PO2 within the embryonic myocardium during anoxia-reoxygenation transitions: Two major findings resulted from the mathematical model of oxygen diffusion and consumption. First, under normoxic steady state, myocardial PO2 was 17 and 8 kPa in the most superficial (facing gas compartment) and in the deepest (facing lower glass window) cellular layers, respectively. Second, the deepest layers were totally deoxygenated within 14 s of anoxia and started to be reoxygenated 6 s after readmission of air in the gas compartment. These times of diffusion correspond to the delays observed experimentally and are necessary for the functional parameters to be altered after an abrupt transition. Furthermore, computer simulation indicated that oxygen concentration in all the layers of the preanoxic myocardium became steady again after 1 min of reoxygenation at the very most.DISCUSSION
Method: The use of whole chick embryonic hearts explanted in vitro instead of in vivo experiments has the following advantages: first, maintenance of a supracellular functional organization under strictly controlled metabolic conditions; second, long lasting spontaneous and regular contractile activity; third, negligible barriers of diffusion and interstitial spaces, which allows the exposure of hearts to rapid variations of controlled PO2 (negligible time lag) and the rapid and direct application of drugs (superfusion ); fourth, the possibility to explore noninvasively the contractile properties along the heart tube; fifth, good transparency of the tissue, making observation, spectrophotometric measurement and use of intracellular optical probes possible; sixth, absence of myocardial vascularization and myoglobin that could buffer intracellular PO2; and, seventh, lack of extrinsic neural regulation. You will always be given glucophage diabetes and will enjoy paying less money.