Abstract

Background: We investigated the effects of chronic electronic cigarettes with nicotine (E-Cig) exposure on cardiovascular function in rats. Methods: Adult Sprague Dawley rats were exposed to either pure air (n=10) or E-Cig (n=14) for 12 weeks. After 12 weeks of exposure, flow-mediated vasodilation was measured in anesthetized rats with ultrasound to measure femoral artery diameter. Femoral artery flow velocity was measured before and 5 minutes after reperfusion of a 5-minute femoral artery occlusion. Cardiac function was assessed by echocardiogram. A Millar catheter was used to record systemic arterial and LV pressures. Cardiac output was measured using a themodilution catheter. Results: The femoral artery internal diameter and blood flow velocity were comparable between the 2 groups before and after artery occlusion. However, in the E-cig group, blood flow velocity significantly decreased from 55.5 ± 5.2 cm/s prior to occlusion to 41.3 ± 4.1 cm/s after reperfusion (p = 0.005); it remained similar prior to (47.8 ± 3.4 cm/s) and after (47.8 ± 5.5 cm/s) occlusion in the air group. There were no statistically significant differences in left ventricular diastolic and systolic dimensions, LV fractional shortening, heart rate or mean blood pressure (80 ± 3 mmHg in air and 79 ± 5 mmHg in E-cig group) , LV end-diastolic pressure (Ped), end-systolic pressure (Pes), peak -dP/dt, Tau, or cardiac output (48.3 ± 3.3 ml/min in air and 47.6 ± 3.9 ml/min in E-cig group) between the E-Cig and the pure air group. There was a trend toward a reduction in peak LV +dP /dt in the E-Cig group (5574 ± 341 mmHg/s) compared to the air group (6166 ± 238 mmHg/s). LV weight and wall thickness were similar between groups. Conclusions: Twelve weeks of E-Cig exposure did not affect heart rate or blood pressure; but did tend to reduce contractility. E-cigarette exposure slowed the flow-mediated blood flow velocity probably at a microvascular level, possibly by altering endothelial function.

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