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  • Title: Cardiomegaly in neonatal rats exposed to 500 ppm carbon monoxide.
    Author: Clubb FJ, Penney DG, Bishop SP.
    Journal: J Mol Cell Cardiol; 1989 Sep; 21(9):945-55. PubMed ID: 2530359.
    Abstract:
    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 x 10(6) versus 32 x 10(6) for controls, P less than 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.
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