Key result
Acute cardiac sympathectomy, propranolol infusion, and reserpinization did not affect the repayment of flow and oxygen debt, indicating reactive hyperemia is primarily a metabolic response.
Sympathetic nervous control and catecholamines do not play a significant metabolic role in the regulation of myocardial reactive hyperemia, indicating it is primarily a metabolic response induced by anoxia.
Supports metabolic dominance of myocardial reactive hyperemia in this model; hypothesis-generating for human studies.
The effects of sympathetic nerves and catecholamines on the characteristics of the myocardial reactive hyperemia were studied in anesthetized open-chest dogs. The flow repayment, the ratio of the reactive hyperemic blood flow to the flow debt, averaged 166 per cent. The calculated oxygen debt was also overpaid, the average repayment being of 118 per cent. The occlusion of the left coronary artery up to 40 sec. did not affect the flow repayment; a constant correlation was observed between flow debt and reactive hyperemic flow. To study the sympathetic effect on the reactive hyperemia characteristics, acute cardiac sympathectomy, intracoronary infusion of propranolol and deprivation of catecholamines by reserpinization were performed. These procedures did not affect the repayment of flow and oxygen debt. From these experimental results the sympathetic nervous control was not observed in the response of the myocardial reactive hyperemia indicating that reactive hyperemia was primarily a metabolic response induced by anoxia. It was also suggested that catecholamines in the heart did not play any significant metabolic role in the regulation of the myocaridal reactive hyperemia.
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Yazaki et al. (1970) studied Myocardial reactive hyperemia. Acute cardiac sympathectomy, intracoronary infusion of propranolol, and deprivation of catecholamines by reserpinization was evaluated on Flow repayment and oxygen debt repayment. Acute cardiac sympathectomy, propranolol infusion, and reserpinization did not affect the repayment of flow and oxygen debt, indicating reactive hyperemia is primarily a metabolic response.
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