Gwathmey J K
Charles A. Dana Research Institute, Harvard Medical School, Boston, MA 02115.
J Comp Pathol. 1991 Jan;104(1):33-45. doi: 10.1016/s0021-9975(08)80086-2.
The purpose of the present study was to examine light microscopic data qualitatively as well as quantitatively from an animal model of dilated cardiomyopathy in the turkey. A previous study reported the gross cardioprotective effect of propranolol and the lack of cardioprotection with digoxin in furazolidone-induced cardiomyopathy. It was therefore important to define whether the response of the myocardium to therapeutic interventions differed from the structural responses seen in their absence. In furazolidone-treated birds with resultant cardiac dilation there was myocyte hypertrophy, enlargement of nuclei and reorientation of subepicardial myocardial fibres. Similar changes were noted in birds receiving both furazolidone and digoxin. However, birds receiving propranolol, a non-selective beta-receptor antagonist, and furazolidone did not demonstrate a hypertrophic response or reorientation of fibres. These data indicate that propranolol maintained myocardial morphology and morphometry and thus prevented the structural sequelae of the disease, which is a better achievement of therapy than simple arrest of the progress. A role for intracellular calcium is implied. The cardioprotective effect seen with beta blockade suggests that membrane related events may lead to the contractile dysfunction that results in dilation and cardiac hypertrophy.
本研究的目的是对来自火鸡扩张型心肌病动物模型的光镜数据进行定性和定量分析。先前的一项研究报道了普萘洛尔对呋喃唑酮诱导的心肌病具有显著的心脏保护作用，而地高辛则缺乏心脏保护作用。因此，确定心肌对治疗干预的反应是否与其在未接受治疗时的结构反应不同非常重要。在因呋喃唑酮治疗而导致心脏扩张的鸟类中，出现了心肌细胞肥大、细胞核增大以及心外膜下心肌纤维重新排列的现象。在同时接受呋喃唑酮和地高辛治疗的鸟类中也观察到了类似的变化。然而，接受普萘洛尔（一种非选择性β受体拮抗剂）和呋喃唑酮治疗的鸟类并未表现出肥大反应或纤维重新排列。这些数据表明，普萘洛尔维持了心肌的形态和形态测量指标，从而预防了该疾病的结构后遗症，这是比单纯阻止疾病进展更好的治疗成果。这暗示了细胞内钙的作用。β受体阻滞剂所显示的心脏保护作用表明，与膜相关的事件可能导致收缩功能障碍，进而导致心脏扩张和心肌肥大。
