Cardiovascular Toxicity of Ambient Particles in Rats with Myocardial Injury

• Main Authors: Wei-Liang Li, 李偉量
• Other Authors: 鄭尊仁
• Format: Others
• Language: zh-TW
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/06008439375766025628

碩士 === 國立臺灣大學 === 職業醫學與工業衛生研究所 === 96 === Numerous epidemiologic studies have shown that the mortality and hospital admissions of heart failure are associated with ambient particle. However, the toxicological researches on the relationship between ambient particle and heart failure are limited. Thus, we used an animal model of myocardial injury to investigate the cardiovascular toxicity of ambient particle. Our study are composed of two major parts： Part Ⅰ：Rats were received 150 mg/kg isoproterenol by subcutaneous injection to induce myocardial injury. Then, rats were exposed to PM2.5、PM10 and saline by intratracheal instillation one and eight weeks after the injection of ISO. The acute and chronic cardiovascular effects were observed using echocardiography. The results showed that acute PM2.5 exposure would lead to decreased LV function, but the similar effects were not observed in PM10. Further, we didn’t observe chronic effect of particles. Because of limitations of echocardiography and study design, the exact relationship between ambient particle and heart failure need further study. Part Ⅱ：Ultrafine particle concentrator (UFPC) was used to conduct a subchronic exposure in rats administered with 150 mg/kg of isoproterenol by subcutaneous injection. Animals were exposed to concentrated ambient particles (CAPs) for 5-hr/day, 4-day/week for 4-weeks, and controls were exposed to filtered air (FA). BNP for left ventricular function status and cTnI for myocardial injury were measured before exposure, 2 and 4 weeks after exposure. Results of BNP concentration suggest that animals exposed to CAPs may return to normal level later than FA group. As to cTnI, PM didn’t induce further myocardial injury at both CAPs and FA group. Our results suggest that CAPs may cause LV dysfunction shortly after myocardial injury.