Hypoxia and hypercapnia increase the sympathoadrenal medullary functions in anesthetized, artificially ventilated rats.
Hypoxia and hypercapnia increase the sympathoadrenal medullary functions in anesthetized, artificially ventilated rats.
复制标题
缺氧和高碳酸血症会增加麻醉、人工通气大鼠的交感肾上腺髓质功能。
DOI：
10.2170/jjphysiol.39.511
复制
发表时间：
1989
期刊：
影响因子：
--
通讯作者：
A. Trzebski
中科院分区：
文献类型：
--
作者：
D. Biesold;M. Kurosawa;A. Sato;A. Trzebski
分别对乌拉坦麻醉和人工通气的大鼠施加分级缺氧（FETO2 14-6%）和高碳酸血症（FETCO2 6-10%）45秒和2分钟，导致肾上腺交感传出神经活动增加，同时肾上腺静脉流出物中测得的肾上腺素和去甲肾上腺素分泌增加。肾上腺素和去甲肾上腺素的增加百分比几乎相等。在双侧颈动脉窦神经（CSN）被切断的大鼠中，缺氧不会对肾上腺交感神经活动或儿茶酚胺分泌产生任何影响。相比之下，CSN 去神经大鼠的兴奋性肾上腺神经和儿茶酚胺分泌反应对高碳酸血症保持不变。切断其分支支配肾上腺的内脏神经后，通过低频刺激内脏神经末梢端维持儿茶酚胺分泌的静息水平，缺氧并没有导致儿茶酚胺分泌的任何增加。然而，高碳酸血症（FETCO2 8 和 10%）会诱导去神经肾上腺髓质分泌儿茶酚胺，尽管其反应强度明显低于肾上腺神经完整的动物。结论是缺氧通过颈动脉化学感受器反射刺激肾上腺髓质，而高碳酸血症主要通过颈动脉化学感受器以外的机制起作用，例如中枢化学感受器，对肾上腺髓质有一些直接刺激作用。讨论了缺氧和高碳酸血症期间交感肾上腺兴奋的双重机制的功能意义。
Graded hypoxia (FETO2 14-6%) and hypercapnia (FETCO2 6-10%), which were applied for 45s and 2 min, respectively, to urethane anesthetized and artificially ventilated rats produced an increase in adrenal sympathetic efferent nerve activity in parallel with increases in adrenaline and noradrenaline secretion measured in the adrenal venous effluent. Percentage increases in adrenaline and noradrenaline were almost equal. In rats whose carotid sinus nerves (CSN) were bilaterally cut, hypoxia did not produce any effect on adrenal sympathetic nerve activity or catecholamine secretion. In contrast, excitatory adrenal nerve and catecholamine secretory responses to hypercapnia remained unchanged in CSN denervated rats. After severing a splanchnic nerve whose branches innervated the adrenal gland, while maintaining the resting level of catecholamine secretion by low-frequency stimulation of the peripheral end of the splanchnic nerve, hypoxia did not produce any increase in catecholamine secretion. Hypercapnia (FETCO2 8 and 10%), however, induced catecholamine secretion from denervated adrenal medulla, although the magnitude of the response was significantly lower than that in animals with adrenal nerve intact. It is concluded that hypoxia stimulates the adrenal medulla via the carotid chemoreceptor reflex whereas hypercapnia acts mainly via mechanisms besides carotid chemoreceptors such as central chemoreceptors with some direct stimulatory effect on the adrenal medulla. The functional significance of these dual mechanisms of sympathoadrenal excitation during hypoxia and hypercapnia is discussed.
血流动力学和血管活性介质对实验性呼吸衰竭的反应。
DOI：
10.1152/jappl.1982.52.5.1230
发表时间：
1982
期刊：
Journal of applied physiology: respiratory, environmental and exercise physiology
影响因子：
--
作者：
O'Brodovich,HM;Stalcup,SA;Pang,LM;Mellins,RB
通讯作者：
Mellins,RB
急性低氧血症和高碳酸血症：意识清醒的狗血浆儿茶酚胺增加。
DOI：
10.1152/ajpheart.1983.245.6.h924
发表时间：
1983
期刊：
The American journal of physiology
影响因子：
--
作者：
RoseJr,CE;Althaus,JA;Kaiser,DL;Miller,ED;Carey,RM
通讯作者：
Carey,RM