Myocardial reactive hyperaemia in perfused guinea pig heart

Reactive hyperaemia (RH) was induced by occlusion of coronary flow (1-60 s) in perfused guinea pig heart. It was inhibited by 100-60%, by NG-nitro-L-arginine (100 microM) and to a lesser extent (up to 35%) by 8-phenyltheophylline (10 microM). Indomethacin (5 microM), did not affect RH. During RH the heart generated prostacyclin, nitric oxide and adenosine as indicated by the appearance of 6-keto-PGF1 alpha, cyclic GMP, inosine, hypoxanthine, xanthine and urate in the perfusate. Only nitric oxide (NO) and adenosine but not prostacyclin were responsible for RH. NO mediated RH which followed short-term (1-10 s) coronary occlusion whereas a combined effort of NO and adenosine was required to maintain RH that followed longer (20-60 s) periods of interruption of coronary inflow. Prostacyclin did not participate in RH at any circumstances.