EFFECTS OF ADENOSINE IN SIMULATED ISCHEMIA AND REPERFUSION IN GUINEA-PIG VENTRICULAR MYOCYTES

Effects of adenosine (ADN) on cardiac cellular electrical and contract ile activity were determined during ischemia and reperfusion. Electric al activity was recorded with conventional and voltage-clamp technique s. Contractions were monitored with a video edge detector. Myocytes we re exposed to simulated ischemia (20 min), in the presence or absence of ADN (1-50 mu M), and reperfused with Tyrode solution. ADN had no ef fects under control conditions. However, action potential abbreviation during ischemia was greater in the presence of ADN than for control, and recovery was delayed. In ischemia, Ca2+ current declined equally, and contractions were abolished in control and ADN-treated myocytes. I n early reperfusion, oscillatory afterpotentials (GAP), transient inwa rd current (I-TI) and aftercontractions appeared, and contractions inc reased above preischemic levels. ADN abolished contractile overshoot a nd reduced incidence of GAP, I-TI, and aftercontractions from 78 to 37 .5%. The effects of exogenous ADN were inhibited by ADN A(1)-receptor blockade. Inhibition of endogenous ADN by 8-phenyltheophylline only in creased incidence of I-TI Thus exogenous ADN in ischemia may protect t he myocardium in reperfusion via A(1) receptors.