Hemodynamic changes in HH stage 34 chick embryos after treatment with all-trans-retinoic acid.
To obtain insight into the hemodynamics of abnormal cardiac development, a chick embryo model was recently developed in which a spectrum of double outlet right ventricle was induced with all-trans-retinoic acid. In Hamburger and Hamilton (HH) stage 34 white Leghorn chick embryos, we simultaneously measured dorsal aortic flow velocities with a 20 MHz pulsed Doppler velocity meter and vitelline artery blood pressures with a servonull system. These measurements were performed in embryos treated at HH stage 15 with 1 microgram of all-trans-retinoic acid (n = 47), or with the solvent DMSO (n = 15), and in control embryos (n = 21). After the wave form recordings were collected, all embryos were examined histologically. Embryos treated with all-trans-retinoic acid showed in 15 cases hearts with a rightward positioned aorta with an additional subaortic ventricular septal defect and 32 cases without septation abnormalities of the heart. The hemodynamic data were correlated with the morphology. Statistical comparison was performed between control and experimental values. There was no significant discrepancy in hemodynamics of sham-operated and control embryos. Heart rate, peak systolic and mean velocities, peak systolic and mean blood flows, and peak acceleration and stroke volume were reduced in embryos treated with all-trans-retinoic acid (p < 0.01). Furthermore, in the presence of a subaortic ventricular septal defect the diameter of the dorsal aorta was reduced. Pressure readings were not statistically significant. Our findings suggest that the hemodynamic changes are the result of a decrease in cardiac contraction force.
D000818:Animals; D001011:Aorta / Q000002:abnormalities; D001783:Blood Flow Velocity / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002642:Chick Embryo; D004195:Disease Models, Animal; D006321:Heart / Q000196:embryology*; D006330:Heart Defects, Congenital / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D006345:Heart Septal Defects, Ventricular / Q000139:chemically induced; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D009929:Organ Size / Q000187:drug effects; D014212:Tretinoin / Q000633:toxicity*; D014655:Vascular Resistance / Q000187:drug effects
D014212:Tretinoin