Ultrastructure of right ventricular myocardium subjected to acute pressure load

• Published in: The Thoracic and cardiovascular surgeon Vol. 52; no. 6; p. 328
• Main Authors: Mühlfeld, C, Coulibaly, M, Dörge, H, Sellin, C, Liakopoulos, O, Ballat, C, Richter, J, Schoendube, F
• Format: Journal Article
• Language: English
• Published: Germany 01.12.2004
• Subjects: Acute Disease; Animals; Blood Pressure; Disease Models, Animal; Glycogen - metabolism; Heart - physiopathology; Heart Ventricles - ultrastructure; Microscopy, Electron; Mitochondria, Heart - metabolism; Mitochondria, Heart - ultrastructure; Myocardium - pathology; Myocardium - ultrastructure; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - pathology; Perfusion; Pulmonary Artery - physiopathology; Swine; Vasoconstriction
• ISSN: 0171-6425
• DOI: 10.1055/s-2004-821272

Ultrastructural data on acute right ventricular pressure load in pigs are rare. In control (n = 7) and banding groups (n = 6), right ventricular pressure (micromanometry) and function (sonomicrometry) were measured. Right ventricular pressure was increased 2.5-fold in the banding group by pulmonary artery constriction. Right ventricular biopsies were taken at baseline and after 6 h and processed for electron microscopy. Parameters of cellular injury were determined stereologically. Three perfusion -fixed hearts were investigated qualitatively in each group. Stereology revealed an increase in the sarcoplasmic volume fraction and the cellular edema index in the banding group ( p < 0.05). Mitochondrial surface-to-volume ratio and volume fraction did not show significant alterations. Subendocardial edema and small amounts of severely injured myocytes were observed in the perfusion-fixed hearts after banding. Ultrastructure was normal in controls. After an initial increase, the right ventricular work index declined progressively in the banding group but remained unchanged in controls. Ultrastructural alterations resulting from acute right ventricular pressure load were characterized by edema of subendocardial myocytes and single cell necrosis. Focal adrenergic overstimulation and mechanical stress are probably more relevant in the pathogenesis of these lesions than ischemia.