Response of vasopressin and norepinephrine to lower body negative pressure in humans.
Response of vasopressin and norepinephrine to lower body negative pressure in humans.
复制标题
加压素和去甲肾上腺素对人体较低身体负压的反应。
DOI：
10.1152/ajpheart.1982.243.6.h970
复制
发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Cohn,JN
中科院分区：
文献类型：
--
作者：
Goldsmith,SR;Francis,GS;Cowley,AW;Cohn,JN
为了研究心肺压力感受器和窦主动脉压力感受器对正常人精氨酸加压素(AVP)非渗透性释放的作用，我们对9名没有高血压或心脏病证据的个体进行了分级下体负压(LBNP)。我们还以血浆去甲肾上腺素(NE)为指标研究了该动作对交感神经系统活动的影响。测量心率(HR)、平均动脉压(MAP)、脉压(PP)和中心静脉压(CVP)。每一阶段采血检测AVP和NE。AVP采用放射免疫法测定，去甲肾上腺素(NE)采用放射酶法测定。在第一次下体负压期间，中心静脉压下降，而心率、平均动脉压和脉压没有变化。NE由147+/-47升至212+/-53(SD)pg/ml，P<0.01，而AVP(5.0+/-1.0pg/ml)无明显变化。随着负压的增加，CVP进一步下降，HR增加，PP变窄，但MAP无明显变化。NE进一步升高至291+/-58pg/ml(P<0.01)，但AVP仍无明显变化。一名受试者血压明显降低，他的AVP从2.6 pg/ml增加到81pg/ml。CVP的下降可能通过心肺受体导致交感神经激活，因此不会增加AVP的水平；CVP的进一步下降导致窦主动脉压力感受器的轻度卸载和交感神经活动的进一步增加也不能刺激AVP。然而，低血压伴随着循环中AVP的迅速而深刻的增加。
To examine the contributions of cardiopulmonary and sinoaortic baroreceptors to the nonosmotic release of arginine vasopressin (AVP) in normal humans, we subjected nine individuals without evidence of hypertension or heart disease to graded, lower body negative pressure (LBNP). We also studied the effects of this maneuver on sympathetic nervous system activity using plasma norepinephrine (NE) as an index. Heart rate (HR), mean arterial pressure (MAP), pulse pressure (PP), and central venous pressure (CVP) were measured in the control state and during two consecutive levels of increasingly intense LBNP. At each stage blood was sampled for AVP and NE. AVP was analyzed by radioimmunoassay, NE by a radioenzymatic method. During the first level of LBNP, CVP decreased with no change in HR, MAP, or PP. NE increased from 147 +/- 47 to 212 +/- 53 (SD) pg/ml, P less than 0.01, whereas AVP (5.0 +/- 1.0 pg/ml) did not change. With increased suction CVP fell further, HR increased, and PP narrowed, but MAP did not change. NE further increased to 291 +/- 58 pg/ml (P less than 0.01), but AVP still did not change significantly. One subject became markedly hypotensive, and his AVP increased from 2.6 to 81 pg/ml. A fall in CVP that results in sympathetic activation presumably via cardiopulmonary receptors does not therefore increase AVP levels; a further fall in CVP that leads to modest unloading of the sinoaortic baroreceptor and further increased sympathetic activity also fails to stimulate AVP. Hypotension, however, is accompanied by a rapid and profound increase in circulating AVP.