Effect of vasopressin on systemic capacity.

Effect of vasopressin on systemic capacity.
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加压素对全身能力的影响。

DOI:
10.1152/ajpheart.1991.261.5.h1494
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发表时间:
1991
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Rutlen,DL
Rutlen,DL
中科院分区:
--
文献类型:
--
作者:
Welt,FG;Rutlen,DL

文献摘要

被引文献

相似文献

为了评估血管加压素(VP)对全身容量(SC)的影响,将血液从腔静脉引流至氧合器并以恒定速率返回主动脉,以便在17只麻醉猪中测量SC的变化作为氧合器体积变化的倒数。VP给药(1.1 U/min ia)10分钟后,平均动脉压从67 +/- 2升高至144 +/- 7 mmHg(P <0.001)。SC迅速下降,最低值为110 +/- 32 ml(P <0.02,5.5 ml/kg)5 min时低于对照组,但恢复至35 +/- 65 ml(P =不显著,1.8 ml/kg)低于对照组。门静脉压从19.3 +/- 2.6 mmHg降至16.6 +/- 2.7 mmHg(P小于0.001),门静脉血流量从828 +/- 68降至458 +/- 92 ml/min(P小于0.001)。经肠系膜静脉阻力增加。内脏摘除后,VP只引起SC增加。因此,VP导致初始SC递减完全是由于内脏容量的减少。内脏容量的减少至少部分是由于胃肠道动脉流入量的减少和随后门静脉压力的降低引起的。VP对SC的这些初始作用预期会增强完整动物的心室充盈和心输出量,并且在对出血的急性代偿反应中可能很重要。
To assess the effect of vasopressin (VP) on systemic capacity (SC), blood was drained from the venae cavae to an oxygenator and returned to the aorta at a constant rate so that changes in SC could be measured as the inverse of changes in oxygenator volume in 17 anesthetized pigs. After 10 min of VP administration (1.1 U/min ia), mean arterial pressure increased from 67 +/- 2 to 144 +/- 7 mmHg (P less than 0.001). SC decreased promptly and reached a nadir of 110 +/- 32 ml (P less than 0.02, 5.5 ml/kg) below control at 5 min but returned to 35 +/- 65 ml (P = not significant, 1.8 ml/kg) below control at 10 min. Portal venous pressure decreased from 19.3 +/- 2.6 to 16.6 +/- 2.7 mmHg (P less than 0.001), and portal flow decreased from 828 +/- 68 to 458 +/- 92 ml/min (P less than 0.001). Transhepatic venous resistance increased. After evisceration, VP caused only an increase in SC. Thus VP causes an initial SC decrement due entirely to a decrease in splanchnic capacity. The decrease in splanchnic capacity must be caused, at least in part, by the decrease in gastrointestinal arterial inflow and subsequent decrease in portal venous pressure. These initial effects of VP on SC would be expected to enhance ventricular filling and cardiac output in the intact animal and could be important in the acute compensatory response to hemorrhage.