Studies on the pathogenesis of cardiomyopathy by quantitation of messenger RNA.

为了探讨病毒性心肌炎和继发性心肌疾病中心肌损伤的发病机制，我们通过聚合酶链式反应合成了一个病毒性心肌炎的动物模型，定量检测了超氧化物歧化酶信使RNA的表达。4周龄的BALB/c小鼠接种脑心肌炎病毒后，给予卡托普利或N，2-巯基丙酸甘氨酸(MPG)治疗，从第4天到第14天，与感染对照组相比，卡托普利和MPG显著改善了小鼠的存活和心肌损伤(坏死、细胞浸润和钙化)，并呈剂量依赖关系。因此，卡托普利和MPG是治疗病毒性心肌炎的有效药物。此外，与年龄匹配的未感染小鼠心脏相比，锰超氧化物歧化酶(Mn-SOD)和铜/锌超氧化物歧化酶(铜/锌超氧化物歧化酶)的诱导作用显著。MPG完全抑制这两种mRNAs的增加，即使在第4天开始治疗也是如此。因此，氧自由基可能在病毒性心肌炎的发病机制中起重要作用，通过消除氧自由基的治疗方法似乎是可能的。

In order to investigate the pathogenesis of myocaradial injury in viral myocarditis and subsequent myocardial disorders, we measured quantitatively expression of superoxide dismutase messenger RNA in an animal model of viral myocarditis in which cDNA was synthesized by the polymerase chain reaction.4-wk-old BALB/c mice were inoculated with the encephalomyocarditis virus, and treated with captopril or N, 2-mercapto-propionyl glycine(MPG), a sulfhydryl-containing amino acid derivative without ACE inhibiting property, from days 4 to 14. On day 14, captopril and MPG significantly improved survival of mice and myocardial injury (necrosis, cellular infiltration, and calcification) in a dosedependent manner compared with the infected control group. Thus, captopril and MPG were effective for the treatment of virus-induced myocarditis. Furthermore, a striking induction of manganese superoxide dismutase (Mn-SOD) and copper / zinc SOD (Cu / ZnSOD) when compared with age-matched uninfected mice hearts. MPG completely inhibited the increase of both mRNAs, even when treatment was started on day 4. Thus, oxygen radicals may play an important role in the pathogenesis of viral myocarditis, and a therapeutic approach by eliminating oxygen radicals seems possible.