Hypoxia and hypercapnia increase the sympathoadrenal medullary functions in anesthetized, artificially ventilated rats
| Autor: | Andrzej Trzebski, Dietmar Biesold, Mieko Kurosawa, Akio Sato |
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| Rok vydání: | 1989 |
| Předmět: |
Male
medicine.medical_specialty Sympathetic Nervous System Epinephrine Physiology Splanchnic nerves Efferent nerve Catecholamines Internal medicine medicine Animals Ventilators Mechanical Central chemoreceptors Adrenal gland business.industry Carotid sinus Rats Inbred Strains Splanchnic Nerves General Medicine Carbon Dioxide Chemoreceptor Cells Rats Oxygen Carotid Sinus medicine.anatomical_structure Endocrinology Adrenal Medulla Catecholamine business Adrenal medulla circulatory and respiratory physiology medicine.drug |
| Zdroj: | The Japanese Journal of Physiology. 39:511-522 |
| ISSN: | 1881-1396 0021-521X |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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