Why the study?
Does strenuous sympathetic nerve activity suppress myocardial contractility during recovery in an open-chest dog model?
Does strenuous sympathetic nerve activity suppress myocardial contractility during recovery in an open-chest dog model?
Strenuous sympathetic nerve activity causes transient myocardial suppression that can be reversed by glucose administration, suggesting high-energy phosphate depletion as the underlying mechanism.
Should not change clinical practice after sympathetic stress; leaves open glucose-reversible energy depletion in myocardial recovery.
To examine whether myocardial contractility is suppressed during recovery from strenuous sympathetic nerve activity, the cardiac sympathetic nerve was stimulated for 1 min at 20 Hz in open-chest anesthetized dogs (n = 6). Myocardial contractility was compared between stimulation at 20 Hz (strenuous) and stimulation at 2 Hz (physiological range). Inotropic activity was assessed as the maximal value of the first derivative of left ventricular pressure. The inotropic activity was significantly below the prestimulation control level at 5 min after the end of the strenuous stimulation (68+/-7% of the control value; p < 0.05). The inotropic activity then increased toward the prestimulation level. In contrast, the inotropic activity with 2-Hz stimulation decreased toward the prestimulation level but never fell below that level during recovery. In another experiment (n = 10), 50% glucose solution was injected 5 min after the end of the strenuous stimulation (20 Hz), i.e. when the inotropic activity reached the nadir. The inotropic activity increased significantly (p < 0.01) above the prestimulation level between 7 and 20 min after stimulation. Maximal response (121+/-7% of the control value) was observed at approximately 10 min. These results suggest that transient myocardial suppression occurs after strenuous sympathetic nerve activity and that high-energy phosphate is substantially consumed during strenuous sympathetic activity, resulting eventually in myocardial suppression.
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Yukitaka Masuda (2001) studied this question.
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