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This Article Full Text Full Text (PDF) All Versions of this Article: 292/4/H1747    most recent 01037.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Brickson, S. Articles by Moss, R. L. Search for Related Content PubMed PubMed Citation Articles by Brickson, S. Articles by Moss, R. L.

In vivo left ventricular functional capacity is compromised in cMyBP-C null mice

Department of Physiology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin

Submitted 21 September 2006 ; accepted in final form 17 November 2006

Cardiac myosin binding protein-C (cMyBP-C) is a thick filament-associated protein that binds tightly to myosin and has a potential role for modulating myocardial contraction. We tested the hypothesis that cMyBP-C 1) contributes to the enhanced in vivo contractile state following -adrenergic stimulation and 2) is necessary for myocardial adaptation to chronic increases in afterload. In vivo pressure-volume relations demonstrated that left ventricular (LV) systolic and diastolic function were compromised under basal conditions in cMyBP-C^–/– compared with WT mice. Moreover, whereas -adrenergic treatment significantly improved ejection fraction, peak elastance, and the time to peak elastance in WT mice, these functional indexes remained unchanged in cMyBP-C^–/– mice. Morphological and functional changes were measured through echocardiography in anesthetized mice following 5 wk of aortic banding. Adaptation to pressure overload was diminished in cMyBP-C^–/– mice as characterized by a lack of an increase in posterior wall thickness, increased LV diameter, deterioration of fractional shortening, and prolonged isovolumic relaxation time. These results suggest that the absence of cMyBP-C significantly diminishes in vivo LV function and markedly attenuates the increase in LV contractility following -adrenergic stimulation or adaptation to pressure overload.

aortic banding; pressure-volume relations; dobutamine

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