(Hypertension. 1996;28:609-614.)
© 1996 American Heart Association, Inc.
Articles |
the Department of Anatomy and Structural Biology, University of South Dakota, College of Medicine, Vermillion, and the Department of Food Science and Technology, Ohio State University, Columbus (S.A.M.).
Correspondence A. Martin Gerdes, PhD, Department of Anatomy and Structural Biology, University of South Dakota, College of Medicine, 414 E Clark St, Vermillion, SD 57069. E-mail mgerdes@sundance.usd.edu.
Regional changes in cardiac myocyte shape during the progression to failure with hypertension have not been clearly established. To address this issue, we examined left and right ventricular myocytes from lean, female spontaneously hypertensive/heart failure rats with compensated hypertrophy (approximately 12 months of age) and congestive heart failure (approximately 24 months of age). During this period, body weight did not change, but heart weight increased 59% and lung weight increased 93%. Left ventricular function declined with the onset of failure. Left ventricular myocyte volume increased 27% exclusively because of myocyte lengthening (29% increase). The onset of left ventricular failure resulted in a 72% increase in right ventricular myocyte volume. Right ventricular myocyte growth, however, was proportional, with a 23% increase in myocyte length and 18% increase in myocyte width. Changes in left ventricular myocyte shape were virtually identical to data collected previously from patients with similar disease, suggesting that this is a relevant animal model. Evidence suggests that left ventricular myocyte transverse growth is defective because dilation and failure were associated with cell lengthening, without a change in myocyte diameter. Although severe hypertrophy was present in the right ventricle as a result of left ventricular failure, myocyte growth was proportional, suggesting that cell shape was properly regulated in this chamber.
Key Words: heart failure, congestive ventricular function cell size
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