Olivetti G, Ricci R, Anversa P
Department of Pathology, University of Parma, Italy.
J Clin Invest. 1987 Dec;80(6):1818-21. doi: 10.1172/JCI113278.
In contrast to observations made in the human heart, hyperplasia of myocyte nuclei has never been demonstrated in experimental cardiac hypertrophy. To test the hypothesis that the duration of the mechanical load more than the magnitude of ventricular hypertrophy may be the inciting stimulus for myocyte nuclei hyperplasia, constriction of the pulmonary artery was produced in rats and the hearts were examined 6 mo later. A 76% increase in right ventricular weight was measured. This hypertrophic response was accompanied by a 41% increase in the total number of myocyte nuclei in the ventricle. Furthermore, average myocyte cell volume per nucleus increased by 28%. No changes in weight, myocyte size, and nuclear number were observed in the left ventricle. In conclusion, myocyte nuclear hyperplasia and cellular hypertrophy both participate to the adaptive response of the right ventricular myocardium in long-standing pressure overload cardiac hypertrophy.
与在人类心脏中观察到的情况相反,实验性心脏肥大中从未证实过心肌细胞核的增生。为了检验机械负荷的持续时间而非心室肥大的程度可能是心肌细胞核增生的刺激因素这一假说,对大鼠进行肺动脉缩窄,并在6个月后检查心脏。测得右心室重量增加了76%。这种肥大反应伴随着心室内心肌细胞核总数增加41%。此外,每个细胞核的平均心肌细胞体积增加了28%。左心室的重量、心肌细胞大小和核数量未观察到变化。总之,在长期压力超负荷性心脏肥大中,心肌细胞核增生和细胞肥大均参与了右心室心肌的适应性反应。