Effect of hypoxia on sympathoadrenal activity in dogs with myocardial insufficiency

¹ Department of Physiology, University of Oregon Medical School, Portland, Oregon

This study was undertaken to determine if a mild circulatory stress (hypoxia) caused a greater than normal activation of the sympathoadrenal system in dogs with cardiac insufficiency. Plasma concentration and urinary excretion of epinephrine and norepinephrine were used as indices of sympathoadrenal activity. Hypoxic stress (breathing 8–10% O₂) was applied to normal dogs and to the same animals after myocardial damage (coronary embolization) and after myocardial damage plus anemia. Only coronary embolization plus anemia produced overt evidence for cardiac insufficiency. None of the animals, either before or after induction of cardiac insufficiency, showed any significant increase in catecholamine output in response to hypoxia. Ability of the method to detect increased catecholamine concentration was validated by responses to carbamylcholine injection and acute hemorrhage. These results suggest that although the method will detect increased adrenal medullary secretion, it may not detect release of small quantities of norepinephrine from postganglionic neuroeffector junctions. Further, increased sympathetic nervous system activity in these dogs was insufficient to provoke adrenal medullary secretion.