Abstract To determine the effects of long-term pressure overload on the structural mechanisms implicated in wall remodeling of the right ventricle, a mild pulmonary artery banding was applied to rats approximately 2 months old, and the animals were killed 150 days later. The surgical procedure resulted in a 60% reduction in the cross-sectional area of the constricted vessel and a 52% increase in the weight of the right ventricle. The hypertrophic myocardial response was associated with an elevation in right ventricular systolic pressure (from 33 +/- 11 mm Hg to 71 +/- 12 mm Hg), right ventricular end-diastolic pressure (from 3 +/- 1 mm Hg to 10 +/- 3 mm Hg), and central venous pressure (from 2 +/- 0.2 mm Hg to 10 +/- 3 mm Hg). The 76% increase in wall thickness after pulmonary artery stenosis was the result of a 24% lateral expansion of cardiac muscle cells and a 44% increase in the number of myocytes across the ventricular wall. The intermyocyte distance was also increased by 22%. These cellular adaptations occurred with no alterations in total myocyte length, average sarcomere length, and volume composition of the myocardium. Ventricular wall area was decreased by 14%, which suggests a small reduction in chamber volume. Myocyte growth was accompanied by proportional expansions of mitochondrial and myofibrillar components, so that the ratio of mitochondria to myofibrils in the cytoplasm remained essentially constant. In conclusion, ventricular remodeling in this model of chronic pressure hypertrophy is characterized by increases in cellular diameter and number that would both tend to decrease the magnitude of systolic and diastolic stresses on a per cell basis and thus improve the myocardial response to a prolonged and sustained mechanical load.
Cellular basis of wall remodeling in long-term pressure overload-induced right ventricular hypertrophy in rats / G. Olivetti; R. Ricci; C. Lagrasta; E. Maniga; EH. Sonnenblick; P. Anversa. - In: CIRCULATION RESEARCH. - ISSN 0009-7330. - 63(3)(1988), pp. 648-657. [10.1161/01.RES.65.5.1182]
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