{"title":"[Collagen remodeling of a mitral periannular cardiac muscle lesion in experimental mitral regurgitation rabbits induced by vagus stimulation].","authors":"S Naito, K Imataka, Y Seko, J Fujii","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>A peculiar mitral periannular cardiac muscle lesion was developed in experimental mitral regurgitation rabbits induced by vagus stimulation. In this model, a pansystolic murmur was heard during one week after vagus stimulation, and it disappeared thereafter. We investigated the periannular cardiac muscle lesion one week (MR-1 group, N = 30) and four weeks (MR-4 group, N = 15) after vagus stimulation using pathohistological, immunohistochemical and biochemical techniques, and found that the lesion had regressed in four weeks. Non-treated rabbits (C-1 group and C-4 group) were used as controls. The periannular cardiac muscle lesion in MR-1 group was characterized by swelling and increased stiffness which corresponded to swelling and degeneration of the myocardial cells and interstitial fibrosis on microscopic observation. On the other hand, in MR-4 group, the swelling and degeneration of the myocardial cells restored and an increase of interstitial collagen was regressed. The hydroxyproline content of the periannular cardiac muscle lesion in MR-1 group was significantly abundant compared with that in C-1 group (10.5 +/- 1.6 mg/g. wet wt, vs 7.8 +/- 0.9, mean +/- SD, p less than 0.01). In MR-4 group, the hydroxyproline content was significantly decreased compared with that in MR-1 group (8.8 +/- 1.4 vs 10.5 +/- 1.6, p less than 0.05). Immunohistochemical study clearly indicated that the increased collagen in the periannular cardiac muscle lesion in MR-1 group was type III collagen, and that the increased type III collagen regressed in MR-4 group.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":77193,"journal":{"name":"Journal of cardiology. Supplement","volume":"25 ","pages":"53-9, discussion 60-1"},"PeriodicalIF":0.0000,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of cardiology. Supplement","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
A peculiar mitral periannular cardiac muscle lesion was developed in experimental mitral regurgitation rabbits induced by vagus stimulation. In this model, a pansystolic murmur was heard during one week after vagus stimulation, and it disappeared thereafter. We investigated the periannular cardiac muscle lesion one week (MR-1 group, N = 30) and four weeks (MR-4 group, N = 15) after vagus stimulation using pathohistological, immunohistochemical and biochemical techniques, and found that the lesion had regressed in four weeks. Non-treated rabbits (C-1 group and C-4 group) were used as controls. The periannular cardiac muscle lesion in MR-1 group was characterized by swelling and increased stiffness which corresponded to swelling and degeneration of the myocardial cells and interstitial fibrosis on microscopic observation. On the other hand, in MR-4 group, the swelling and degeneration of the myocardial cells restored and an increase of interstitial collagen was regressed. The hydroxyproline content of the periannular cardiac muscle lesion in MR-1 group was significantly abundant compared with that in C-1 group (10.5 +/- 1.6 mg/g. wet wt, vs 7.8 +/- 0.9, mean +/- SD, p less than 0.01). In MR-4 group, the hydroxyproline content was significantly decreased compared with that in MR-1 group (8.8 +/- 1.4 vs 10.5 +/- 1.6, p less than 0.05). Immunohistochemical study clearly indicated that the increased collagen in the periannular cardiac muscle lesion in MR-1 group was type III collagen, and that the increased type III collagen regressed in MR-4 group.(ABSTRACT TRUNCATED AT 250 WORDS)