L-Arginine has been tested in various cardiovascular diseases, mainly to improve endothelial function through NO production. However, as the results have been partly unpredictable, we assessed the hemodynamic, energetic and metabolic effects of L-arginine to clarify any potential benefits in postischemic left ventricular (LV) dysfunction.
LV dysfunction was induced by repetitive brief coronary occlusions in 12 anesthetized, open chest pigs. L-Arginine was subsequently infused (bolus 400 mg·kg−1 and continuously for 1 hour, 250 mg·kg−1·h−1). Hemodynamic parameters, metabolites of L-arginine and myocardial energetics were assessed sequentially.
L-Arginine infusions caused a substantial rise in plasma L-arginine (3474 ± 358 μmole·L−1) accompanied by a 2-fold increase in plasma L-citrulline. No significant alterations in vascular resistance or LV contractility were observed from L-arginine. Mean arterial pressure dropped from 78 ± 11 to 72 ± 10 mm Hg (P = 0.019) and 70 ± 8 mm Hg (P = 0.003) after bolus and infusions, respectively. Myocardial oxygen consumption was unaltered, and myocardial creatine content was not increased after 90 minutes of L-arginine infusion.
L-Arginine infusion did not influence the energetic cost of myocardial contractility, and only minor hemodynamic changes were observed despite a demonstrable turnover of L-arginine. These findings question the use of L-arginine to promote therapeutic NO formation in the acute setting.