Cardiomegaly in neonatal rats exposed to 500 ppm carbon monoxide.
Cardiomegaly in neonatal rats exposed to 500 ppm carbon monoxide.
复制标题
暴露于 500 ppm 一氧化碳的新生大鼠心脏肥大。
DOI：
10.1016/0022-2828(89)90762-1
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发表时间：
1989
影响因子：
5
通讯作者：
Bishop,SP
中科院分区：
文献类型：
--
作者：
ClubbJr,FJ;Penney,DG;Bishop,SP
在生长中的新生大鼠中诱导增加的血流动力学工作量，以研究心肌细胞结构和数量的变化，并确定一氧化碳 (CO) 是否产生体积诱导的心脏肥大模型。新生大鼠暴露于 500 ppm CO 长达 32 天，此时暴露于 CO 的剩余大鼠和环境空气对照在室内空气中继续发育至 200 天。在 CO 组中，6 日龄时心室重量与体重的比率比对照组高 26%，15 日龄时增加一倍多，28 日龄时仍高出 47%。尽管两组之间在任何时间段的绝对肌细胞体积都没有差异，但在 CO 暴露期间，CO 组相对于体重确实具有更大的肌细胞体积。在暴露期间，两个心室的双核肌细胞比对照组长，但宽度没有增加。 200日龄时，CO暴露组大鼠左心室及室间隔的肌细胞显着变短，并且CO暴露组的肌细胞总数比对照组多（36×106与对照组32×106，P<0·05）。在这项研究中，从出生到 32 天龄，500 ppm CO 诱导的心脏肥大主要是由于肌细胞肥大，肌细胞的长宽比增加（即与体积诱导模型一致的变化）。脱离二氧化碳暴露后，心脏肥大和肌细胞肥大均有所消退。随着去除二氧化碳后时间的增加，与年龄匹配的对照组相比，肌细胞趋于变得更短、更小。这种趋势在 105 天时出现，并在 200 天龄时具有统计学意义，导致大鼠脱离 CO 暴露后很长时间内心肌中的肌细胞数量增加。我们得出的结论是，新生儿接触 CO 会通过细胞长度和细胞体积的增加导致心脏肥大，这与心脏肥大的体积超负荷模型一致。
Increased hemodynamic workload was induced in growing neonatal rats to study alterations in myocyte structure and number and to determine if carbon monoxide (CO) produced a volume-induced model of cardiomegaly. Newborn rats were exposed to 500 ppm CO for up to 32 days of age, at which time the remaining CO exposed rats and ambient air controls continued development in room air to 200 days of age. In the CO group, ventricular weight to body weight ratio was 26% greater than controls at 6 days of age, more than double at 15 days, and remained 47% greater at 28 days. Although absolute myocyte volumes were not different between the two groups at any time period, the CO group did have greater myocyte volume relative to body weight during the CO exposure period. Binucleated myocytes of both ventricles were longer than controls during the exposure period, but did not have increased width. By 200 days of age, myocytes from left ventricle plus septum of CO exposed rats were significantly shorter and CO exposed rats had more total myocytes than controls (36 × 106versus 32 × 106for controls,P< 0·05). In this study, cardiomegaly induced by 500 ppm CO from birth to 32 days of age was primarily due to myocyte hypertrophy with myocytes having increased length to width ratios (i.e., alterations consistent with a volume-induced model). Following removal from CO exposure, there was regression of both cardiomegaly and myocyte hypertrophy. With increasing time after removal from CO, myocytes tended to become shorter and smaller compared to age matched controls. This trend was present at 105 days and statistically significant by 200 days of age, resulting in an increased number of myocytes in the myocardium long after removal of rats from CO exposure. We conclude that neonatal exposure to CO causes cardiomegaly by increase in cell length and cell volume, consistent with a volume overload model of cardiac hypertrophy.