Cohen-Gould L, Robinson T F, Factor S M
Am J Pathol. 1987 May;127(2):327-34.
Significant connective tissue abnormalities occurring in hearts of cardiomyopathic Syrian hamsters are reported. These abnormalities include a pronounced loss of the intrinsic connective tissue skeletal framework around foci of myocytolytic necrosis within the non-necrotic myocardium. These changes were demonstrated by a silver impregnation technique, and they were confirmed by scanning electron microscopy. Quantitation demonstrated more than a twofold increase in the area of ventricular wall affected by pathologic changes, when the connective tissue alterations were included with the myocardial necrosis. In addition, the authors also observed focal, thick "tethering" connective tissue fibers at the termini of necrotic lesions, seemingly connecting them to normal muscle. These connective tissue abnormalities may contribute to the progressive loss of ventricular function that occurs in this model of cardiomyopathy. They may permit greater wall thinning than would occur with focal necrosis alone, and they may increase focal mural stiffness in the tethered regions. Further investigation of the pathogenesis of these changes and their mechanical significance is indicated.
据报道,患心肌病的叙利亚仓鼠心脏出现了明显的结缔组织异常。这些异常包括非坏死心肌内肌溶解坏死灶周围固有结缔组织骨骼框架的显著丧失。这些变化通过银浸染技术得以证实,并通过扫描电子显微镜得到确认。定量分析表明,当将结缔组织改变与心肌坏死一并考虑时,受病理变化影响的心室壁面积增加了两倍多。此外,作者还观察到坏死病变末端有局灶性、粗大的“系留”结缔组织纤维,似乎将它们与正常肌肉相连。这些结缔组织异常可能导致该心肌病模型中出现的心室功能逐渐丧失。它们可能比仅局灶性坏死时允许更大程度的心室壁变薄,并且可能增加系留区域的局灶性壁僵硬。有必要对这些变化的发病机制及其力学意义进行进一步研究。