Transmural sheet strains in the lateral wall of the ovine left ventricle

被引:21
作者
Cheng, A
Langer, F
Rodriguez, F
Criscione, JC
Daughters, GT
Miller, DC
Ingels, NB
机构
[1] Palo Alto Med Fdn, Res Inst, Lab Cardiovasc Physiol & Biophys, Palo Alto, CA 94301 USA
[2] Stanford Univ, Sch Med, Dept Cardiovasc & Thorac Surg, Stanford, CA 94305 USA
[3] Texas A&M Univ, Dept Biomed Engn, College Stn, TX USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2005年 / 289卷 / 03期
关键词
wall thickening; myocardium; systolic function;
D O I
10.1152/ajpheart.00119.2005
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
In an attempt to provide a better understanding of our finding that regions with contracting left ventricular myofibers need not develop a significant transmural systolic wall thickening gradient, the analytic approach of Costa et al. (Am J Physiol Heart Circ Physiol 276: H595-H607, 1999) was applied to the four-dimensional dynamic data obtained 1 and 8 wk after surgical implantation of transmural radiopaque beads in the lateral equatorial left ventricular wall in seven ovine hearts. Quantitative histology of tissue blocks demonstrated that fiber angles varied linearly across the wall in this region from -37 degrees in the subepicardium to +18 degrees in the subendocardium. Sheet angles exhibited a pleated-sheet behavior, alternating sign from subepicardium to subendocardium. From end diastole ( reference configuration) to end systole ( deformed configuration), fiber strain was uniformly negative, sheet extension and sheet thickening were uniformly positive, and sheet-normal shear contributed to wall thickening at all wall depths. Subepicardial radial wall thickening increased significantly from week 1 to week 8, with significant increases in the contributions from subepicardial sheet extension and sheet-normal shear. At 1 and 8 wk, the contribution of sheet-normal shear to wall thickening was substantial at all transmural depths; the contribution of sheet extension to wall thickening was greatest in the subepicardium and least in the subendocardium, and the contribution of sheet thickening to wall thickening was greatest in the subendocardium and least in the subepicardium. A mechanistic model is proposed that provides a working hypothesis that a selective decrease in subepicardial intercellular matrix stiffness is responsible for elimination of the transmural wall thickening gradient 1-8 wk after marker implantation surgery.
引用
收藏
页码:H1234 / H1241
页数:8
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