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心脏容量感受器在人体急性模拟失重期间抗利尿激素释放控制中的作用。

Role of cardiac volume receptors in the control of ADH release during acute simulated weightlessness in man.

作者信息

Convertino V A, Benjamin B A, Keil L C, Sandler H

机构信息

Biomedical Research Division, NASA-Ames Research Center, Moffett Field, California 94035, USA.

出版信息

Physiologist. 1984;27(6 Suppl):S51-2.

Abstract

Hemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce central blood volume shifts in ten cardiac and one heart-lung transplant recipients to assess the contribution of cardiac volume receptors in the control of ADH release during the initial acute phase of exposure to weightlessness. Each subject underwent 15 min of a sitting-control period (C) followed by 30 min of -6 degrees headdown tilt (T) and 30 min of resumed sitting (S). Venous blood samples and cardiac dimensions were taken at 0 and 15 min of C; 5, 15, and 30 min of T; and, 5, 15, and 30 min of S. Blood samples were analyzed for hematocrit, plasma osmolality, plasma renin activity (PRA), and ADH. Heart rate (HR) and blood pressure (BP) were recorded every two min. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P < .05) from 90 ml in C to 106 ml in T and returned to 87 ml in S. Plasma ADH was reduced by 20% (P < .05) with T and returned to control levels with S. These responses were similar in six normal cardiac-innervated control subjects. These data may suggest that cardiac volume receptors are not the primary mechanism for the control of ADH release during acute central volume shifts in man.

摘要

在旨在引起中心血容量变化的体位改变过程中,对10名心脏移植受者和1名心肺移植受者的血流动力学反应及抗利尿激素(ADH)进行了测量,以评估在暴露于失重状态的初始急性期,心脏容量感受器在控制ADH释放中的作用。每位受试者先进行15分钟的坐位对照期(C),随后进行30分钟的 -6度头低位倾斜(T),再进行30分钟恢复坐位(S)。在C期的0和15分钟、T期的5、15和30分钟以及S期的5、15和30分钟采集静脉血样本并测量心脏尺寸。分析血样中的血细胞比容、血浆渗透压、血浆肾素活性(PRA)和ADH。每两分钟记录心率(HR)和血压(BP)。体位改变未改变血浆渗透压。平均左心室舒张末期容积从C期的90毫升增加(P < .05)至T期的106毫升,在S期又回到87毫升。T期时血浆ADH降低了20%(P < .05),S期时恢复到对照水平。这些反应在6名正常心脏有神经支配的对照受试者中相似。这些数据可能表明,在人体急性中心血容量变化期间,心脏容量感受器并非控制ADH释放的主要机制。

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