The effect of electronic cigarettes on young versus old normal hearts and pathologic hearts

项目摘要/摘要 电子烟(E-C)继续流行，但E-C对心血管系统(CV)的影响 无论是正常人还是心脏病患者都是未知的。吸烟会增加烟雾 心率、血压，加重内皮功能障碍，加速动脉粥样硬化。一些人 建议替代E-C可能是降低吸烟风险的更安全的方法，因为它们缺乏 焦油和其他一些与香烟烟雾有关的有毒化学物质。然而，E-C仍然可以 提供尼古丁和其他潜在危险的化学品，如丙烯醛、丙二醇、甘油、 醛和调味品。此外，E-C蒸发可能产生的小颗粒尺寸可能 导致对肺部和心血管系统的毒性增加。……有很大的知识差距 目前还没有研究表明慢性暴露于E-C对心血管系统的影响。 其他健康的年轻人，与老年人相比，他们的E-C使用量迅速增加 可能将电子烟作为戒除标准香烟的一种方式的个人。另外，没有数据 E-C对已知心血管疾病受试者的长期疗效。因此，在提出建议之前， 个人可以放心地认为，他们使用电子邮件不会导致或加剧心血管疾病，严谨 需要进行对照研究来评估E-C对CV表型和基因的影响。我们的目标是 是为了确定电子烟与标准香烟烟雾相比的急性和慢性影响 关于年轻的和老年的心血管系统，以及患病的心血管系统，包括左心室(LV) 因既往心肌梗死(MI)而导致的功能障碍。我们将确定电子邮件是否更安全， 对有这些潜在心血管疾病的受试者与标准受试者同样安全或不那么安全 香烟。我们假设，E-C，特别是如果它们携带尼古丁，将会导致不良的LV 心肌梗死后的重塑，加重心力衰竭和内皮功能障碍。我们会 确定如果E-C不含尼古丁，这些影响是否会减弱，以及某些 治疗可以逆转这种效果。将使用一个成熟的MI啮齿动物模型，并将有 具有使啮齿动物暴露在环境中的丰富经验的实验室之间的合作努力 在分析烟雾和污染方面有丰富经验的实验室 活体心脏疾病模型的病理生理学包括超声心动图、心脏 导尿术，详细的组织学和组织化学分析，生化分析，评估 内皮功能、线粒体功能评估、超微结构分析和评估 基因表达。

Project Summary/Abstract E-cigarettes (E-C) continue to gain popularity, but the effects of E-C on the cardiovascular (CV) system of either normal individuals or those with heart disease are unknown. Cigarette smoke can increase heart rate, blood pressure, worsen endothelial dysfunction, and accelerate atherosclerosis. Some suggest that substituting E-C could be a safer approach to reduce cigarette smoking risks as they lack tar and some of the other noxious chemicals associated with cigarette smoke. However, E-C can still deliver nicotine and other potentially dangerous chemicals such as acrolein, propylene glycol, glycerol, aldehydes, and flavorings. In addition, the small particle size that may result from E-C vaping could result in increased toxicity to the lungs and cardiovascular system. There is a large knowledge gap in that there are no studies that have examined the effect of chronic exposure to E-C on the CV system in otherwise healthy young individuals where there has been a rapid increase in E-C use versus older individuals who may be turning to E-C as a way to quit standard cigarettes. In addition there is not data on the long-term effect of E-C on subjects with known CV disease. Thus, before suggesting that individuals can feel safe that their use of E-C is not going to cause or exacerbate CV disease, rigorous controlled studies are needed to assess the effect of E-C on CV phenotype and genotype. Our goal will be to determine the acute and chronic effects that E-C has in comparison to standard cigarette smoke on the young versus the old CV system and on the diseased CV system, including left ventricular (LV) dysfunction due to previous myocardial infarction (MI). We will determine whether E-C are safer, equally safe or less safe for subjects who have these underlying CV conditions versus standard cigarettes. We hypothesize that E-C, especially if they carry nicotine, will contribute to adverse LV remodeling post myocardial infarction, worsen heart failure, and endothelial dysfunction. We will determine whether these effects will be lessened if E-C does not contain nicotine, and whether certain therapies can reverse the effects. A well-established rodent model of MI will be used and there will be collaborative effort between a laboratory that has extensive experience subjecting rodents to exposure to smoke and pollution with a laboratory that has extensive experience with analyzing the pathophysiology of in vivo cardiac disease models including assessment by echocardiography, cardiac catheterization, detailed histologic and histochemical analyses, biochemical analyses, assessment of endothelial function, assessment of mitochondrial function, ultrastructural analysis, and assessment of gene expression.