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Am J Physiol Heart Circ Physiol (February 7, 2002). doi:10.1152/ajpheart.00759.2001
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Articles in PresS, published online ahead of print February 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00759.2001
Submitted on August 23, 2001
Accepted on February 5, 2002

Heart Size Independent Analysis of Myocardial Function in Murine Pressure Overload Hypertrophy

Hideyuki Takaoka1, Giovanni Esposito1, Lan Mao1, Hiroyuki Suga2, and Howard A Rockman1*

1 Medicine, Duke University Medical Center, Durham, NC, USA
2 National Cardiovascular Center Research Institute, Osaka, Japan

* To whom correspondence should be addressed. E-mail: rockm001{at}mc.duke.edu.

Pressure overload cardiac hypertrophy may be a compensatory mechanism to normalize systolic wall stress and preserve LV function. To test this concept, we developed a novel in vivo method to measure myocardial stress ({sigma})-strain ({epsilon}) relations in normal and hypertrophied mice. LV volume was measured using 2 pairs of miniature omnidirectional piezoelectric crystals implanted orthogonally in the endocardium and 1 crystal placed on the anterior free wall to measure instantaneous wall thickness. Highly linear {sigma}-{epsilon} relations were obtained in control (n=7), and hypertrophied mice produced by 7 days of transverse aortic constriction (TAC, n=13). Administration of dobutamine in control mice significantly increased the load-independent measure of LV contractility, systolic myocardial stiffness. In TAC mice, systolic myocardial stiffness was significantly greater than in control mice (3156±1433 vs. 1435±467 g/cm2, p<0.01), indicating enhanced myocardial contractility with pressure overload. However, despite the increased systolic performance, both active (time constant of LV pressure decay) and passive (diastolic myocardial stiffness constant) diastolic properties were markedly abnormal in TAC mice compared to the control mice. These data suggest that the development of cardiac hypertrophy is associated with a heightened contractile state, perhaps as an early compensatory response to pressure overload.




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