Zhu J L, Leadley R J
Division of Experimental Medicine, St. Luke's Hospital and Foundation, Kansas City, Missouri 64111.
Proc Soc Exp Biol Med. 1995 Apr;208(4):361-9. doi: 10.3181/00379727-208-43863.
During episodes of blood loss, several apparently redundant mechanisms are activated to maintain arterial blood pressure. This study was designed to examine one such compensatory mechanism involving enhanced vasopressin release during hemorrhage when the autonomic nervous system (ANS) is pharmacologically blocked. First, to confirm that this compensatory mechanism exists in canines, conscious dogs were hemorrhaged under normal conditions and during ANS blockade. In dogs with intact cardiac nerves (intact, n = 7), hemorrhage at 0.8 ml/kg/min increased plasma vasopressin (PAVP) from 3.0 +/- 0.7 to 6.6 +/- 2.4 and 78 +/- 50 pg/ml at blood losses of 10 and 20 ml/kg, respectively. At the same amount of blood loss during hemorrhage with ANS blockage, PAVP was enhanced significantly from 33 +/- 17 to 230 +/- 90 and 610 +/- 270 pg/ml. ANS blockade did not, however, alter the hemorrhage-induced increases in plasma renin activity. Next, to examine the afferent mechanisms responsible for the enhanced PAVP response, cardiac-denervated dogs (CD, n = 9) were hemorrhaged with and without ANS blockade. Without blockade, PAVP increased from 3.7 +/- 0.9 to 5.2 +/- 0.8 and 26 +/- 11 pg/ml at blood losses of 10 and 20 ml/kg. PAVP was significantly higher in response to hemorrhage with ANS blockade, increasing from 17 +/- 6 to 76 +/- 18 and 330 +/- 80 pg/ml. The rise in PAVP in the CD dogs suggested that peripheral baroreceptors were involved in eliciting vasopressin release under these conditions. Therefore, the influence of arterial baroreceptors was examined by infusing norepinephrine during hemorrhage in order to maintain blood pressure constant. Under these conditions, PAVP increased significantly in the intact dogs at 10 ml/kg blood loss, but did not change in the CD dogs. These results demonstrate that the enhanced release of AVP during hemorrhage with ANS blockade can be mediated either by cardiac or arterial baroreceptors; however, the maximum response is elicited only when both sets of receptors are functioning normally.
在失血期间，会激活几种看似多余的机制来维持动脉血压。本研究旨在探讨一种这样的代偿机制，即在自主神经系统（ANS）被药物阻断时，出血期间血管加压素释放增强。首先，为了证实这种代偿机制在犬类中存在，在正常条件下和ANS阻断期间对清醒犬进行出血实验。对于心脏神经完整的犬（完整组，n = 7），以0.8 ml/kg/min的速度出血时，在失血10和20 ml/kg时，血浆血管加压素（PAVP）分别从3.0±0.7升高到6.6±2.4和78±50 pg/ml。在ANS阻断的出血过程中，失血量相同时，PAVP从33±17显著升高到230±90和610±270 pg/ml。然而，ANS阻断并未改变出血诱导的血浆肾素活性升高。接下来，为了研究导致PAVP反应增强的传入机制，对心脏去神经的犬（CD组，n = 9）在有和没有ANS阻断的情况下进行出血实验。在没有阻断的情况下，在失血10和20 ml/kg时，PAVP从3.7±0.9升高到5.2±0.8和26±11 pg/ml。在ANS阻断的出血情况下，PAVP显著更高，从17±6升高到76±18和330±80 pg/ml。CD组犬中PAVP的升高表明在这些条件下外周压力感受器参与了血管加压素的释放。因此，通过在出血期间输注去甲肾上腺素以维持血压恒定来研究动脉压力感受器的影响。在这些条件下，完整组犬在失血10 ml/kg时PAVP显著升高，但CD组犬中未发生变化。这些结果表明，在ANS阻断的出血期间AVP释放增强可由心脏或动脉压力感受器介导；然而，只有当两组感受器都正常运作时才会引发最大反应。
