Reversibility of the structural effects of pressure overload hypertrophy of cat right ventricular myocardium.
The purpose of the present quantitative structural study was to determine whether the histological alterations seen in pressure overloaded myocardium return to normal, as in vitro contractile function does, upon removal of the pressure overload stimulus. Three experimental groups of four cats each were studied: a group with pulmonary artery banding to create a pressure overload, a group that had been subjected to an equivalent duration of pressure overload and then had that pressure overload removed, and a group of sham-operated controls. Seven to 10 weeks after each operative procedure, the right ventricular pressure was elevated only in the pulmonary artery-banded group. The right ventricle/body weight ratio was significantly increased in the pressure overloaded group only. The body weight at sacrifice, the left ventricle/body weight ratio, and the right ventricular end-diastolic pressure did not differ significantly in the three groups. The striking histological changes in the right ventricular myocardium hypertrophing in response to a pressure overload were the decrease in the volume density of cardiocytes and the increase in connective tissue in papillary muscles. These were reversed when the pressure overload was removed. This study demonstrates that when a pressure overload is removed, myocardial structure returns to normal as the function returns to normal. Given the critical importance of the proportion of cardiocytes and connective tissue components to both systolic and diastolic cardiac function, these data support the hypothesis that the abnormal proportions of these structures provide a potential morphological basis for at least some of the functional abnormalities observed in pressure overload hypertrophy of the cat right ventricle.
D000818:Animals; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D002415:Cats; D004195:Disease Models, Animal; D006333:Heart Failure / Q000209:etiology; D006352:Heart Ventricles; D006976:Hypertension, Pulmonary / Q000150:complications; D008929:Mitochondria, Heart / Q000473:pathology; D009200:Myocardial Contraction; D009210:Myofibrils / Q000473:pathology