Myocardial necrosis, fibrosis, and DNA synthesis in experimental cardiac hypertrophy induced by sudden pressure overload.
The development of myocardial fibrosis as a result of cardiac hypertrophy was studied in 11 cats in which the pulmonary artery was banded, six rabbits in which the ascending aorta was banded, and eight cats with various congenital cardiac anomalies. Histological examination of the myocardium revealed multifocal areas of degeneration and necrosis with healing by fibrosis in the right ventricle of cats in which the pulmonary artery was banded and in the left ventricle of rabbits in which the aorta was banded. In five of eight cats with congenital anomalies, myocardial necrosis and fibrosis were not present in spite of heart weight to body weight ratios 2-4 times greater than in the experimental models. In the other three cats, fibrosis was subendocardial or diffuse rather than multifocal as in the banded animals. This suggests that the increased connective tissue found in animals with cardiac hypertrophy induced by banding the aorta or pulmonary artery is an artifact of the preparation. Autoradiographic studies of the myocardium of pulmonary artery-banded cats indicated that all newly synthesized DNA in this model is restricted to interstitial cell and endothelial cell proliferation.
D000818:Animals; D001794:Blood Pressure; D006332:Cardiomegaly / Q000378:metabolism / Q000473:pathology*; D002415:Cats; D003326:Coronary Circulation; D004247:DNA / Q000096:biosynthesis*; D006330:Heart Defects, Congenital / Q000473:pathology; D006352:Heart Ventricles / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009336:Necrosis; D011817:Rabbits
D004247:DNA