Catecholamine release as mediator of intracellular enzyme activation in ischaemic perfused rat hearts.

Isolated rat hearts perfused at suboptimal pressures have been studied as a model for generalised myocardial ischaemia. Glycogen phosphorylase a and hormone-sensitive triglyceridase activities, measured as markers for endogenous catecholamine release, were significantly increased at low perfusion pressures. Pharmacological blockage of noradrenaline re-uptake accentuated these effects, and depletion of catecholamine reserves eliminated them. This phenomenon may be important in the pathophysiology of cardiac ischaemia and its serious complications.