TREATMENT OF VIRAL MYOCARDITIS WITH RIBAVIRIN IN AN ANIMAL PREPARATION
TREATMENT OF VIRAL MYOCARDITIS WITH RIBAVIRIN IN AN ANIMAL PREPARATION
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DOI：
10.1161/01.cir.71.4.834
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发表时间：
1985-01-01
期刊：
影响因子：
37.8
通讯作者：
CRUMPACKER, CS
中科院分区：
文献类型：
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作者：
MATSUMORI, A;WANG, H;CRUMPACKER, CS
观察广谱抗病毒药物利巴韦林对脑心肌炎(EMC)病毒所致实验性心肌炎的治疗作用。将10株EMC病毒空斑形成单位(PFU)接种四周龄DBA/2小鼠。利巴韦林100(第1组，n=20)、200(第2组，n=10)和400 mg/(kg·d，第3组，10只)皮下注射。于病毒接种后0~12d，观察动物12d。对照组注射生理盐水(n=20)。用利巴韦林治疗的小鼠存活时间比对照组长(组1平均存活6.7d，组2平均存活7.4d，组3平均存活7.7d，对照组平均存活5.2d；P<；0.005)。心肌病毒滴度在第6天至第8天显著低于对照组(3.24±-.0.49log10pfu/mg；P<；0.005)和组3(1.70+-)。0.65log10pfu/mg；P<；0.001)与对照组(4.09+-)相比。0.57log10pfu/mg)。1组(13/20，65%)、2组(2/10，20%)、3组(0/20，0)心肌肉眼病变发生率明显低于对照组(20/20,100%)(P<；0.05)。组织学检查显示未治疗组有广泛的心肌坏死和细胞浸润，2组和3组的细胞浸润较少(P<；0.01)，3组的坏死较轻(P<；0.01)。利巴韦林能有效抑制病毒性心肌炎的心肌病毒复制，减轻炎症反应和心肌损伤。
The therapeutic effects of ribavirin, a broad-spectrum, antiviral agent, on experimental myocarditis caused by encephalomyocarditis (EMC) virus were investigated. Four-week-old DBA/2 mice were inoculated with 10 plaque-forming units (pfu) of EMC virus. Ribavirin in a dose of 100 (group 1, n = 20), 200 (group 2, n = 10) or 400 mg/kg per day (group 3, n = 10) was administered s.c. on days 0 to 12 after virus inoculation, and animals were observed for 12 days. Control animals were injected with saline (n = 20). Mice treated with ribavirin survived longer than controls (mean survival 6.7 days for group 1, 7.4 days for group 2, 7.7 days for group 3, and 5.2 days for control; P < 0.005). Myocardial virus titers on days 6 to 8 were significantly lower in group (3.24 .+-. 0.49 log10 pfu/mg; P < 0.005) and in group 3 (1.70 .+-. 0.65 log10 pfu/mg; P < 0.001) compared with controls (4.09 .+-. 0.57 log10 pfu/mg). The incidence of gross myocardial lesions was significantly lower in group 1 (13/20, 65%), group 2 (2/10, 20%) and group 3 (0/20, 0%) compared with controls (20/20, 100%) (P < 0.05). Histologic examination showed extensive myocardial necrosis and cellular infiltration in untreated groups; there was less infiltration in groups 2 and 3 (P < 0.01) and less severe necrosis in group 3 (P < 0.01). Ribavirin effectively inhibited myocardial virus replication and reduced the inflammatory response and myocardial damage in an experimental preparation of viral myocarditis.