In canine left ventricular myocardium, laminar extension and interlaminar shear contributed approximately 60% and 40%, respectively, of mean transmural thickening during systole.
Previous studies suggest that the laminar architecture of left ventricular myocardium may be critical for normal ventricular mechanics. However, systolic three-dimensional deformation of the laminae has never been measured. Therefore, end-systolic finite strains relative to end diastole, from biplane radiography of transmural markers near the apex and base of the anesthetized open-chest canine anterior left ventricular free wall (n = 6), were referred to three-dimensional laminar microstructural axes reconstructed from histology. Whereas fiber shortening was uniform -0.07 +/- 0.04 (SD), radial wall thickening increased from base (0. 10 +/- 0.09) to apex (0.14 +/- 0.13). Extension of the laminae transverse to the muscle fibers also increased from base (0.08 +/- 0. 07) to apex (0.11 +/- 0.08), and interlaminar shear changed sign 0. 05 +/- 0.07 (base) and -0.07 +/- 0.09 (apex), reflecting variations in laminar architecture. Nevertheless, the apex and base were similar in that at each site laminar extension and shear contributed approximately 60 and 40%, respectively, of mean transmural thickening. Kinematic considerations suggest that these dual wall-thickening mechanisms may have distinct ultrastructural origins.
Costa et al. (1999) studied Normal ventricular mechanics (n=6). In canine left ventricular myocardium, laminar extension and interlaminar shear contributed approximately 60% and 40%, respectively, of mean transmural thickening during systole.