Tobacco and marijuana induce adverse effects on cardiac function and platelet activity and reduce tissue preservation following myocardial infarction.

IF 3.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Xiaoyin Wang, Daniel D Han, Huiliang Qiu, Chaitanya Punnati, Natasha Goyal, Alyssa Parangan, Jayita Mukunda, Parmis Tabibiazar, Lam Tran, Kelly Tan, Arailym Kamzabek, Ronak Derakhshandeh, Matthew L Springer
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引用次数: 0

Abstract

Smoking disrupts cardiac autonomic regulation, vascular biology, and platelet function; however, the acute and longer-term cardiovascular effects of resurging and emerging tobacco and marijuana products remain incompletely characterized. We investigated the impact of exposure to smoke and aerosol from several tobacco and marijuana products on cardiac function, platelet activity, and myocardial susceptibility to ischemia-reperfusion myocardial infarction (MI). Male and female Sprague-Dawley rats underwent single or daily 5-min pulsatile exposure sessions to emissions from tobacco cigarettes, e-cigarettes (JUUL), heated tobacco products (IQOS), marijuana cigarettes, or cannabinoid-depleted ("placebo") marijuana cigarettes, with an air negative control. Cardiac function was assessed immediately after single exposure by echocardiography and intraventricular hemodynamics. Platelet aggregation was measured immediately after single exposure and 1 day after repeated (2-wk) exposure. Myocardial infarct size, normalized to area at risk, was assessed following MI after repeated (4-wk) exposure. Single exposure to tobacco smoke or JUUL aerosol reduced left ventricular ejection fraction relative to preexposure. Acute marijuana smoke exposure similarly impaired left ventricular function assessed by hemodynamics. Single exposure to tobacco, marijuana, and placebo marijuana smoke increased collagen-induced platelet aggregation, with more pronounced responses in females, whereas repeated (2-wk) exposure to smoke/aerosol from tobacco cigarettes, JUUL, IQOS, and placebo marijuana increased platelet aggregation across groups. Notably, repeated (4-wk) exposure to tobacco smoke/aerosol or marijuana smoke before MI reduced myocardial tissue preservation, resulting in greater infarct size post MI. These findings indicate that individual tobacco and marijuana smoking and vaping similarly impair cardiac function, enhance platelet reactivity, and reduce myocardial tolerance to ischemia-reperfusion injury.NEW & NOTEWORTHY Inhalable products marketed as reduced-harm alternatives to combustible cigarettes, including e-cigarettes, heated tobacco products, and marijuana, produce rapid and sustained adverse cardiovascular effects. Even brief exposure impairs cardiac function and enhances platelet aggregation, whereas prior exposure increases myocardial susceptibility to ischemia-reperfusion injury, resulting in larger infarcts following myocardial infarction. These findings challenge the perception that noncombustible or "reduced-harm" products are cardiovascularly benign.

烟草和大麻诱导心肌梗死后心功能和血小板活性的不良影响并减少组织保存。
吸烟破坏心脏自主调节、血管生物学和血小板功能;然而,复苏和新出现的烟草和大麻产品的急性和长期心血管影响仍然没有完全表征。我们研究了暴露于几种烟草和大麻产品的烟雾和气溶胶对心功能、血小板活性和心肌对缺血/再灌注心肌梗死(MI)的易感性的影响。雄性/雌性Sprague-Dawley大鼠接受单次或每日5分钟脉冲暴露于烟草香烟、电子烟(JUUL)、加热烟草产品(IQOS)、大麻香烟或大麻素耗尽(“安慰剂”)大麻香烟的排放物;带空气负控制。单次暴露后立即使用超声心动图和室内血流动力学评估心功能。单次暴露后立即测量血小板聚集,重复(2周)暴露后1天测量血小板聚集。心肌梗死面积归一化为危险区域,在重复(4周)暴露后进行心肌梗死评估。与暴露前相比,单次暴露于烟草烟雾或JUUL气溶胶可降低左心室射血分数。急性大麻烟雾暴露同样损害左心室功能通过血流动力学评估。单次暴露于烟草、大麻和安慰剂大麻烟雾中会增加胶原诱导的血小板聚集,女性的反应更为明显,而重复(2周)暴露于烟草香烟、JUUL、IQOS和安慰剂大麻的烟雾/气溶胶中会增加各组的血小板聚集。值得注意的是,心肌梗死前反复(4周)暴露于烟草烟雾/气溶胶或大麻烟雾中会减少心肌组织保存,导致心肌梗死后梗死面积增大。这些结果表明,个体吸烟和吸大麻对心功能的损害类似,血小板反应性增强,心肌对缺血/再灌注损伤的耐受性降低。
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来源期刊
CiteScore
9.60
自引率
10.40%
发文量
202
审稿时长
2-4 weeks
期刊介绍: The American Journal of Physiology-Heart and Circulatory Physiology publishes original investigations, reviews and perspectives on the physiology of the heart, vasculature, and lymphatics. These articles include experimental and theoretical studies of cardiovascular function at all levels of organization ranging from the intact and integrative animal and organ function to the cellular, subcellular, and molecular levels. The journal embraces new descriptions of these functions and their control systems, as well as their basis in biochemistry, biophysics, genetics, and cell biology. Preference is given to research that provides significant new mechanistic physiological insights that determine the performance of the normal and abnormal heart and circulation.
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