Effects of adenosine in simulated ischemia and reperfusion in guinea pig ventricular myocytes

Effects of adenosine (ADN) on cardiac cellular electrical and contractile activity were determined during ischemia and reperfusion. Electrical activity was recorded with conventional and voltage-clamp techniques. Contractions were monitored with a video edge detector. Myocytes were exposed to simulated ischemia (20 min), in the presence or absence of ADN (1-50 microM), and reperfused with Tyrode solution. ADN had no effects 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. In early reperfusion, oscillatory afterpotentials (OAP), transient inward current (ITI) and aftercontractions appeared, and contractions increased above preischemic levels. ADN abolished contractile overshoot and reduced incidence of OAP, ITI, and aftercontractions from 78 to 37.5%. The effects of exogenous ADN were inhibited by ADN A1-receptor blockade. Inhibition of endogenous ADN by 8-phenyltheophylline only increased incidence of ITI. Thus exogenous ADN in ischemia may protect the myocardium in reperfusion via A1 receptors.