Neonatal Diesel Exhaust Particulate Exposure Does Not Predispose Mice to Adult Cardiac Hypertrophy or Heart Failure.

Neonatal Diesel Exhaust Particulate Exposure Does Not Predispose Mice to Adult Cardiac Hypertrophy or Heart Failure.
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DOI:
10.3390/ijerph13121178
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发表时间:
2016-11-24
影响因子:
--
通讯作者:
Chin MT
Chin MT
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Liu Y;Weldy CS;Chin MT

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背景资料:我们以前曾报道,在子宫内和生命早期暴露于柴油机废气颗粒物易使小鼠成年心力衰竭,而在子宫内暴露本身就足以赋予这种倾向。这项后续研究探讨了新生儿单独接触是否也会导致这种易感性。研究方法:新生雄性C57 BL/6小鼠在出生后立即暴露于柴油机废气(DE)颗粒,直至21日龄断奶,然后将其转移到过滤空气(FA)条件下。在12周龄时,进行横向主动脉缩窄术(TAC),然后每周进行超声心动图检查,持续3周。最后一次超声心动图检查后,对小鼠实施安乐死,进行器官收获、重量分析和组织学检查。结果如下:与FA暴露对照组相比,新生儿暴露于DE颗粒不会增加TAC后心脏肥大或心力衰竭的易感性(心室重量/体重比7.505 vs 7.517 mg/g,p =不显著(NS))。在术后1周、2周和3周,两组之间TAC后的左心室射血分数相似。组织学分析显示,心脏肥大或纤维化程度无差异。结论:新生儿暴露于DE颗粒不会使小鼠在成年期易患TAC诱导的心脏肥大和心力衰竭,与先前发表的结果相反,这些结果表明子宫内暴露导致易感性。
Background: We have previously reported that in utero and early life exposure to diesel exhaust particulates predisposes mice to adult heart failure, and that in utero exposure alone is sufficient to confer this predisposition. This follow up study addresses whether neonatal exposure alone can also confer this predisposition. Methods: Newborn male C57BL/6 mice were exposed to diesel exhaust (DE) particulates immediately after birth until weaning at 21 days of age, whereupon they were transferred to filtered air (FA) conditions. At the age of 12 weeks, transverse aortic constriction (TAC) was performed followed by weekly echocardiography for three weeks. After the last echocardiogram, mice were euthanized for organ harvest, gravimetry and histology. Results: Neonatal exposure to DE particulates did not increase susceptibility to cardiac hypertrophy or heart failure after TAC when compared to FA exposed controls (ventricular weight/body weight ratio 7.505 vs. 7.517 mg/g, p = Not Significant (NS)). The left ventricular ejection fraction after TAC was similar between groups at one week, two weeks, and three weeks after procedure. Histological analysis showed no difference in the degree of cardiac hypertrophy or fibrosis. Conclusions: Neonatal exposure to DE particulates does not predispose mice to TAC-induced cardiac hypertrophy and heart failure in adulthood, in contrast to previously published results showing susceptibility due to in utero exposure.
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