Raff H, Kane C W, Wood C E
Department of Physiology, University of Florida College of Medicine, Gainesville 32610.
Am J Physiol. 1991 Jun;260(6 Pt 2):R1077-81. doi: 10.1152/ajpregu.1991.260.6.R1077.
The purpose of this study was to determine the interaction of hypoxia and hypercapnia in the control of arginine vasopressin (AVP) secretion in fetal sheep and to determine the role of the peripheral arterial chemoreceptors in that response. We measured the plasma AVP response to hypercapnia and/or hypoxia in catheterized intact or sinoaortic-denervated fetal sheep between 123 and 144 days of gestation. Ewes were exposed to the following inspired gases: two successive 30-min periods of normocapnic normoxia, 30 min of normocapnic normoxia followed by 30 min of normocapnic hypoxia, two successive 30-min periods of hypercapnic normoxia, or 30 min of hypercapnic normoxia followed by 30 min of hypercapnic hypoxia (i.e., asphyxia). Hypercapnia per se had no significant effect on fetal plasma AVP. Normocapnic hypoxia per se resulted in a significant increase in fetal plasma AVP. Although hypercapnia resulted in a significant acidemia, the decrease in arterial pH was more marked under hypoxic conditions. Hypercapnia/acidemia augmented the AVP response to hypoxia. Fetal sinoaortic denervation did not significantly attenuate any of the AVP responses. We conclude that hypercapnia augments the fetal AVP response to hypoxia and that the AVP response to neither normocapnic nor hypercapnic hypoxia is dependent on afferent information carried in the carotid sinus or aortic nerves.
本研究的目的是确定低氧和高碳酸血症在调控胎羊精氨酸加压素（AVP）分泌中的相互作用，并确定外周动脉化学感受器在该反应中的作用。我们在妊娠123至144天的完整或经窦主动脉去神经支配的插管胎羊中，测量了对高碳酸血症和/或低氧的血浆AVP反应。母羊暴露于以下吸入气体：两个连续30分钟的常碳酸常氧期、30分钟常碳酸常氧后接30分钟常碳酸低氧、两个连续30分钟的高碳酸常氧期、或30分钟高碳酸常氧后接30分钟高碳酸低氧（即窒息）。高碳酸血症本身对胎羊血浆AVP无显著影响。常碳酸低氧本身导致胎羊血浆AVP显著增加。虽然高碳酸血症导致显著的酸血症，但在低氧条件下动脉pH的下降更为明显。高碳酸血症/酸血症增强了AVP对低氧的反应。胎羊窦主动脉去神经支配并未显著减弱任何AVP反应。我们得出结论，高碳酸血症增强了胎羊AVP对低氧的反应，并且AVP对常碳酸或高碳酸低氧的反应均不依赖于通过颈动脉窦或主动脉神经传入的信息。
