Anversa P, Palackal T, Sonnenblick E H, Olivetti G, Capasso J M
Department of Pathology, New York Medical College, Valhalla 10595.
J Clin Invest. 1990 Apr;85(4):994-7. doi: 10.1172/JCI114576.
To determine whether long-term hypertension leads to hyperplasia of myocyte nuclei in the heart, a phenomenon suspected to occur in humans, renal hypertension was produced in rats and the animals were killed 8 mo later. Arterial blood pressure remained elevated for approximately 5 mo, but decreased progressively in the last 3 mo so that at 8 mo this parameter was practically identical to that found in controls. Moreover, left ventricular end diastolic pressure was markedly increased in experimental animals in association with a substantial decrease in left ventricular dP/dt. The alteration of these physiological measurements was indicative of severe ventricular dysfunction. Quantitative analysis of the transmural distribution of myocyte nuclei in the left ventricle showed 36 and 23% increases in myocyte nuclei concentration in the epimyocardium and endomyocardium, respectively. These changes in nuclei were accompanied by 25 and 16% reductions in myocyte cell volume per nucleus in the outer and inner layers of the wall. In conclusion, long-term hypertension leads to impairment of ventricular function and proliferation of nuclei in myocytes.
为了确定长期高血压是否会导致心脏肌细胞核增生(一种疑似在人类中发生的现象),研究人员在大鼠中诱发肾性高血压,并在8个月后处死这些动物。动脉血压在大约5个月内持续升高,但在最后3个月逐渐下降,因此在8个月时,该参数实际上与对照组相同。此外,实验动物的左心室舒张末期压力显著升高,同时左心室dP/dt大幅下降。这些生理测量值的改变表明存在严重的心室功能障碍。对左心室肌细胞核跨壁分布的定量分析显示,心外膜和心内膜的肌细胞核浓度分别增加了36%和23%。这些细胞核的变化伴随着壁外层和内层每核肌细胞体积分别减少25%和16%。总之,长期高血压会导致心室功能受损和心肌细胞核增殖。