摘要
Many studies have shown the negative relationship between long term exposure to PM_(2.5)and cardiac dysfunction.Recently,studies have shown that even a single exposure of PM_(2.5)from air sample in permissible range can induce very mild cardiac pathological changes.In the present study,we revisited the toxic effect of PM_(2.5)on rat heart by adopting single and multiple exposure durations.FemaleWistar ratswere exposed to PM_(2.5)at a concentration of 250μg/m3 daily for 3 hr for single(1 day)and multiple(7,14,21 days)durations.The major pathological changes noted in 21 days exposed myocardium comprised of an elevated ST segment(the segment between the S wave and the T wave),development of cardiac fibrosis,hypertrophy,cardiac injury,tissue inflammation and declined cardiac function.With 14 days exposed heart,the electrocardiograms(ECG),data showed insignificantly declined heart rate and an increased QT(the time from the start of the Q wave to the end of the T wave)interval along with mild fibrosis,hypertrophy and lesser number of TUNEL positive cells.On the other hand,single-and 7-days exposure to PM_(2.5)did not impart any significant changes in the myocardium.To determine the reversibility potential of PM_(2.5)induced cardiotoxicity,a washout period of 24 hours was adopted and all observed changes in the myocardium were reversed till day 7,but not in 14-and 21-days exposed samples.Based on the above findings we concluded that PM_(2.5)associated cardiac dysfunction is the cumulative outcome of ineffective cardiac adaptive and repair process that accumulate additively over the time due to prolonged exposure durations.
基金
the Indian Council of Medical Research(No.3/1/2(22)/Env/2021-NCD-II)
Department of science and technology,India(CRG/2021/000227)for funding this research.
