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[迷走神经刺激诱导的实验性二尖瓣反流兔二尖瓣环周心肌病变的胶原重塑]

[Collagen remodeling of a mitral periannular cardiac muscle lesion in experimental mitral regurgitation rabbits induced by vagus stimulation].

作者信息

Naito S, Imataka K, Seko Y, Fujii J

机构信息

Institute for Adult Disease, Asahi Life Foundation, Tokyo.

出版信息

J Cardiol Suppl. 1991;25:53-9, discussion 60-1.

PMID:1832282
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)

摘要

在通过迷走神经刺激诱导的实验性二尖瓣反流兔中,出现了一种特殊的二尖瓣瓣环心肌病变。在该模型中,迷走神经刺激后一周内可听到全收缩期杂音,此后杂音消失。我们使用病理组织学、免疫组织化学和生化技术,对迷走神经刺激后1周(MR - 1组,N = 30)和4周(MR - 4组,N = 15)的瓣环心肌病变进行了研究,发现病变在4周时已消退。未处理的兔子(C - 1组和C - 4组)作为对照。MR - 1组的瓣环心肌病变表现为肿胀和硬度增加,在显微镜下观察对应于心肌细胞的肿胀和变性以及间质纤维化。另一方面,在MR - 4组中,心肌细胞的肿胀和变性恢复,间质胶原增加有所消退。MR - 1组瓣环心肌病变的羟脯氨酸含量与C - 1组相比显著丰富(10.5±1.6mg/g湿重,vs 7.8±0.9,平均值±标准差,p<0.01)。在MR - 4组中,羟脯氨酸含量与MR - 1组相比显著降低(8.8±1.4 vs 10.5±1.6,p<0.05)。免疫组织化学研究清楚地表明,MR - 1组瓣环心肌病变中增加的胶原是III型胶原,并且在MR - 4组中增加的III型胶原消退。(摘要截断于250字)

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