Convertino V A, Thompson C A, Benjamin B A, Keil L C, Savin W M, Gordon E P, Haskell W L, Schroeder J S, Sandler H
Life Sciences Research Office, National Aeronautics and Space Administration, Kennedy Space Center, Florida 32899.
Clin Physiol. 1990 Jan;10(1):55-67. doi: 10.1111/j.1475-097x.1990.tb00083.x.
Haemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce blood volume shifts in 10 cardiac transplant recipients to assess the contribution of cardiac and vascular volume receptors in the control of ADH secretion. Each subject underwent 15 min of a control period in the seated posture, then assumed a lying posture for 30 min at 6 degrees head-down tilt (HDT) followed by 30 min of seated recovery. Venous blood samples and cardiac dimensions (echocardiography) were taken at 0 and 15 min before HDT, 5, 15 and 30 min of HDT, and 5, 15 and 30 min of seated recovery. Blood samples were analysed for haematocrit, plasma osmolality, plasma renin activity (PRA) and ADH. Resting plasma volume (PV) was measured by Evans blue dye and per cent changes in PV during posture changes were calculated from changes in haematocrit. Heart rate (HR) and blood pressure (BP) were recorded every 2 min. In the cardiac transplant subjects, mean HR decreased (BP less than 0.05) from 102 b.p.m. pre-HDT to 94 b.p.m. during HDT and returned to 101 b.p.m. in seated recovery while BP was slightly elevated (P less than 0.05). PV was increased by 6.3% (P less than 0.05) by the end of 30 min of HDT but returned to pre-HDT levels following seated recovery. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P less than 0.05) from 90 +/- 5 ml pre-HDT to 105 +/- 4 ml during HDT and returned to 88 +/- 5 ml in seated recovery. Plasma ADH was reduced by 28% (P less than 0.05) by the end of HDT and returned to pre-HDT levels with seated recovery. PRA was also reduced by 28% (P less than 0.05) with HDT. These responses were similar to those of six normal cardiac-innervated control subjects and one heart-lung recipient. Therefore, cardiac volume receptors are not the only mechanism for the control of ADH release during acute blood volume shifts in man.
在旨在诱导血容量变化的体位改变过程中，对10名心脏移植受者的血流动力学反应和抗利尿激素（ADH）进行了测量，以评估心脏和血管容量感受器在控制ADH分泌中的作用。每位受试者先在坐姿下进行15分钟的对照期，然后以头向下倾斜6度的姿势躺30分钟，接着进行30分钟的坐姿恢复。在头向下倾斜前0分钟和15分钟、头向下倾斜5分钟、15分钟和30分钟以及坐姿恢复5分钟、15分钟和30分钟时采集静脉血样本并测量心脏尺寸（超声心动图）。对血样进行血细胞比容、血浆渗透压、血浆肾素活性（PRA）和ADH分析。用伊文思蓝染料测量静息血浆容量（PV），并根据血细胞比容的变化计算体位改变期间PV的百分比变化。每2分钟记录心率（HR）和血压（BP）。在心脏移植受试者中，平均心率从倾斜前的102次/分钟降至倾斜期间的94次/分钟（P<0.05），并在坐姿恢复时回到101次/分钟，而血压略有升高（P<0.05）。头向下倾斜30分钟结束时，PV增加了6.3%（P<0.05），但在坐姿恢复后回到倾斜前水平。体位改变未改变血浆渗透压。平均左心室舒张末期容积从倾斜前的90±5毫升增加到倾斜期间的105±4毫升（P<0.05），并在坐姿恢复时回到88±5毫升。头向下倾斜结束时，血浆ADH降低了28%（P<0.05），并在坐姿恢复时回到倾斜前水平。头向下倾斜时PRA也降低了28%（P<0.05）。这些反应与6名正常心脏受神经支配的对照受试者和1名心肺移植受者的反应相似。因此，在人体急性血容量变化期间，心脏容量感受器并非控制ADH释放的唯一机制。
