Sweet W D, Freeman R H, Davis J O, Vari R C
Am J Physiol. 1985 Nov;249(5 Pt 2):H1038-44. doi: 10.1152/ajpheart.1985.249.5.H1038.
Chronic constriction of the thoracic inferior vena cava decreases venous return and cardiac output, increases the secretion of renin and aldosterone, and produces sodium retention with ascites and edema formation. The arterial pressure is maintained at normotensive levels in this caval model by an increase in total peripheral resistance. The objective of the present study was to compare renal and hemodynamic responses to ganglionic blockade in the conscious thoracic caval dog to responses obtained in another low-output model, the chronic sodium-deplete dog, and also to the responses obtained in the normal sodium-replete dog. The control base-line pressures averaged 103 +/- 2, 110 +/- 3, and 110 +/- 3 mmHg, respectively, in the sodium-replete, sodium-deplete, and thoracic caval dogs (P greater than 0.05). Ganglionic blockade in the conscious dog with caval constriction resulted in a sustained 20- to 30-mmHg fall in the arterial pressure; a sustained fall of 20 mmHg occurred in the sodium-deplete dogs. In contrast, ganglionic blockade failed to decrease the blood pressure at any time in the normal sodium-replete animals. Effective renal blood flow and creatinine clearance failed to demonstrate sustained changes after ganglionic blockade in any group of dogs; renal sodium excretion increased only in the normal sodium-replete dogs. These results suggest an enhanced contribution of the sympathetic nervous system to blood pressure maintenance in both the sodium-deplete and the caval dogs. Although the data fail to demonstrate an important contribution of the adrenergic system in the chronic sodium retention in these two experimental models, decreases in renal perfusion pressure may have blunted any potential natriuresis in these animals following ganglionic blockade.
慢性缩窄胸段下腔静脉会减少静脉回流和心输出量,增加肾素和醛固酮的分泌,并导致钠潴留伴腹水和水肿形成。在这个腔静脉模型中,通过增加总外周阻力将动脉血压维持在正常血压水平。本研究的目的是比较清醒胸段腔静脉犬对神经节阻断的肾脏和血流动力学反应,与另一个低输出量模型(慢性缺钠犬)以及正常钠充足犬的反应。在钠充足、缺钠和胸段腔静脉犬中,对照基线压力平均分别为103±2、110±3和110±3 mmHg(P>0.05)。清醒的腔静脉缩窄犬进行神经节阻断会导致动脉血压持续下降20至30 mmHg;缺钠犬的动脉血压持续下降20 mmHg。相比之下,神经节阻断在任何时候都未能降低正常钠充足动物的血压。在任何一组犬中,神经节阻断后有效肾血流量和肌酐清除率均未显示出持续变化;仅在正常钠充足犬中肾钠排泄增加。这些结果表明,交感神经系统在缺钠犬和腔静脉犬维持血压方面的作用增强。尽管数据未能证明肾上腺素能系统在这两个实验模型的慢性钠潴留中有重要作用,但神经节阻断后肾灌注压的降低可能削弱了这些动物潜在的利钠作用。