Abstract 13788: Acute Administration of Nicotine Induces Transient Elevation of Blood Pressure and Increases Myocardial Infarct Size in an Acute Myocardial Ischemia/reperfusion Rat Model

Abstract

Introduction: Nicotine is a major bioactive component in tobacco cigarettes and electronic cigarettes. Despite the fact that smokers are at higher risk of experiencing an acute myocardial infarction (AMI), there are few studies that have examined the acute effects of nicotine on AMI.To address this issue, our present study was to examine the acute effects of nicotine on myocardial infarct size, no reflow, cardiac hemodynamics and cardiac function in a rat myocardial infarct model. Methods: Forty-six female Sprague-Dawley rats were randomly divided into nicotine group and control group (n=23/group) and received an intravenous loading dose of nicotine at 2.0 μg/kg/min or saline for 30 minutes before starting coronary artery occlusion, then followed by a maintenance dose 0.35 μg/kg/min of nicotine to the end of 3.5 hours of occlusion (30 minutes) and reperfusion (3 hours). Results: At baseline, there were no difference between the two study groups, in systolic blood pressure (BP in mmHg) (nicotine, 69.0±2.7; control, 69.3±4.4; p > 0.05), or diastolic BP (nicotine, 45.7±3.2; control, 48.2±4.2; p > 0.05). Nicotine initially increased systolic BP (nicotine, 97.0±8.6; control, 69.2±3.3, p <0.05) and diastolic BP (nicotine, 65.6±6.4; control, 47.4±3.1, p < 0.01) at 10 minutes after starting injection of the loading dose; pressures dropped to control levels in both groups at 30 minutes. During occlusion/reperfusion, the BP and heart rate were not altered by nicotine. Nicotine significantly increased myocardial infarct size as a percentage of the ischemic risk zone compared to the controls (nicotine, 54.9 ± 1.9 %; control, 48.6 ± 2.7 %, p < 0.05), but nicotine did not affect the no-reflow size (nicotine, 34.8 ± 3.10 %; control, 33.7 ± 3.0%, p > 0.05). Nicotine did not alter fractional shortening assessed by echocardiography. Conclusions: Nicotine infusion can transiently increase blood pressure in anesthetized rats. During coronary occlusion and reperfusion, nicotine increased myocardial infarct size, but did not affect hemodynamics or fractional shortening, suggesting that the increase in infarct size was not simply due to an increase in oxygen demand due to altered afterload, heart rate or contractility, but may reflect a more direct effect on the myocardium.