Release of myocardial noradrenaline during acute hibernation in the isolated rat heart

摘要

Objective: To explore the release of myocardial noradrenaline during acute hibernation. Methods: The hearts were gained from rats and set up as modified Langendorf preparations beating isometrically. They were perfused with modified Krebs-Hense-leit buffer under controlled pressure. Mechanical measurements and coronary effluent were recorded simultaneously at 30 min intervals for 150 min. Lactate dehydrogenase in coronary effluent was assayed at the beginning, 60 min and 120 min low-flow ischemia. Noradrenaline in coronary effluent was determined at the beginning of low-flow and 120 min of low-flow ischemia and also in control, during hibernation and after 30 min reperfusion during stimulation, myocardial noradrenaline response on tyramine was investigated in absence or presence of desipramine after 30 min reperfusion. Results: In the control, there was nosignificant chant in noradrenaline overflow during 120 min per-fusion; In the acute myocardial hibernation group, there was also nosignificant difference in noradrenaline overflow between the beginning and 120 min low-flow ischemia. The electrical field stimulation-induced overflow of noradrenaline during hibernation myocardium was significantly less than preischemia or after reperfusion, but there was nosignificant difference between preischemia and reperfusion group. Tyramine induced significant noradrenaline release in absence of desipramine after 30 min reperfusion, but this increase in noradrenaline release had nosignificant in the presence of desipramine. These studies indicated that there was not significant spontaneous noadrenaline overflow during acute myocardial hibernation in isolated rat hearts, the stimulation-induced noradrenaline overflow decreased during hibernation and restored to the level of preischemia after reperfusion, myocardial noradrenaline response to tyramine remained after 30 min reperfusion. Conclusion: Myocardial noradrenaline overflow may not contribute to the development of acute myocardial hibernation and the function of sympathetic nerve may also maintain in hibernation as myocardium does during acute myocardial hibernation, reperfusion of myocardium may contribute to restoring the function of sympathetic nerve.