Breslow M J, Ball T D, Miller C F, Raff H, Traystman R J
Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
Am J Physiol. 1989 Nov;257(5 Pt 2):H1458-65. doi: 10.1152/ajpheart.1989.257.5.H1458.
To evaluate whether hypoxia-induced increases in adrenal cortical (CQ) and medullary (MQ) blood flow (radiolabeled microspheres) occur secondary to hypoxia-induced secretory activity, pentobarbital-anesthetized ventilated dogs were pretreated with dexamethasone (DEX) to prevent adrenocorticotropic hormone (ACTH) and corticosteroid secretory changes or underwent unilateral adrenal denervation to prevent adrenal catecholamine secretory responses. In nonsurgically stressed dogs, DEX completely prevented increases in ACTH or corticosteroid levels during reduction of arterial oxygen content to 8 vol% but had no effect on hypoxia-induced doubling of CQ. In dogs in which adrenal oxygen consumption (VO2) was measured, DEX reduced VO2 by 50% without altering CQ. Unilateral adrenal denervation prevented hypoxia-induced increases in adrenal catecholamine secretion and MQ but had no effect on the CQ response. These results suggest that hypoxia-induced medullary vasodilation is associated with adrenal catecholamine secretory activity but that increases in CQ occur independent of secretory activity and likely represent direct vascular effects of hypoxia.
为评估低氧诱导的肾上腺皮质（CQ）和髓质（MQ）血流增加（放射性微球法）是否继发于低氧诱导的分泌活动，对戊巴比妥麻醉通气的犬，用地塞米松（DEX）预处理以防止促肾上腺皮质激素（ACTH）和皮质类固醇分泌变化，或进行单侧肾上腺去神经支配以防止肾上腺儿茶酚胺分泌反应。在非手术应激犬中，DEX完全阻止了动脉氧含量降至8 vol%时ACTH或皮质类固醇水平的升高，但对低氧诱导的CQ加倍无影响。在测量肾上腺氧耗（VO2）的犬中，DEX使VO2降低50%而不改变CQ。单侧肾上腺去神经支配可防止低氧诱导的肾上腺儿茶酚胺分泌增加和MQ增加，但对CQ反应无影响。这些结果表明，低氧诱导的髓质血管舒张与肾上腺儿茶酚胺分泌活动有关，但CQ的增加独立于分泌活动发生，可能代表低氧对血管的直接作用。
