Xs. Li et al., ROLE OF L-ARGININE IN PREVENTING MYOCARDIAL AND ENDOTHELIAL INJURY FOLLOWING ISCHAEMIA REPERFUSION IN THE RAT ISOLATED HEART/, Acta Physiologica Scandinavica, 156(1), 1996, pp. 37-44
The protective effect of L-arginine on ischaemia/reperfusion-induced m
yocardial injury was investigated in the rat isolated Langendorff perf
used heart. Six groups of hearts subjected to 30 min global ischaemia
and 30 min reperfusion received either vehicle, D-arginine. L-arginine
, the nitric oxide (NO)-donor S-Nitroso-N-Acetyl-D, L-Penicillamine (S
NAP), the inhibitor of NO formation N-G-nitro-L-arginine (L-NNA), or L
-arginine plus L-NNA. The recoveries of left ventricular double produc
t and coronary flow at the end of reperfusion were significantly highe
r in the L-arginine group (85 +/- 5 and 75 +/- 6%. respectively) than
in the vehicle group (37 +/- 6 and 34 +/- 5%. respectively. P < 0.05).
During both the ischaemic and reperfusion periods. left ventricular e
nd diastolic pressure was lower in the L-arginine group than in the ve
hicle group. Creatine kinase outflow and the area of no-reflow were sm
aller in the L-arginine treated hearts (P < 0.01). There were no diffe
rences between vehicle and D-arginine treated groups. L-NNA did not af
fect recovery per se but abolished the protective actions of L-arginin
e. SNAP produced the same protective effects as L-arginine. Acetylchol
ine-induced endothelium-dependent vasodilation was reduced after ischa
emia and reperfusion in the vehicle group but not in the L-arginine gr
oup. It is concluded that L-arginine reduces ischaemia/reperfusion-ind
uced myocardial and endothelial injury. The results suggest that the b
eneficial effects of L-arginine are related to preserved synthesis and
release of NO.