L-ARGININE DECREASES INFARCT SIZE IN RATS EXPOSED TO ENVIRONMENTAL TOBACCO-SMOKE

This study examined the effects of L-arginine on myocardial infarct si ze, hemodynamics, and vascular reactivity in environmental tobacco smo ke (ETS)-exposed and non-ETS-exposed rats. We previously demonstrated that exposure to ETS increased myocardial infarct size in a rat model of ischemia and reperfusion. If reduced reperfusion was caused by endo thelial cell damage and increased vascular tone, L-arginine (ARG) woul d increase nitric oxide and better protect the heart. Sixty Sprague-Da wley rats were randomly divided into four groups: ETS or non-ETS (cont rol) with and without ARG (2.25% ARG in drinking water). The ETS group s were exposed to passive smoking (4 Marlboro cigarettes per 15 minute s, 6 hours a day) for 6 weeks. After 6 weeks, all rats were subjected to 35 minutes of left coronary artery occlusion and 120 minutes of rep erfusion, with hemodynamic monitoring. Aortic rings were harvested to evaluate vascular reactivity. Average air nicotine, carbon monoxide, a nd total particulate concentrations were 1304 +/- 215 mu g/m(3), 78 +/ - 2.0 ppm, and 31 +/- .7 mg/m(3) (mean +/- SEM) for the ETS-exposed ra ts. Infarct size (infarct mass/risk area x 100%) increased with ETS ex posure but decreased significantly in the ETS-with-ARG group compared with the ETS-without-ARG group (42% +/- 6% vs 64% +/- 6%, mean +/- SEM ; p = 0.043). The benefit of ARG was dependent on ETS exposure (ETS x ARG interaction, p = 0.043). There were no significant differences bet ween groups in heart rate, systolic pressure, and rate-pressure produc t. ARG significantly decreased myocardial infarct size after ischemia and reperfusion in ETS-exposed rats. Neither the adverse effects of ET S on infarct size nor the blockage of this effect by ARG appears to be the result of ETS-induced alterations in hemodynamics.