972-107 L-Arginine Decreases Infarct Size in Rats Exposed to Environmental Tobacco Smoke

Abstract

We previously showed that environmental tobacco smoke (ETS) increased myocardial infarct size in a rat model of ischemia and reperfusion. If reduced reperfusion was caused by endothelial cell damage and increased vascular tone, we postulated that L-arginine (ARG) would increase nitric oxide and better protect the heart. 60 rats were randomly divided into 4 groups: ETS or Control (C) with and without ARG (2.25% ARG in drinking water). The ETS groups were exposed (4 Marlboro cigarettes per 15 minutes. 6 hours a day) for 6 weeks. During ETS-exposure, average air nicotine, carbon monoxide and total particulate concentrations were 1304 μg/m 3 , 78 ppm and 31 mg/m 3 , respectively. After 6 weeks, all rats were subjected to 35 min LAD occlusion (0) and 120 min reperfusion, with hemodynamic monitoring via the carotid artery. Aortic rings were harvested to evaluate vascular reactivity. Infarct size (infarct mass/risk area x 100%) decreased significantly in the ETS with ARG group compared to the ETS without ARG group. There were no significant differences among groups in heart rate (HR), systolic pressure (SP), and rate pressure product. Tlere were positive correlations between infarct size and heart rates from baseline to reperfusion 120 min (r = 0.4-0.6. p = 0.01-0.001). There was no relationship between vascular reactivity and infarct size. Group No. of Rats Inf/LV (%) Inf/RA (%) 0-35’HR (beats/m) 0-35'SP (mmHg) Max Relax (%) C 11 25 ± 3 51 ± 6 408 ± 11 120 ± 7 84 ± 11 C+ ARG 10 25 ± 2 52 ± 3 415 ± 10 103 ± 11 112 ± 15 ETS 10 34 ± 4 64 ± 6 427 ± 16 108 ± 8 128 ± 16 ETS + ARG 11 22 ± 3 * 42 ± 6 * 410 ± 17 106 ± 10 127 ± 18 Values are Means ± SEM * p < 0.05, p values from two-way ANOVA L-arginine decreases myocardial infarct size after ischemia and reperfusion in ETS-exposed rats. This effect does not appear to be secondary to alterations in hemodynamics.