Study on cardiovascular toxicity of ambient particles in rats with left ventricular dysfunction 1. Decreased left ventricular function in spontaneously hypertensive rats exposed to diesel exhaust particles2. Establishment of a left ventricle-dysfunctio

碩士 === 國立臺灣大學 === 職業醫學與工業衛生研究所 === 95 === Decreased left ventricular function in spontaneously hypertensive rats exposed to diesel exhaust particles Objective: Epidemiologic studies have shown that the death and hospital admissions of heart failure are associated with particulate matter, but the as...

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Bibliographic Details
Main Authors: Yu-Fang Huang, 黃于芳
Other Authors: 鄭尊仁
Format: Others
Language:en_US
Published: 2007
Online Access:http://ndltd.ncl.edu.tw/handle/e9v8kn
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Summary:碩士 === 國立臺灣大學 === 職業醫學與工業衛生研究所 === 95 === Decreased left ventricular function in spontaneously hypertensive rats exposed to diesel exhaust particles Objective: Epidemiologic studies have shown that the death and hospital admissions of heart failure are associated with particulate matter, but the association is not consistent. Resent studies reported that patients with heart failure were more sensitive to particulate matter with median aerodynamic diameter <2.5μg/m3 (PM2.5). Here, we conducted an animal study to further investigate the causal relationship between diesel exhaust particles (DEP) exposure and left ventricular function. Method: A total of 24 14- or 16-month-old male spontaneously hypertensive rats (SHR) were exposed intra-tracheally to DEP of 500μg/rat (n=12) and saline as the control (n=12) every 2 weeks for three times. Left ventricular systolic (LVDs) and diastolic (LVDd) diameter and the fraction shortening (FS) were measured before and after treatment using echocardiography. Result: Compared to the control group, DEP exposed SHRs have lower survival rate (50% v.s. 67%), but this did not reach a statistic signification. After DEP exposure, FS in SHR was decreased from 55.7% to 45.5% (p<0.05), and LVDd was increased from 0.49 cm to 0.56cm (p=.056). The change of these values in control group was statistically insignificant. Conclusion: Our results suggest that DEP may impair LV function, which may lead to decompensation in subjects with existing LV impairment. The findings also support previous epidemiology studies. Establishment of a left ventricle-dysfunction animal model induced by isoproterenol Objective: Epidemiologic studies showed that the increasing hospital admissions for heart failure are associated with the concentration of particulate matter in the air. In order to investigate the underlying mechanism, it is needed to establish an appropriate animal model of left ventricular impairment, and further to evaluate the function and the degree of impairment. Method: A total of 20 8-week-old male Wistar rats randomly received 150 mg/kg isoproterenol (ISO group, n=16) or IDD water (control group, n=4) twice for 2 days. Rat was drawn blood from each tail vain at 3 weeks after injection. At 6 weeks after injection, rats were assessed the left ventricular diastolic diameters (LVDd) and fractional shortening (FS) by echocardiography, and sacrificed to get the blood and the heart. The BNP concentration of blood was measured by ELISA. We also observed the difference of mortality between ISO and control groups during experimental period. Result: The immediate (24-hour) and total mortality were 43.75% and 50% in ISO group. In echocardiography, the FS of ISO group (35.25%) was lower than that of control group (44.59%) significantly (p=0.0197). The concentration of blood BNP was increased from 0.359 ng/ml to 0.435 ng/ml (p=0.0001) in the ISO group at 3 to 6 weeks after injection. Conclusion: This study successfully established the left ventricle-dysfunction animal model by using 8-week-old male Wistar rats received 150 mg/kg isoproterenol twice for 2 days, and rats were myocardial impaired and decreased LV function at 6 weeks after injection.