RELEASE OF TISSUE-PLASMINOGEN ACTIVATOR DURING REPERFUSION AFTER DIFFERENT TIMES OF ISCHEMIA IN ISOLATED, PERFUSED RAT HEARTS

Tissue plasminogen activator (t-PA) is a potential marker of endotheli al cell activation or injury. The relationship between duration of isc haemia and release of t-PA during reperfusion was investigated in isol ated rat hearts exposed to either 5, 10, 20, 30, 40, or 60 min of glob al, normothermic ischaemia followed by 30 min of reperfusion (n = 8 in each group). t-PA activity was measured (chromogenic peptide substrat e assay) in the effluent before ischaemia, and after 2.5, 5, 7.5, 10, 20, and 30 min of reperfusion. Release of lactate dehydrogenase (LD), a marker of myocyte injury, was measured before ischaemia and after 5 min reperfusion. Left ventricular pressures were measured by a balloon in the left ventricle. Ischaemia for 20 min or less had only minor ef fects on cardiac function. Thirty min or more of ischaemia induced ven tricular fibrillation during reperfusion in most hearts. After ischaem ia t-PA outflow increased, but without any significant difference betw een groups. Peak release occurred after either 2.5 or 5 min of reperfu sion. After 10 min reperfusion the release was not different from the basal value. in contrast, postischaemic release of LD correlated to th e length of ischaemia. To conclude, t-PA release from the ischaemic-re perfused rat heart is independent of the length of ischaemia. Thus the potential of t-PA to quantify endothelial injury appears to be limite d.