytes ( P < .01) in CBDL rats but not in controls. CBDL rats showed an increased expression of ANF and CK–B genes ( P < .01). Isolated perfused CBDL hearts showed pressure/end–diastolic pressure curves and response to isoproterenol identical to sham hearts, although generated wall tension was reduced because of the increased wall thickness. Coronary resistance was markedly reduced. This reduction was abolished by inhibition of NO synthesis with N –nitro–L–arginine. Expression of eNOS was increased in CBDL hearts. In conclusion, portal hypertension associated to biliary cirrhosis induces marked LV hypertrophy and increased myocardial NO synthesis without detectable fibrosis or functional impairment. This observation could be relevant to patients with cirrhosis.

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