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去窦弓神经大鼠出血期间的脑代谢和激素激活

Cerebral metabolic and hormonal activations during hemorrhage in sinoaortic-denervated rats.

作者信息

Kadekaro M, Summy-Long J Y, Terrell M L, Lekan H, Gary H E, Eisenberg H M

机构信息

Division of Neurosurgery, University of Texas Medical Branch, Galveston 77550.

出版信息

Am J Physiol. 1990 Aug;259(2 Pt 2):R305-12. doi: 10.1152/ajpregu.1990.259.2.R305.

DOI:10.1152/ajpregu.1990.259.2.R305
PMID:2386241
Abstract

Denervation of sinoaortic baroreceptors in normovolemic rats selectively increases glucose utilization in the median eminence and pituitary neural lobe and enhances secretion of vasopressin and oxytocin. Hemorrhage in denervated animals increases further glucose metabolism in these structures and stimulates the release of both neurohypophysial hormones with preferentially a greater effect on vasopressin. Similar increases in glucose metabolism in these structures with a greater release of vasopressin are observed in sham-operated animals during hemorrhage. Absence of high-pressure receptors, therefore, does not modify the preferential release of vasopressin during hypovolemia. Hemorrhage also increases glucose utilization in the paraventricular and supraoptic nuclei, area postrema, and subfornical organ in sham-operated and denervated rats but only after a 20% blood reduction. The results indicate that decreased inputs from low-pressure receptors during hemorrhage increase the activity of the hypothalamoneurohypophysial system after small reductions in blood volume and that the activity of this system is tonically inhibited by baroreceptors. The activities of structures responsive to circulating angiotensin II (subfornical organ and area postrema) are stimulated by larger reductions in blood volume and their metabolic activities are not tonically influenced by high-pressure receptors.

摘要

正常血容量大鼠的窦主动脉压力感受器去神经支配选择性增加正中隆起和垂体神经叶的葡萄糖利用,并增强血管加压素和催产素的分泌。去神经支配动物的出血进一步增加了这些结构中的葡萄糖代谢,并刺激了两种神经垂体激素的释放,对血管加压素的影响尤为显著。在假手术动物出血期间,观察到这些结构中葡萄糖代谢有类似增加,且血管加压素释放更多。因此,缺乏高压感受器并不会改变低血容量时血管加压素的优先释放。出血还会增加假手术和去神经支配大鼠室旁核、视上核、最后区和穹窿下器官的葡萄糖利用,但仅在失血20%后出现。结果表明,出血期间低压感受器输入减少,在血容量稍有减少后会增加下丘脑-神经垂体系统的活性,且该系统的活性受到压力感受器的紧张性抑制。对循环血管紧张素II有反应的结构(穹窿下器官和最后区)的活性在血容量大幅减少时受到刺激,其代谢活性不受高压感受器的紧张性影响。

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