目的　全国十二家大型医院协作观察中西医结合治疗急性病毒性心肌炎疗效。方法 对1 028 例临床诊断为急性病毒性心肌炎患者随机各分两组,治疗组602 例,用中西医结合(黄芪、牛磺酸、泛葵利酮、抗心律失常药等) 治疗;对照组426 例,用常规(极化液、抗心律失常药等) 治疗。结果 中西医结合治疗组临床症状改善、外周血肠道病毒阴转、心电图ST2T改变及房室传导阻滞、阵发性心房颤动、窦房传导阻滞等恢复均优于对照组( P < 0. 01、0. 05) ;对早搏及心功能改善两组间无统计学差异( P < 0. 05) 。结论　在目前对急性病毒性心肌炎无特效药物治疗的情况下,采用中西医结合治疗可作为一种治疗手段。

Dysregulation of intracellular Ca2+ homeostasis plays an important role in mediating myocardial injury. We tested the hypothesis that treatment with trimetazidine (TMZ) would improve intracellular Ca2+ handling in myocardial injury of rats. The control group received saline only (10 ml kg-1 day-1, I.P.) for 7 days. In a second group, isoprenaline (ISO; 5 mg kg-1 day-1,S.C.) was administered to rats for 2 days to induce an acute injury of the myocardium. In a third group, treatment with TMZ (10 mg kg-1 day-1, I.P.) was initiated 1 day before ISO administration and continued for 7 days (n=7 rats in each group).Histopathological evaluation showed that TMZ prevented ISO-induced myocardial damage. TMZ preserved the ATP levels and decreased the maleic dialdehyde (MDA) content in the hearts compared with ISO-treated rats. The diastolic [Ca2+]I measured by loading with fura-2AM in isolated cardiomyocytes was increased significantly in ISO-treated rats compared to the control animals. TMZ prevented the rise of diastolic [Ca2+]I and the depression of caffeine-induced Ca2+ transients caused by ISO administration. The reduction in sarcoplasmic reticulum (SR) Ca2+ content in the heart cells and in cardiac SR Ca2+-ATPase activity in ISO-treated rats was abolished by TMZ, although there were no differences in SR Ca2+-ATPase protein levels between the control, ISO and ISO + 7 mz-treated rats. In addition, TMZ prevented the reduction in sarcolemmal L-type Ca2+ current density in the heart cells induced by ISO treatment. These results demonstrate that the treatment of rats with TMZ inhibited the increase of diastolic [Ca2+]I and prevented the decrease of SR Ca2+ content, SR Ca2+-ATPase activity and L-type Ca2+ current density in cardiomyocytes in ISO-mediatedmyocardial injury of rats. These changes inCa2+ handling could help to explain the favourable action of TMZ in myocardial injury.

This study was designed to determine the effect of pteridines, R-and S-tetrahydrobiopterin, sepiapterin, and dihydrobiopterin on endothelium-dependent contractions to acetylcholine in isolated aortas from spontaneously hypertensive rat and normotensive Wistar-Kyoto rat. The noncumulative addition of redox-active pteridines R- and S-tetrahydrobiopterin (but not the oxidized analogues sepiapterin and dihydrobiopterin) produced a concentrationdependent transient contraction in isolated aortic rings from both normotensive and hypertensive rats. R-and S-tetrahydrobiopterin (but not sepiapterin or dihydrobiopterin) potentiated the endothelium-dependent contractions to acetylcholine but only in aortas from hypertensive rats and in the presence of NG-nitro-L-arginine. In these aortas, the generation of oxygen-derived free radicals by the combination of xanthine plus xanthine oxidase also potentiated the endothelium-dependent contractions to acetylcholine. The presence of R-tetrahydrobiopterin did not alter the characteristics of the endothelium-dependent contractions because they were inhibited by valeryl salicylate, an inhibitor of cyclooxygenase-1, by S18886, a TP-receptor antagonist or by Tiron, a cell permeable superoxide anion scavenger. However, the contractions to acetylcholine, which are unaffected by the combination of superoxide dismutase and catalase, become significantly inhibited by these two scavengers in the presence of R-tetrahydrobiopterin. In the presence of NG-nitro-L-arginine, R-tetrahydrobiopterin did not affect the contractions to phenylephrine, U 46619, or to oxygen-derived free radicals generated by xanthine plus xanthine oxidase. These results indicate that the production of superoxide by the autoxidation of tetrahydrobiopterin selectively enhances endothelium-dependent contractions in the spontaneously hypertensive rat when nitric oxide synthase is inhibited.

We extracted Astragalosides (AS) from Astragalus membranaceus, a nature herb using as a Chinese traditional medicine, and postulated Astragalosides would exert beneficial effect in myocardial injury by preserving both energy metabolism and Ca2+ homeostasis. Sprague-Dauley (SD) rats were injected with isoproterenol (ISO) s.c. at a dose of 5mg/kg/day consecutively for two days. Astragalosides and trimetazidine were treated to isoproterenol-administrated rats by injecting i.p. at a dose of 5mg/kg/day one day prior to isoproterenol and lasted for 8 days, respectively. The histological changes were alleviated in isoproterenol-damaged SD rats treated with astragalosides. Compared with those in isoproterenol group, myocardial intracellular [Ca2+]i was decreased, L-type Ca2+ density and sarcoplasmic reticulum (SR) Ca2+ load were improved by astragalosides administration. Meanwhile myocardial ATP content was increased, phosphocreatine (PCr) was decreased in the same group. In conclusion, astragalosides is expected to be an efficacious treatment for myocardial injury by regulating intracellular Ca2+ homeostasis and energy metabolism.