Keller B B, Yoshigi M, Tinney J P
National Institutes of Health Specialized Center of Research in Pediatric Cardiovascular Diseases, Strong Children's Research Center, Department of Pediatrics, University of Rochester School of Medicine and Dentistry, New York 14642, USA.
Am J Physiol. 1997 Dec;273(6):H2861-6. doi: 10.1152/ajpheart.1997.273.6.H2861.
Embryonic ventricular diastolic and systolic function was evaluated during normal ejection (coupled) and during acute ventricular outflow tract occlusion (uncoupled) in the stage 21 chick embryo. We simultaneously measured ventricular pressure with a servo-null system and ventricular dimensions using video microscopy. Experimental protocols included 1) baseline recording followed by acute conotruncal (CT) ligation (n = 15) and 2) baseline recording, preload increase using Krebs-Henseleit buffer (3 microliters), preload reduction via venous hemorrhage, and then CT occlusion (n = 20). Ventricular epicardial cross-sectional area was converted to internal volume using wall volume measures and assuming an ellipsoid geometry to produce pressure-volume loops. We calculated the time constant of ventricular pressure decline using a monoexponential decay function with a pressure asymptote. As previously noted, heart rate was unaffected by acutely altered preload or afterload. CT ligation increased end-systolic pressure, maximal +dP/dt, and the time constant of ventricular pressure decline and decreased stroke volume indexed for end-diastolic volume. Thus the embryonic ventricle has significant contractile reserve masked in vivo by the dynamic coupling between the ventricle and arterial circulation.