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心房肽24通过Frank-Starling机制调节清醒犬的心肌功能。

Atriopeptin 24 regulates myocardial function via Frank-Starling mechanism in conscious dogs.

作者信息

Patel M B, Hintze T H

机构信息

Department of Physiology, New York Medical College, Valhalla 10595.

出版信息

Am J Physiol. 1990 Jan;258(1 Pt 2):H183-90. doi: 10.1152/ajpheart.1990.258.1.H183.

DOI:10.1152/ajpheart.1990.258.1.H183
PMID:2137297
Abstract

Recent studies have shown that the infusion of atriopeptins decreases blood volume because of the diuresis and also because of changes in vascular volume. In dogs chronically instrumented for the measurement of left ventricular pressure and internal left ventricular diameter, infusion of atriopeptin 24 (500 ng.kg-1.min-1 for 1 h), steady-state plasma levels of 6,000 pg/ml resulted in 5.9 +/- 1.7% decrease in left ventricular (LV) end-diastolic diameter (EDD) from 34.7 +/- 2.3 mm (P less than 0.05) and no significant change in LV first derivative of pressure with time (dP/dt), LV first derivative of dimension with time, LV dP/dt divided by internal diastolic circumference or percent shortening. Hematocrit increased from 42 to 46% (P less than 0.05). During pacing, infusion of atriopeptin 24 still reduced LV EDD by 7.5 +/- 1.8% from 32 +/- 2.8 mm (P less than 0.05), although there were no changes in the indexes of inotropic state. These results were unaffected by combined autonomic receptor blockade or by ganglionic blockade. Inflation of a hydraulic occluder around the aorta during the infusion of atriopeptin 24 to return LV EDD to preinfusion levels did not cause any index of myocardial contractility to increase significantly. At lower infusion rates that resulted in plasma atriopeptin levels of 2,000 pg/ml, atriopeptin 24 still reduced LV EDD without effect on inotropic state. Thus in the conscious dog, atriopeptins reduce preload independent of neuronal influences and without affecting inotropic state.

摘要

最近的研究表明,输注心房肽可降低血容量,这是由于利尿作用以及血管容量的变化所致。在长期植入用于测量左心室压力和左心室内径的犬中,输注心房肽24(500 ng·kg-1·min-1,持续1小时),稳态血浆水平达6000 pg/ml,导致左心室(LV)舒张末期直径(EDD)从34.7±2.3 mm降低5.9±1.7%(P<0.05),而左心室压力随时间的一阶导数(dP/dt)、左心室尺寸随时间的一阶导数、左心室dP/dt除以舒张期内径周长或缩短百分比均无显著变化。血细胞比容从42%增至46%(P<0.05)。在起搏期间,输注心房肽24仍使左心室EDD从32±2.8 mm降低7.5±1.8%(P<0.05),尽管心肌收缩状态指标无变化。这些结果不受联合自主神经受体阻断或神经节阻断的影响。在输注心房肽24期间,通过主动脉周围液压闭塞器充气使左心室EDD恢复到输注前水平,并未导致任何心肌收缩性指标显著增加。在较低输注速率下,导致血浆心房肽水平为2000 pg/ml时,心房肽24仍可降低左心室EDD,而不影响心肌收缩状态。因此,在清醒犬中,心房肽可独立于神经影响降低前负荷,且不影响心肌收缩状态。

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