Abnormal myocardial and coronary vasculature development under hypoxia leads to embryonic heart failure and death

Oxygen availability is one of the prerequisites for embryonic development. In our previous study we found that quail embryos incubated under hypoxic conditions (16%O2) die at embryonic day (ED) 9 with signs of heart failure. By ED4 and 6 we found thinner ventricular wall and increased capillary density. We thus hypothesized that the cause would lie in severe myocardial and coronary maldevelopment. ED6 and 7 hypoxic hearts had thinner ventricular wall. There was a simultaneous increase in capillary density, most pronounced in the interventricular septum. This site corresponds to an area of tissue hypoxia and ensuing increased angiogenesis, and also formation of conduction system. Hypoxia had a positive effect on normal sequence of maturation of the conduction evaluated by optical mapping at ED7.In sections from ED9 hypoxic hearts we found irregularities in development of coronary tree. This deficiency was due to decreased myocyte proliferation rather than to increased apoptosis. By Indian ink injection we found in normoxic specimens regular coronary branching, while in the hypoxic ones there was often only an irregular plexus. Embryonic hypoxia thus leads to increased capillarity and trabeculation to minimize diffusion distance. In the subsequent period there is a failure in organization of vascular plexus into normal vasculature, leading to heart failure. Supported by MSMT VZ 206100‐3