Shen Y T, Cowley A W, Vatner S F
Department of Medicine, Harvard Medical School, Brigham & Women's Hospital, Boston, Mass.
Circ Res. 1991 May;68(5):1422-36. doi: 10.1161/01.res.68.5.1422.
To determine the relative roles of cardiac and sinoaortic baroreceptors in mediation of arginine vasopressin (AVP) release, hemorrhage was performed in five groups of conscious splenectomized dogs: 1) all nerves intact; 2) either chronic surgical or acute pharmacological (intrapericardial lidocaine) cardiac denervation (CD); 3) chronic sinoarotic denervation (SAD); 4) combined chronic sinoartic denervation plus either chronic or acute cardiac denervation (SAD + CD); and 5) all nerves intact, but with ganglionic blockade. Hemorrhage (0.5 ml/min/kg) reduced mean arterial pressure similarly in the intact and CD groups. Decreases in mean arterial pressure were augmented in SAD, SAD + CD, and ganglion-blocked groups compared with responses in intact and CD groups. There were no differences in responses of plasma AVP to hemorrhage in the intact and CD groups, but the AVP response was significantly blunted in the SAD + CD group as compared with SAD alone. When compared during the early stage of hemorrhage, at the same reduction in mean arterial pressure, the rise in AVP was greater in the ganglion-blocked group than in the SAD + CD group, but was less than in the intact group. With a protocol to reduce mean arterial pressure by 20 mm Hg over the same period (42 +/- 0.6 minutes) in four of the groups, the blood volume required to reduce mean arterial pressure by 20 mm Hg was similar in the intact (20 +/- 1 ml/kg) and CD (21 +/- 1 ml/kg) groups, but was less in the SAD (12 +/- 1 ml/kg) and SAD + CD (12 +/- 1 ml/kg) groups. Again, similar increases were observed in AVP between the intact (50 +/- 9 pg/ml) and CD (51 +/- 9 pg/ml) groups, whereas increases in AVP were diminished in the SAD (11 +/- 3 pg/ml) and SAD + CD (7 +/- 2 pg/ml) groups. In the presence of an AVP antagonist, decreases in mean arterial pressure and increases in total peripheral resistance with hemorrhage were affected similarly in both the intact and CD groups, whereas hemodynamic impairment by AVP blockade was less marked in the SAD and SAD + CD groups. These results indicate that cardiac receptors are not the major regulators of AVP release during progressive hemorrhage in conscious dogs. However, when the complicating influences of sinoaortic reflexes were eliminated, a modest role for cardiac receptors was uncovered.
为了确定心脏和窦主动脉压力感受器在精氨酸血管加压素（AVP）释放介导中的相对作用，对五组清醒脾切除犬进行了出血实验：1）所有神经完整；2）慢性手术或急性药理学（心包内注射利多卡因）心脏去神经支配（CD）；3）慢性窦主动脉去神经支配（SAD）；4）慢性窦主动脉去神经支配加慢性或急性心脏去神经支配（SAD + CD）；5）所有神经完整，但进行神经节阻断。出血（0.5 ml/min/kg）使完整组和CD组的平均动脉压以相似幅度降低。与完整组和CD组的反应相比，SAD组、SAD + CD组和神经节阻断组的平均动脉压下降幅度增大。完整组和CD组血浆AVP对出血的反应无差异，但与单独的SAD组相比，SAD + CD组的AVP反应明显减弱。在出血早期，当平均动脉压下降幅度相同时，神经节阻断组AVP的升高幅度大于SAD + CD组，但小于完整组。在四组中采用在相同时间段（42±0.6分钟）将平均动脉压降低20 mmHg的方案，完整组（20±1 ml/kg）和CD组（21±1 ml/kg）降低平均动脉压20 mmHg所需的血量相似，但SAD组（12±1 ml/kg）和SAD + CD组（12±1 ml/kg）所需血量较少。同样，完整组（50±9 pg/ml）和CD组（51±9 pg/ml）的AVP升高相似，而SAD组（11±3 pg/ml）和SAD + CD组（7±2 pg/ml）的AVP升高减弱。在存在AVP拮抗剂的情况下，完整组和CD组出血时平均动脉压的降低和总外周阻力的增加受到的影响相似，而在SAD组和SAD + CD组中，AVP阻断对血流动力学的损害不太明显。这些结果表明，在清醒犬进行性出血期间，心脏感受器不是AVP释放的主要调节因素。然而，当消除窦主动脉反射的复杂影响时，发现心脏感受器有适度作用。
