Abstract
The rapid increase in use of electronic-cigarettes (e-cigarettes), especially among youth, raises the urgency for regulating bodies to make informed decisions, guidance, and policy on these products. This study evaluated cardiac function in an experimental model following exposure to e-cigarettes. We subjected C57BL/6 mice to e-cigarette vaping for 2-weeks, and cardiac function was assessed using echocardiography. Cardiac tissues were collected at the end of e-cigarette exposure for pathological analysis. The experimental data showed that e-cigarette vaping (3 h/day for 14 days) had no significant effect on cardiac contractility as measured by ejection fraction. However, it significantly increased angiogenesis in mouse heart tissue. We found that e-cigarette exposure increased the endothelial cell marker CD31 and CD34 to approximately 2 fold (p < 0.05) in heart tissue from female mice and about 150% (p < 0.05) in male mice. E-cigarette vaping also caused slower weight gain compared to mice exposed to room air. In addition, short-term e-cigarette exposure slightly increased collagen content in heart tissue but did not result in significant tissue fibrosis. These results suggest that short-term exposure to e-cigarettes has no acute effect on cardiac contractile function or tissue fibrosis, but it increases cardiac angiogenesis.
Highlights
Some early studies showed that e-cigarette liquid or vapor were less toxic compared to c-cigarettes in cultured cardiac myocytes and endothelial cells[18,19,20,21]
To study the effect of e-cigarette smoking on the cardiac functional change, we performed echocardiographic measurements on animals exposed to e-cigarette vapor
Our current research showed that short term exposure to e-cigarette vaping does not have significant effect on cardiac contractility and geometric properties, but it significantly increases the angiogenesis represented by capillary density in mouse heart tissue
Summary
Some early studies showed that e-cigarette liquid or vapor were less toxic compared to c-cigarettes in cultured cardiac myocytes and endothelial cells[18,19,20,21]. Habitual e-cigarette use was found to shift cardiac autonomic balance toward sympathetic predominance and increased oxidative stress, which are associated with increased cardiovascular risk[25]. These results raised questions regarding the safety of e-cigarette use and its beneficial effect as a substitute for c-cigarettes. Our recent studies suggest that chronic exposure to e-cigarette vaping disrupts airway barrier function, induces tissue fibrosis in the heart and kidney, and causes systemic inflammation in mice[26]. We investigated the acute effect of short-term exposure to e-cigarettes on cardiac function and tissue injury in mice
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