In perfused isolated guinea pig hearts reactive hyperemia (RH) was ind
uced by occlusion of coronary flow for periods ranging from 1-60 s. RH
was hampered by 100-60 % in the presence of an inhibitor of NO syntha
se, N-G-nitro-L-arginine (100 mu M) and, to a lesser extent (up to 35
%),by an antagonist of adenosine receptors, 8-phenyltheophylline (10 m
u M). An inhibitor of PGH synthase, indomethacin (5 mu M), did not aff
ect RH. During RH the heart generated prostacyclin, nitric oxide, and
adenosine as indicated by the appearance of 6-keto-PGF(1a), cyclic GMP
, urate, inosine, hypoxanthine and xanthine in the perfusate. Out of t
hese factors only NO and adenosine were responsible for RH. NO was res
ponsible for RH which was evoked by short - term (1-10 s) coronary occ
lusion, whereas concurrent efforts of NO and adenosine were required t
o maintain RH that followed longer (20-60 s) periods of interruption o
f coronary inflow. Thus, in the investigated system nitric oxide and a
denosine but not prostacyclin can be considered as the mediators of my
ocardial reactive hyperemia.