Ischemia-induced local release of myocardial noradrenaline.

The isolated perfused rat heart, prelabelled with 3H-noradrenaline (NA), was used to examine the ischemia-induced release of myocardial NA, and to investigate to what extent reperfusion of an ischemic myocardium per se causes a release of NA. In a model of global myocardial ischemia with 90% flow reduction and the use of lactate as perfusion substrate, release of 3H-NA into the perfusate was already observed during the first 10-20 min of ischemia. The quantities of 3H-NA released increased further with increasing duration of ischemia. In another model with regional ischemia produced by left coronary artery ligation, a similar, though less marked, release of 3H-NA into the perfusate was observed during ischemia. Reperfusion after 60 min of ischemia was associated with a marked outflow of 3H-NA and 3H-NA metabolites, which was not reduced if reperfusion was performed with a Ca2+-free buffer. Furthermore, in the globally ischemic heart model, the relative amounts of 3H-NA and the various 3H-NA metabolites in the effluent remained constant during the last minute of ischemia and the first minute of reperfusion. We concluded that ischemia is associated with early local release of myocardial NA. NA can partly be trapped in the ischemic tissue and washed out during reperfusion.