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实验性病毒性心肌炎后的心肌性能

Heart muscle performance after experimental viral myocarditis.

作者信息

Adesanya C O, Goldberg A H, Phear W P, Thorp K A, Young N A, Abelmann W H

出版信息

J Clin Invest. 1976 Mar;57(3):569-75. doi: 10.1172/JCI108312.

DOI:10.1172/JCI108312
PMID:1249200
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC436689/
Abstract

As part of an inquiry into possible antecedents of idiopathic cardiomyopathy, acute experimental coxsackie virus myocarditis was studied for late structural and functional sequelae. Myocarditis was induced in 12- and 22-day-old hamsters by inoculation with coxsackie virus B3. Early viremia occurred, followed by virus replication in heart muscle. Maximum peak developed tension (Tpd) of isometrically contracting isolated heart muscle was depressed 17 and 43% in the animals inoculated at 12 days, and studied 18 and 90 days later, respectively, as compared to their uninoculated controls. In both infected groups, less muscle stretch was required to reach the length at which Tpd was produced. Animals studied 180 days after inoculation did not differ from controls. The muscles from animals inoculated at 22 days of age and studied 18 days later showed a 15% depression of Tpd compared to their controls. Glycerinated muscles from this infected group developed 50% less tension than their controls. The muscles of hamsters inoculated with virus at 22 days and studied 90 and 180 days later showed no change in Tpd. The data suggest that contractility and compliance of heart muscle are decreased 18 days after inoculation, but recover by 90 days if the animals are inoculated at age 22 days. However, if the animals are inoculated at a younger age (12 days), depression of myocardial performance persists for at least an additional 90 days. It is concluded that the inflammatory stage of experimental acute coxsackie virus B3 myocarditis in the Syrian golden hamster may be followed by residual alterations in contractile proteins and myocardial function.

摘要

作为对特发性心肌病可能病因进行调查的一部分,对急性实验性柯萨奇病毒心肌炎的晚期结构和功能后遗症进行了研究。通过接种柯萨奇病毒B3,在12日龄和22日龄的仓鼠中诱发心肌炎。早期出现病毒血症,随后病毒在心肌中复制。与未接种的对照组相比,在12日龄接种病毒并分别在18天和90天后进行研究的动物中,等长收缩的离体心肌的最大峰值发展张力(Tpd)分别降低了17%和43%。在两个感染组中,达到产生Tpd的长度所需的肌肉拉伸较小。接种后180天研究的动物与对照组没有差异。22日龄接种病毒并在18天后进行研究的动物的肌肉,其Tpd比对照组降低了15%。该感染组的甘油化肌肉产生的张力比对照组低50%。22日龄接种病毒并在90天和180天后进行研究的仓鼠的肌肉,其Tpd没有变化。数据表明,接种后18天心肌的收缩性和顺应性降低,但如果动物在22日龄接种,90天后会恢复。然而,如果动物在较年轻的年龄(12日龄)接种,心肌性能的降低至少会持续另外90天。得出的结论是,叙利亚金黄仓鼠实验性急性柯萨奇病毒B3心肌炎的炎症阶段之后,收缩蛋白和心肌功能可能会出现残留改变。

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引用本文的文献

1
Viral myocarditis. A review.病毒性心肌炎。综述。
Am J Pathol. 1980 Nov;101(2):425-84.
2
Prognosis and treatment of cardiomyopathy and myocarditis.
Heart Vessels Suppl. 1985;1:175-9. doi: 10.1007/BF02072388.
3
Natural history of left ventricular function in neonatal Coxsackie myocarditis.
Pediatr Cardiol. 1985;6(3):151-6. doi: 10.1007/BF02336555.

本文引用的文献

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Coxsackie B myopericarditis in adults.成人柯萨奇B组病毒感染性心肌心包炎
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