Key result
Depletion of cardiac noradrenaline by reserpine or guanethidine markedly enhanced G-6-P accumulation during myocardial ischaemia in rat hearts, without altering ATP decrease or glycogen breakdown.
Endogenous noradrenaline release during myocardial ischaemia is not essential for glycogen breakdown but is important for later steps in anaerobic carbohydrate metabolism, likely phosphofructokinase activation.
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Noradrenaline may regulate late glycolytic steps in ischaemic myocardium; animal findings leave open its relevance to human ischaemia.
We have investigated the role of endogenous catecholamines in myocardial carbohydrate metabolism in isolated, perfused rat hearts after left coronary artery occlusion for 30 min. A significant decrease in ATP and glycogen, and an increase in glucose-6-phosphate (G-6-P) content in the ischaemic myocardium was obtained. After depletion of the cardiac noradrenaline stores by reserpine or guanethidine pretreatment the increase in the G-6-P levels was very markedly enhanced, and the myocardial glycogen content of non-ischaemic control hearts was significantly increased by reserpine. However, the amount of glycogen broken down during the ischaemia in pretreated animals was similar to that in the ischaemic myocardium from control animals, and the decrease in the myocardial ATP was not altered by reserpine or guanethidine. Thus the well known release of noradrenaline during myocardial ischaemia is not an essential prerequisite for the activation of the ischaemic breakdown of glycogen. Rather, it is of importance for later steps in anaerobic carbohydrate metabolism, probably for the activation of phosphofructokinase, as suggested by the large ischaemic accumulation of G-6-P in noradrenaline depleted hearts.
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Metz et al. (1989) studied myocardial ischaemia. reserpine or guanethidine pretreatment vs. control animals was evaluated on myocardial carbohydrate metabolism (ATP, glycogen, G-6-P). Depletion of cardiac noradrenaline by reserpine or guanethidine markedly enhanced G-6-P accumulation during myocardial ischaemia in rat hearts, without altering ATP decrease or glycogen breakdown.
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