Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarction.

INTRODUCTION: The long-term effects of chronic electronic cigarette (e-cigarette) exposure on lung and heart inflammation during the healing phase of myocardial infarction (MI) remain unexplored. Additionally, the impact of e-cigarette exposure on blood parameters in this context is unclear. This study aims to assess e-cigarette with nicotine (e-cig Nic+) effects on lung histology, inflammatory gene expression in cardiac tissue, and blood parameters during MI recovery. METHODS: Sprague Dawley rats of both sexes underwent proximal left coronary artery occlusion to induce a large anterior wall MI. After one week, rats were randomized to either air or e-cig Nic+ exposure for 12 weeks. RESULTS: In the lungs, e-cig Nic+ exposure led to a significant accumulation of inflammatory cells within the alveolar spaces and increased inflammatory cell numbers in the lung parenchyma compared to the air group. Numerically elevated levels of malondialdehyde (MDA), an oxidative stress biomarker, were observed in the e-cig Nic+ group. In the heart, a PCR array analysis of inflammatory cytokines and receptors revealed that 70 out of 84 inflammatory-related genes were downregulated in the e-cig Nic+ group, with 11 reaching statistical significance. Additionally, the blood of rats exposed to e-cig Nic+ exhibited significantly lower white blood cell, lymphocyte, and platelet counts compared to the air group. CONCLUSIONS: Chronic exposure to e-cig Nic+ exacerbates lung inflammation, alters inflammatory gene expression in the heart, and suppresses immune cell counts in the blood during MI recovery. These findings suggest that e-cigarette with nicotine aerosol inhalation contributes to lung lesions and dampens immune and inflammatory responses in an already compromised MI setting.