[Peculiar mitral periannular cardiac muscle lesion in rabbits with experimentally-induced mitral regurgitation by vagus stimulation: investigation of a collagen increase and a myosin heavy chain isozyme change].

Abstract

A peculiar mitral periannular cardiac muscle lesion was developed in rabbits with experimentally-induced mitral regurgitation by vagus stimulation. We investigated the cardiac muscle lesion of mitral regurgitation rabbits (MR group, N = 30) using pathohistological, immunohistochemical and biochemical methods. Control group consisted of 21 non-treated rabbits. The periannular cardiac muscle lesion in the MR group was characterized by swelling and increased stiffness of the muscle which were observed as swelling and degeneration of the myocardial cells and interstitial fibrosis on the microscopic observation, and increase in the amount and dimension of collagen tendon, strands, and struts on the scanning electron microscopic study. Hydroxyproline content of the periannular cardiac muscle lesion in the MR group was significantly abundant compared with that in the control group (10.5 +/- 1.6 vs 7.8 +/- 0.9 mg/g.wet wt, mean +/- SD, p less than 0.01) and that of the cardiac muscle in the left ventricular free wall in the MR group (10.5 +/- 1.6 vs 7.1 +/- 0.9, p less than 0.01). Furthermore, the immunohistochemical study clearly indicated that the increased collagen in the periannular cardiac muscle lesion in the MR group was type III collagen. A significant myosin heavy chain isozyme change from V1 myosin to V3 myosin on pyrophosphate gel electrophoresis was observed at the periannular cardiac muscle lesion in the MR group compared with that in the control group (%V1: %V3, 4.2: 92.7 vs 15.4: 74.7, p less than 0.01) and that of the cardiac muscle in the left ventricular free wall in the MR group (4.2: 92.7 vs 14.1: 75.4, p less than 0.01). These results suggested that the mitral periannular cardiac muscle in experimental mitral regurgitation rabbits induced by vagus stimulation suffers a strong mechanical load compared with the cardiac muscle in the left ventricular free wall.