POSTISCHEMIC CELL-DEATH IN REPERFUSED PORCINE HEARTS IS NOT ATTENUATED BY THE SPIN TRAP AGENT PBN DURING EARLY REPERFUSION

Ischemic, reperfused porcine hearts were used to investigate whether t he spin trap agent PBN (N-tert-butyl-alpha-phenylnitrone) attenuates p ostischemic cell death by scavenging of free radicals. The left anteri or descending coronary artery (LAD) was ligated distally in 16 pigs fo r 45 min and then reperfused for 3 h. PBN (coronary concentration appr oximately 1 mM) was infused into the LAD of eight pigs during the firs t 45 min of reperfusion. Electron spin resonance spectroscopy (ESR) wa s performed to identify free radical adducts in the reperfused coronar y venous blood. Regional systolic shortening (SS%) was determined by s onomicrometry. Infarct size was evaluated as the percentage of infarct ed (tetrazolium stain) to ischemic (dye technique) myocardium. The tra nsmural ultrastructural degree of myocardial injury as well as myocard ial ATP levels were assessed at the end of the experiment. Intracorona ry treatment with PBN during early reperfusion did not attenuate myoca rdial damage. Infarct sizes (control group 59 +/- 19 %, treated group 55 +/- 14 %), transmural ultrastructural alterations, myocardial ATP c oncentrations (control group 1.8 +/- 0.3 mumol/mg frozen weight, treat ed group 1.7 0.4 mumol/mg) and regional systolic shortening at the end of the experiments (control group - 1 +/- 5 %, treated group -2 +/- 6 % did not differ significantly. Furthermore, under various experimenta l conditions of spin trapping, free radical adducts could not be ident ified in coronary venous blood during early reperfusion. The results s uggest that the spin trap agent PBN (1 mM) does not affect postischemi c cell death in porcine hearts.