A NONSTEROID ANTI-INFLAMMATORY DRUG EXACERBATES COXSACKIE-B3 MURINE MYOCARDITIS
A NONSTEROID ANTI-INFLAMMATORY DRUG EXACERBATES COXSACKIE-B3 MURINE MYOCARDITIS
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DOI：
10.1016/s0735-1097(85)80312-0
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发表时间：
1985-01-01
影响因子：
24
通讯作者：
SCANLON, PJ
中科院分区：
文献类型：
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作者：
COSTANZONORDIN, MR;REAP, EA;SCANLON, PJ
非甾体抗炎药常用于治疗肠道病毒感染引起的肌痛和关节痛，但其对急性病毒性心肌炎的疗效尚不清楚。在75只感染1.75 × 1.75的4周龄雄性BALB/c小鼠中研究了非甾体抗炎药布洛芬对急性病毒性心肌炎的作用。第0天107个科萨基病毒B3噬斑形成单位。每天以15 mg/kg体重的剂量腹膜内给予伊诺明。将小鼠分为四组，即第I组，18只未感染的小鼠，在第1 - 14天给予布洛芬;第II组，18只感染的未治疗小鼠;第III组，20只感染的小鼠，在第1 - 14天给予布洛芬;和第IV组，17只感染的小鼠，在第7 - 14天给予布洛芬。第7天处死第I组9只动物、第II组8只动物和第III组7只动物;第7天处死剩余小鼠;第14天处死剩余小鼠。进行心脏病毒培养和组织学分析。第7天和第14天的培养物均为阴性。在每只动物中分析的炎症和坏死分级为0至4级，4级代表广泛的炎症和坏死。仅给予布洛芬的所有18只未感染小鼠（组I）的心脏组织学正常。在第7天处死的第II组（感染，未治疗）和第III组（感染，从第1天开始治疗）小鼠中，炎症和坏死没有显著差异。在第14天处死的小鼠的炎症评分为2.1 ± 0.1。0.6（第二组），3.1 .+-。0.7（第三组）和2.9 .+-。1.0（第IV组感染，处理第7 - 14天）。在第14天处死的小鼠的坏死评分为1.5 ± 0.5。0.8（第二组），3.0 .+-。0.9（第三组）和2.7 .+-。1.1（第四组）。当与组II（感染，但未治疗）相比时，组III（p < 0.01）和组IV（p < 0.05）中的炎症和坏死均显著恶化。提示布洛芬可减轻急性病毒性心肌炎时心肌的炎症和坏死。这种效果，不归因于病毒在心肌中的持久性，可能与布洛芬对伊兰定敏感的单核细胞的免疫调节特性。
Nonsteroid anti-inflammatory drugs are often used to treat myalgias and arthralgias in enteroviral infections, but their effects on acute viral myocarditis are unknown. The effect of the nonsteroidal anti-inflammatory drug, ibuprofen, on acute viral myocarditis was studied in 75 four week old male BALB/c mice infected with 1.75 .times. 107 plaque-forming units of Coxsackie virus B3 on day 0. Ibuprofen was given intraperitoneally at a dose of 15 mg/kg body weight daily. The mice were assigned to four groups.sbd.Group I, 18 uninfected mice given ibuprofen on days 1 to 14; Group II, 18 infected, untreated mice; Group III, 20 infected mice given ibuprofen on days 1 to 14; and Group IV, 17 infected mice given ibuprofen on days 7 to 14. Nine animals in Group I, eight in Group II and seven in Group III were killed on day 7; the remaining mice were killed on day 7; the remaining mice were killed on day 14. Heart viral cultures and histologic analysis were done. Cultures at days 7 and 14 were all negative. Inflammation and necrosis analyzed in each animal were graded 0 to 4, with grade 4 representing widespread inflammation and necrosis. The heart was histologically normal in all 18 uninfected mice (Group I) given ibuprofen only. Inflammation and necrosis were not significantly different in Group II (infected, untreated) and Group III (infected, treated beginning day 1) mice killed at day 7. Inflammation scores of mice killed on day 14 were 2.1 .+-. 0.6 (Group II), 3.1 .+-. 0.7 (Group III) and 2.9 .+-. 1.0 (Group IV infected, treated days 7 to 14). Necrosis scores of mice killed on day 14 were 1.5 .+-. 0.8 (Group II), 3.0 .+-. 0.9 (Group III) and 2.7 .+-. 1.1 (Group IV). When compared with Group II (infected, but not treated), both inflammation and necrosis were significantly worse in Group III (p < 0.01) and Group IV (p < 0.05). These results indicate that ibuprofen worsens myocardial inflammation and necrosis during acute viral myocarditis. This effect, not attributable to viral persistence in the myocardium, may be related to immunomodulating properties of ibuprofen on prostaglandin-sensitive mononuclear cells.