BRIEF, INTERMEDIATE AND PROLONGED ISCHEMIA IN THE ISOLATED CRYSTALLOID PERFUSED RAT-HEART - RELATIONSHIP BETWEEN SUSCEPTIBILITY TO ARRHYTHMIAS AND DEGREE OF ULTRASTRUCTURAL INJURY

Isolated Langendorff-perfused rat hearts were used to assess susceptib ility to reperfusion-induced arrhythmias after different durations of ischemia in relationship to structurally related impairment of heart f unction, and to examine whether phase two ischemia-induced arrhythmias occur in crystalloid perfused hearts. This was achieved by subjecting the hearts to 5 min reperfusion following either sustained (240 min), intermediate (30 min), or brief (10 min) regional ischemia. Sustained ischemia induced little arrhythmogenesis upon reperfusion (no ventric ular fibrillation) and impairment of recovery of coronary now (approxi mately 64% of uninvolved zone flow), Electron microscopic investigatio n of the ischemic region revealed severe degenerative damage of the ul trastructure of cardiac myocytes and capillary endothelial cells, In c ontrast, reperfusion following brief ischemia caused all hearts to dev elop ventricular fibrillation (VF), accompanied by a persisting hypere mia throughout the course of reperfusion (flow 149 +/- 33% of that in the uninvolved zone after 1 min of reperfusion). In this group, myocar dial ultrastructure exhibited negligible i.e., almost complete reversa l of injury, upon reperfusion, Intermediate (30 min) ischemia led to a high incidence of reperfusion arrhythmias (92% of hearts developing V F) and modest hyperemia (now 111 +/- 22% of that in the uninvolved zon e after 1 min of reperfusion). Moderate ultrastructural alterations an d their further deterioration upon reperfusion were observed in some b ut not all hearts in this group. During ischemia, phase 1 arrhythmias were common (57% of hearts developed VF during the first 30 min). Howe ver, phase 2 arrhythmias were absent during 120-240 min ischemia in th ese isolated hearts. In conclusion sustained ischemia in the rat heart renders myocardium unviable with a consequent loss of susceptibility to reperfusion arrhythmias, Phase 2 ischemia-induced arrhythmias do no t occur in this model, implicating an intact autonomic nervous system and/or circulating factors from blood (e.g., neutrophils) in phase 2 a rrhythmogenesis. (C) 1995 Academic Press Limited