In the heart, lack of oxygen affects excitability of pacemaker and muscular cells, conduction, excitation-contraction coupling and mechanical performances. Reperfusion of an ischemic heart, instead of being beneficial, can result in functional disturbances depending on the severity and duration of the oxygen deprivation. Although numerous studies have been devoted to this topic in the adult heart, scant attention has been paid to the reactivity of the embryonic myocardium to changes in oxygen concentration. The young embryonic heart beats spontaneously, lacks developed vascularization and innervation, and is dependent primarily on glycolytic metabolism; its oxygen and substrate requirements are met exclusively by diffusion.
Throughout the embryogenesis of many species, PO2 found in the tissue is rather low, and the heart can be acutely or chronically exposed to important fluctuations of PO2. It has been shown that critical values of PO2 that impair normal contractile function and depress ATP production in cultured embryonic and adult cardiomyocytes range from 0.1 to 1.6 kPa ; and that electrical and contractile activities of the fetal heart of mammals and the embryonic heart of the chick are more resistant to hypoxia than those of adult hearts. During the first three days of development of the chick embryo (equivalent to the first nine and 28 days of development of mouse and human embryos, respectively) the heart undergoes considerable morphological as well as functional differentiations, which could make it specially vulnerable to variations of oxygen availability. Dreaming of a reliable pharmacy to find allergy treatment and spend less money?