Middleton K M, Henderson A H, Lewis M J
Adv Myocardiol. 1985;6:339-48.
Catecholamine-induced myocardial hypertrophy and necrosis in rats have been measured and compared following treatment with different catecholamines. Significant degrees of both hypertrophy (whether measured as biventricular weight or biventricular/body weight ratio) and necrosis (measured by enzyme histochemical techniques on a standardized series of cryostat sections through the apex of each heart) occurred following 10 days' treatment with daily isoproterenol (0.5 or 5 mg/kg s.c.) or dobutamine (5 mg/kg s.c.) (N = 6-12). These agents given to conscious restrained animals lowered blood pressure and increased heart rate for 3, 6, or 1 hr, respectively. Neither hypertrophy nor necrosis occurred after norepinephrine (1 mg/kg) or dopamine (5 mg/kg); both these agents acutely increased blood pressure for about 30 min. Hemodynamic factors may therefore contribute to catecholamine-induced necrosis, which may in turn contribute to the associated hypertrophy.
在大鼠经不同儿茶酚胺治疗后，已对儿茶酚胺诱导的心肌肥大和坏死进行了测量和比较。在用每日异丙肾上腺素（0.5或5mg/kg皮下注射）或多巴酚丁胺（5mg/kg皮下注射）治疗10天后，出现了显著程度的肥大（无论是以双心室重量还是双心室/体重比来衡量）和坏死（通过酶组织化学技术在每个心脏心尖的标准化系列低温切片上进行测量）（N = 6 - 12）。给予清醒受限动物这些药物后，分别使血压降低和心率增加3、6或1小时。去甲肾上腺素（1mg/kg）或多巴胺（5mg/kg）给药后既未出现肥大也未出现坏死；这两种药物均使血压急性升高约30分钟。因此，血流动力学因素可能导致儿茶酚胺诱导的坏死，而坏死反过来可能导致相关的肥大。
