Is preconditioning by nicotine responsible for the better prognosis in smokers with acute myocardial infarction?

Cigarette smoking is a well-known risk factor for acute myocardial infarction and sudden death. However, a history of smoking consistently has been associated with better hospital outcome in patients with acute myocardial infarction. The mechanism for the better outcome in smokers is not clear. It has been suggested that nicotine may have a "preconditioning-like" effect. This study assesses whether nicotine attenuates myocardial infarct size. Anesthetized rabbits were randomized to receive infusion of nicotine 80 micrograms/kg (n = 13), or saline (n = 12) over 10 min. Twenty minutes after termination of infusion all rabbits underwent 30 min of coronary artery occlusion and 4 h of reperfusion. Risk zone was assessed by blue dye and infarct size by tetrazolium staining. Nicotine did not affect regional myocardial blood flow 15 min after treatment, during occlusion or during reperfusion. Heart rate and mean systemic blood pressure were similar between the groups. Nicotine serum levels during occlusion were 9.5-22.0 ng/ml in the treated group, which are comparable to levels found in human smokers. No differences were found in the risk zone of nicotine compared to control rabbits (26 +/- 2% vs. 23 +/- 2% of the left ventricle, respectively), or infarct size (31 +/- 5% vs. 37 +/- 4% of risk zone). Since no effect on infarct size was found, a third group receiving higher dose of nicotine, 320 micrograms/kg (n = 6), was added. Infarct size was not different from the control group (39 +/- 6% of risk zone). Nicotine, given intravenously before ischemic insult, does not protect the myocardium. A "preconditioning-like" effect of nicotine is probably not the mechanism of reduced mortality in smoking patients with myocardial infarction.