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AJP - Heart and Circulatory Physiology, Vol 266, Issue 3 1007-H1018, Copyright © 1994 by American Physiological Society
ARTICLES |
D. A. MacKenna, J. H. Omens, A. D. McCulloch and J. W. Covell
Department of Medicine (Cardiology), University of California, San Diego, La Jolla 92093.
Although it makes up only 2-6% of left ventricular dry weight, collagen is thought to be the major structural protein determining passive ventricular stiffness. However, the relationship between structure of the extracellular matrix and passive mechanics is not understood. Hence, to deplete the collagen matrix, 16 rat hearts were perfused with bacterial collagenase for 60 min. Quantitative morphology using picrosirius red revealed a 36% decrease in collagen area fraction predominantly in the medium-sized fibers. Scanning electron microscopy revealed damage to the endomysial struts. Passive pressure-volume curves showed increases in left ventricular volume at all pressures (from 0.203 +/- 0.061 to 0.265 +/- 0.061 ml at 5 mmHg, P < 0.0001). Strain during loading, calculated from lengths obtained from a triplet of piezoelectric crystals, was unchanged with collagen depletion. However, remodeling strain computed from the collagenase-treated state referred to the Krebs solution-treated state at the same ventricular pressure showed both circumferential (0.145 +/- 0.166 to 0.170 +/- 0.158) and longitudinal (0.070 +/- 0.120 to 0.068 +/- 0.069) stretching. Sarcomere lengths increased at all depths (5.2% at midwall). Thus alterations in the extracellular matrix lead to increased ventricular volume and sarcomere lengths without altering ventricular compliance.
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