Sicard R E, Werner J C
Program in Medicine, Brown University, Providence, RI.
In Vivo. 1994 May-Jun;8(3):353-8.
Dexamethasone-induced relative cardiomegaly in neonatal rats mimics hypertrophic cardiomyopathy seen in premature infants receiving dexamethasone for bronchopulmonary dysplasia. Dexamethasone reduced cellular density by approximately 20%. However, dose related increases in mean fiber diameter were seen and mitotic index was doubled at 12.5 micrograms dexamethasone/injection. In addition, dexamethasone induced collagen accumulation throughout the myocardium in an apparently dose dependent manner. These data suggest that dexamethasone promotes (i) myocardial hypertrophy and possibly hyperplasia and (ii) fibrosis and possibly fibroplasia. Further studies are required to determine relationships between disseminated collagen deposition and other suggested metabolic changes and the observed compensatory myocardial hypertrophy and hyperplasia.
地塞米松诱导新生大鼠出现相对心脏肥大,类似于接受地塞米松治疗支气管肺发育不良的早产儿所患的肥厚型心肌病。地塞米松使细胞密度降低了约20%。然而,观察到平均纤维直径呈剂量相关性增加,且在注射12.5微克地塞米松时,有丝分裂指数增加了一倍。此外,地塞米松以明显的剂量依赖性方式诱导整个心肌中的胶原蛋白积累。这些数据表明,地塞米松促进了(i)心肌肥大,可能还有增生,以及(ii)纤维化,可能还有纤维增生。需要进一步研究来确定弥漫性胶原蛋白沉积与其他提示的代谢变化之间的关系,以及观察到的代偿性心肌肥大和增生。