Darlington D N, Chew G, Ha T, Keil L C, Dallman M F
Department of Physiology, University of California San Francisco 94143.
Endocrinology. 1990 Aug;127(2):766-72. doi: 10.1210/endo-127-2-766.
Fed adrenalectomized rats survive the stress of hemorrhage and hypovolemia, whereas fasted adrenalectomized rats become hypotensive and hypoglycemic after the first 90 min and die within 4 h. We have studied the effects of glucose and corticosterone (B) infusions after hemorrhage as well as treatment with B at the time of adrenalectomy on the capacity of chronically prepared, conscious, fasted, adrenalectomized rats to survive hemorrhage. We have also measured the magnitudes of vasoactive hormone responses to hemorrhage. Maintenance of plasma glucose concentrations did not sustain life; however, treatment of rats at the time of adrenalectomy with B allowed 100% survival, and acute treatment of adrenalectomized rats at the time of hemorrhage allowed about 50% survival during the 5-h posthemorrhage observation period. Rats in the acute B infusion group that died exhibited significantly increased plasma B and significantly decreased plasma glucose concentrations by 2 h compared to the rats that lived. Plasma vasopressin, renin, and norepinephrine responses to hemorrhage were markedly augmented in the adrenalectomized rats not treated with B, and plasma vasopressin concentrations were significantly elevated at 1 and 2 h in all of the rats that subsequently died compared to values in those that lived. We conclude that: 1) death after hemorrhage in fasted adrenalectomized rats is not a result of lack of glucose; 2) chronic and, to an extent, acute treatment of fasted adrenalectomized rats with B enables survival; 3) fasted adrenalectomized rats exhibit strong evidence of hepatic insufficiency which is not apparent in either fed adrenalectomized rats or B-treated fasted adrenalectomized rats; 4) death after hemorrhage in fasted adrenalectomized rats may result from hepatic failure as a consequence of marked splanchnic vasoconstriction mediated by the actions of extraordinarily high levels of vasoactive hormones after hemorrhage; and 5) B appears to act to decrease the magnitude of response of vasoactive hormones after hemorrhage in fasted adrenalectomized rats.
切除肾上腺的喂食大鼠能承受出血和血容量过低的应激,而切除肾上腺的禁食大鼠在最初90分钟后会出现低血压和低血糖,并在4小时内死亡。我们研究了出血后输注葡萄糖和皮质酮(B)以及在切除肾上腺时用B治疗对长期制备的、清醒的、禁食的、切除肾上腺的大鼠承受出血能力的影响。我们还测量了对出血的血管活性激素反应的幅度。维持血浆葡萄糖浓度并不能维持生命;然而,在切除肾上腺时用B治疗大鼠可使其100%存活,在出血时对切除肾上腺的大鼠进行急性治疗可使约50%的大鼠在出血后5小时的观察期内存活。与存活的大鼠相比,急性B输注组中死亡的大鼠在2小时时血浆B显著升高,血浆葡萄糖浓度显著降低。未用B治疗的切除肾上腺的大鼠对出血的血浆血管加压素、肾素和去甲肾上腺素反应明显增强,与存活大鼠相比,所有随后死亡的大鼠在1小时和2小时时血浆血管加压素浓度均显著升高。我们得出以下结论:1)禁食的切除肾上腺的大鼠出血后死亡不是由于缺乏葡萄糖;2)用B对禁食的切除肾上腺的大鼠进行长期以及在一定程度上的急性治疗可使其存活;3)禁食的切除肾上腺的大鼠表现出明显的肝功能不全迹象,这在喂食的切除肾上腺的大鼠或用B治疗的禁食的切除肾上腺的大鼠中均不明显;4)禁食的切除肾上腺的大鼠出血后死亡可能是由于出血后极高水平的血管活性激素作用介导的明显内脏血管收缩导致肝功能衰竭;5)B似乎起到降低禁食的切除肾上腺的大鼠出血后血管活性激素反应幅度的作用。