Biesold D, Kurosawa M, Sato A, Trzebski A
Department of Physiology, Tokyo Metropolitan Institute of Gerontology, Japan.
Jpn J Physiol. 1989;39(4):511-22. doi: 10.2170/jjphysiol.39.511.
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.
对经氨基甲酸乙酯麻醉并进行人工通气的大鼠分别施加45秒的分级低氧（终末潮气氧分压14%-6%）和2分钟的高碳酸血症（终末潮气二氧化碳分压6%-10%），结果发现，肾上腺交感传出神经活动增加，同时肾上腺静脉流出液中测得的肾上腺素和去甲肾上腺素分泌也增加。肾上腺素和去甲肾上腺素的百分比增加几乎相等。在双侧切断颈动脉窦神经（CSN）的大鼠中，低氧对肾上腺交感神经活动或儿茶酚胺分泌没有任何影响。相反，在去神经支配的大鼠中，对高碳酸血症的肾上腺神经兴奋性和儿茶酚胺分泌反应保持不变。在切断支配肾上腺的内脏神经分支后，通过低频刺激内脏神经外周端维持儿茶酚胺分泌的静息水平，低氧并未使儿茶酚胺分泌增加。然而，高碳酸血症（终末潮气二氧化碳分压8%和10%）可诱导去神经支配的肾上腺髓质分泌儿茶酚胺，尽管反应幅度明显低于肾上腺神经完整的动物。得出的结论是，低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除颈动脉化学感受器之外的机制起作用，如中枢化学感受器，对肾上腺髓质有一些直接刺激作用。讨论了低氧和高碳酸血症期间交感肾上腺兴奋的这些双重机制的功能意义。
