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 generalized 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.