Cardiac plasma membrane physical properties and β‐adrenergic receptor function are unaltered in portal‐hypertensive rats
Cardiac plasma membrane physical properties and β‐adrenergic receptor function are unaltered in portal‐hypertensive rats
复制标题
门脉高压大鼠的心脏质膜物理特性和β-肾上腺素能受体功能未改变
作者：
Zeng;J. Meddings;Sam Lee
我们之前已经证明，肝硬化大鼠模型中的心肌收缩力受损可能是继发于影响β-肾上腺素能受体功能的心脏质膜物理特性改变的继发性。目前尚不清楚该模型中这是由肝硬化还是门静脉高压引起的，因此我们在无肝硬化的肝前期门静脉高压大鼠模型中研究了心肌细胞质膜的物理性质、脂质组成和β-肾上腺素能受体功能。门静脉高压是由分级门静脉狭窄引起的，而对照组则进行了假手术。使用二苯基己三烯和一系列蒽酰氧基硬脂酸通过荧光偏振方法研究心脏肌膜质膜的物理性质，以分别估计膜流动性的静态和动态成分。使用3 H-二氢阿普洛尔作为放射性配体测量β-肾上腺素能受体密度和结合亲和力。通过放射免疫测定法测量异丙肾上腺素刺激的腺苷酸环化酶活性。与对照组相比，门静脉高压大鼠的膜流动性的静态和动态成分均没有显着差异。两组之间的膜胆固醇、磷脂含量和胆固醇/磷脂比率没有差异。门静脉高压大鼠的β-肾上腺素能受体密度和结合亲和力（分别为1.65±0.06pmol/mg蛋白质和6.78±0.80nmol/L）与对照组（1.76±0.17pmol/mg蛋白质和7.25±1.48nmol/L）没有差异。异丙肾上腺素刺激的门脉高压大鼠膜内腺苷酸环化酶活性与对照组没有显着差异。我们的结论是，门脉高压大鼠的心脏质膜物理特性和β-肾上腺素受体功能未受损，这表明肝硬化心肌病本身并不是由门脉高压引起的。 （肝病学 1995；22：188-193。）
We have previously demonstrated that impairment of cardiac contractility in a rat model of cirrhosis may be secondary to altered cardiac plasma membrane physical properties affecting β‐adrenergic receptor function. It is unclear whether this is caused by the cirrhosis or by the portal hypertension in this model, so we studied cardiomyocyte plasma membrane physical properties, lipid composition, and β‐adrenergic receptor function in a rat model of prehepatic portal hypertension without cirrhosis. Portal hypertension was induced by graded portal vein stenosis, whereas controls had a sham operation. Cardiac sarcolemmal plasma membrane physical properties were studied by fluorescent polarization methods using diphenylhexatriene and a series of anthroyloxy‐stearic acids to estimate, respectively, the static and dynamic components of membrane fluidity. β‐Adrenergic receptor density and binding affinity were measured using <3>H‐dihydroalprenolol as a radioligand. Isoproterenol‐stimulated adenylyl cyclase activity was measured by radioimmunoassay. Neither the static nor the dynamic components of membrane fluidity were significantly different in portal‐hypertensive rats compared with the controls. The membrane cholesterol, phospholipid content, and the cholesterol/phospholipid ratio did not differ between the two groups. β‐Adrenergic receptor density and binding affinity in the portal‐hypertensive rats (respectively, 1.65 ± 0.06 pmol/mg protein and 6.78 ± 0.80 nmol/L) were not different from controls (1.76 ± 0.17 pmol/mg protein and 7.25 ± 1.48 nmol/L). Isoproterenol‐stimulated adenylyl cyclase activity in membranes from portal‐hypertensive rats did not significantly differ from controls. We conclude that cardiac plasma membrane physical properties and β‐adrenoceptor function in portal hypertensive rats remains unimpaired, suggesting that the cardiomyopathy of cirrhosis is not caused by portal hypertension per se. (HEPATOLOGY 1995; 22:188‐193.)
影响因子：
56.9
作者：
PITCHER, JA;INGLESE, J;LEFKOWITZ, RJ
通讯作者：
LEFKOWITZ, RJ