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J Mol Cell Cardiol. 1999 Feb;31(2):307-17.

Chronic pressure overload cardiac hypertrophy and failure in guinea pigs: I. Regional hemodynamics and myocyte remodeling.

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  • 1South Dakota Health Research Foundation Cardiovascular Research Institute, Sioux Falls 57105, USA.


A chronic pressure overload animal model was created in young guinea pigs by surgical constriction of the descending thoracic aorta. Hemodynamics, echocardiography and myocyte size characterization demonstrated compensated pressure overloaded left ventricular (LV) hypertrophy at 4 weeks (4 wk), and congestive left heart failure 6 months (6 mo) after aortic constriction. Compared to age-matched sham-surgery control groups, the cell length and length/width ratio of isolated LV myocytes were significantly increased at 6 mo but not at 4 wk. LV myocyte lengthening was statistically correlated to an increase in LV chamber dimension and diastolic wall stress at 6 mo. These data demonstrate that myocyte lengthening occurs in mechanical overload-induced congestive heart failure, contributes to LV chamber dilatation, and is associated with increased end-diastolic wall stress. Myocytes of the other three chambers remained morphometrically normal at 4 wk. Hypertrophy of left atrial (LA) and right ventricular and atrial myocytes was evident at 6 mo. Increases in both cell length and cross-sectional area contributed significantly to the hypertrophy in the three chambers. More than 85% of LV myocytes were binucleate and the binucleation remained unchanged in the sham-surgery group from the tested 4 wk to 6 mo time point. LV hypertrophy and failure showed no significant effects on the binucleation of LV myocytes. By contrast, over 96% of LA myocytes were mononucleate. The mononucleate percent of LA myocytes was not appreciably altered during either normal growth or hypertrophy induced by secondary hemodynamic overload due to LV failure.

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