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(Hypertension. 1997;30:1041-1046.)
© 1997 American Heart Association, Inc.

Articles

Cardiac Myocyte Membrane Wounding in the Abruptly Pressure-Overloaded Rat Heart Under High Wall Stress

Thomas A. Fischer; Paul L. McNeil; Robert Khakee; Peter Finn; Ralph A. Kelly; Marc A. Pfeffer; Janice M. Pfeffer

From the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (T.A.F., P.F., R.A.K., M.A.P., J.M.P.), and the Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta (P.L.M., R.K.).

Correspondence to Janice M. Pfeffer, Department of Medicine, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail PFEFFER{at}BICS.BWH.HARVARD.EDU

Abstract The potential role of transient sarcolemmal membrane wounding as a signal transduction event for cardiomyocyte hypertrophy was evaluated in rats with short-term pressure overload caused by banding of the proximal aorta. This procedure resulted in significant increases in left ventricular systolic (1.5-fold) and end-diastolic (2.6-fold) pressures and wall stresses that were associated with significant wall thinning and cavitary enlargement. Quantitative image analysis of frozen sections of the stressed ventricles obtained 60 minutes after banding demonstrated a 6- to 10-fold increase in cytosolic staining with a horseradish peroxidase–labeled anti-albumin antibody compared with sham-operated controls, indicating that an increase in transient sarcolemmal membrane permeability (wounding) is an early response to an abrupt increase in hemodynamic load in vivo. We conclude that an intense hemodynamic stress in vivo can result in histologically detectable cardiomyocyte wounding.

Key Words: pressure overload • cardiomyocyte wounding • stress, left ventricular wall

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