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吸入颗粒物可加重异丙肾上腺素诱导的心肌病大鼠模型中的心肺损伤。

Particulate matter inhalation exacerbates cardiopulmonary injury in a rat model of isoproterenol-induced cardiomyopathy.

机构信息

Environmental Sciences and Engineering, UNC Gillings School of Global Public Health, Chapel Hill, North Carolina, USA.

出版信息

Inhal Toxicol. 2010 Apr;22(5):355-68. doi: 10.3109/08958370903365692.

Abstract

Ambient particulate matter (PM) exposure is linked to cardiovascular events and death, especially among individuals with heart disease. A model of toxic cardiomyopathy was developed in Spontaneously Hypertensive Heart Failure (SHHF) rats to explore potential mechanisms. Rats were infused with isoproterenol (ISO; 2.5 mg/kg/day subcutaneous [sc]), a beta-adrenergic agonist, for 28 days and subsequently exposed to PM by inhalation. ISO induced tachycardia and hypotension throughout treatment followed by postinfusion decrements in heart rate, contractility, and blood pressures (systolic, diastolic, pulse), and fibrotic cardiomyopathy. Changes in heart rate and heart rate variability (HRV) 17 days after ISO cessation indicated parasympathetic dominance with concomitantly altered ventilation. Rats were subsequently exposed to filtered air or Harvard Particle 12 (HP12) (12 mg/m(3))--a metal-rich oil combustion-derived PM--at 18 and 19 days (4 h/day) after ISO infusion via nose-only inhalation to determine if cardio-impaired rats were more responsive to the effects of PM exposure. Inhalation of PM among ISO-pretreated rats significantly increased pulmonary lactate dehydrogenase, serum high-density lipoprotein (HDL) cholesterol, and heart-to-body mass ratio. PM exposure increased the number of ISO-pretreated rats that experienced bradyarrhythmic events, which occurred concomitantly with acute alterations of HRV. PM, however, did not significantly affect mean HRV in the ISO- or saline-pretreated groups. In summary, subchronic ISO treatment elicited some pathophysiologic and histopathological features of heart failure, including cardiomyopathy. The enhanced sensitivity to PM exposure in SHHF rats with ISO-accelerated cardiomyopathy suggests that this model may be useful for elucidating the mechanisms by which PM exposure exacerbates heart disease.

摘要

环境颗粒物 (PM) 暴露与心血管事件和死亡有关,尤其是在心脏病患者中。本研究在自发性高血压心力衰竭 (SHHF) 大鼠中建立了一种毒理性心肌病模型,以探讨潜在机制。大鼠接受异丙肾上腺素 (ISO;2.5 mg/kg/天皮下 [sc]) 输注 28 天,随后通过吸入暴露于 PM。ISO 输注期间,大鼠发生心动过速和低血压,随后出现心率、收缩力和血压(收缩压、舒张压、脉搏)下降,以及纤维化性心肌病。ISO 停止后 17 天,心率和心率变异性 (HRV) 的变化表明迷走神经占主导地位,同时伴有通气改变。大鼠随后在 ISO 输注后 17 和 18 天(ISO 输注后 17 和 18 天)通过鼻内吸入仅接受过滤空气或 Harvard Particle 12(HP12)(12 mg/m3)暴露,以确定心脏受损大鼠对 PM 暴露的影响是否更敏感。PM 暴露在 ISO 预处理大鼠中显著增加了肺乳酸脱氢酶、血清高密度脂蛋白 (HDL) 胆固醇和心脏/体重比。PM 暴露增加了 ISO 预处理大鼠发生心动过缓性心律失常的数量,这与 HRV 的急性改变同时发生。然而,PM 并未显著影响 ISO 或盐水预处理组的平均 HRV。总之,亚慢性 ISO 处理引起了心力衰竭的一些病理生理和组织病理学特征,包括心肌病。在 ISO 加速性心肌病的 SHHF 大鼠中,PM 暴露的敏感性增强表明该模型可能有助于阐明 PM 暴露加重心脏病的机制。

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