L-arginine treatment showed significant decrease of infarction size in relation to the area at risk (% IS/AAR) when compared to Lead-intoxicated rats (52.4±7 % in L- arginine treated group versus 65.3±6 % in Lead-intoxicated group), moreover, L-arginine had reduced the extent of injury and attenuated infarction size becoming comparable to the normal control group (52.4±7 % in L- arginine treated group versus 48.6 % ±5 in normal control group).
Because L-arginine is the substrate of NO synthesis, and NO release is significantly attenuated after reperfusion 45, we hypothesized that the administration of exogenous L-arginine would maintain NO levels and thereby attenuated endothelial dysfunction and myocardial necrosis after ischemia/reperfusion.
In agreement with our observations, L-arginine was described to reduce necrotic injury in a cat model of myocardial ischemia plus reperfusion, and this reduction in infarct size is associated with the preservation of endothelial function and attenuation of neutrophil accumulation in ischemic cardiac tissue 45. The exact cardioprotective mechanisms of L-arginine are not known with certainty, but if NO release is maintained close to the site of injury, it could have cytoprotective effects by inhibiting neutrophil aggregation and adherence 45 or by quenching superoxide free radicals which are known to be inactivators of NO 79-82.
These results indicate that chronic Lead intoxication had toxic effects which deteriorate the heart function. NO donation by L-arginine improved myocardial functional recovery after myocardial ischemia / reperfusion and ameliorated lead toxicity. The ability of L-arginine to reduce infarct size and improve inotropic and chronotropic responses to myocardial ischemia / reperfusion is mediated by its antioxidant and hypocholestremic activities rather than having Lead chelating effect.