End-systolic myocardial stiffness is a load-independent index of contractility in stage 24 chick embryonic heart.

Abstract

Cardiac morphogenesis and function are interrelated during cardiovascular development. We evaluated the effects of acute alteration of loading condition to chick embryonic ventricular contractility using end-systolic myocardial stiffness based on the incremental elastic modulus concept. End-systolic stress-strain relations including geometric factor and end-systolic myocardial stiffness were determined from the simultaneous measurement of ventricular pressure and chamber dimension in the following four groups of stage 24 White Leghorn chick embryos: volume infusion (n = 9), conotruncal occlusion (n = 9), calcium suffusion (n = 10), and verapamil suffusion (n = 8). The end-systolic stress-strain relationship was linear in each embryo. There was no correlation between end-systolic myocardial stiffness and end-systolic stress. End-systolic myocardial stiffness increased with calcium suffusion (P < 0.05 vs. volume infusion). The geometric factor increased after verapamil suffusion (P < 0.05). End-systolic myocardial stiffness normalized by geometric factor was not changed by alteration of preload or afterload, increased after calcium suffusion, and decreased after verapamil administration (P < 0.05). These results suggest that normalized end-systolic myocardial stiffness is a load-independent index of ventricular contractility in the developing embryonic chick ventricle.