Elevation of serum endothelins and cardiotoxicity induced by particulate matter (PM2.5) in rats with acute myocardial infarction.
Elevation of serum endothelins and cardiotoxicity induced by particulate matter (PM2.5) in rats with acute myocardial infarction.
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DOI：
10.1385/ct:2:4:253
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发表时间：
2002-01-01
影响因子：
3.2
通讯作者：
Schuchke, Dale A
中科院分区：
文献类型：
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作者：
Kang, Y James;Li, Yan;Schuchke, Dale A
流行病学研究已经确定了一个显着的正相关关系，急性暴露于环境浓度的颗粒物（PM）与每日死亡率和心血管疾病住院率的增加。实验研究表明，预先存在心血管疾病的动物更容易受到PM暴露的心脏效应的影响。本研究旨在探讨内皮素系统的上调可能参与了急性心肌梗死（MI）大鼠PM暴露引起的心脏毒性。使成年雄性Sprague道利大鼠经受左冠状动脉闭塞，并在手术后12小时显示心肌梗塞。心肌梗死动物心率明显减慢，心电图出现室性早搏。通过静脉滴注PM（2.5）2.0 mg溶于0.3 mL生理盐水，可显著加重室性心律失常，沿着心率进一步降低。相同的PM暴露仅引起假手术动物的轻微心脏变化。血清总内皮素浓度显着升高，心肌梗死大鼠和假手术对照响应PM曝光。然而，心肌细胞上内皮素受体A型的数量增加，观察到只有在梗死心肌。因此，本研究表明，心肌梗死大鼠内皮素系统的上调可能参与PM缺血诱导的心脏毒性。
Epidemiological studies have defined a significant positive association of acute exposure to ambient concentrations of particulate matter (PM) with increased daily mortality and hospital admission for cardiovascular diseases. Experimental studies have shown that animals with pre-existing cardiovascular diseases are more susceptible to the cardiac effect of PM exposure. The present study was undertaken to investigate possible involvement of upregulation of the endothelin system in PM exposure-induced cardiotoxicity in rats with acute myocardial infarction (MI). Adult male Sprague Dawley rats were subjected to occlusion of the left coronary artery and displayed myocardial infarction 12 h after the surgery. The heart rate significantly decreased and premature ventricular complexes of the electrocardiogram occurred in the myocardial infarct animals. Exposure to PM(2.5) via intratracheal instillation with 2.0 mg in 0.3 mL normal saline significantly worsened the ventricular arrhythmia along with a further decrease in heart rate. The same PM exposure only caused slight cardiac changes in the sham-operated animals. Serum total endothelin concentrations were significantly elevated in both myocardial infarct rats and shamoperated controls in response to PM exposure. However, increased numbers of the endothelin receptor type A on the cardiomyocytes were observed only in the infarct myocardium. This study thus suggests that upregulation of the endothelin system in rats with MI is likely involved in the PM exposure-induced cardiotoxicity.