The embryonic heart was reoxygenated under stop-flow conditions and, consequently, was not accompanied by a washout of metabolites accumulated during anoxia. This makes our experimental protocol different from that generally used in ischemic-reperfused isolated hearts. Indeed, no reflow accompanied reoxygenation; nevertheless the embryonic ventricle stopped contracting, showing that this mechanical failure (oxygen paradox) was due to an oxygen-dependent phenomenon rather than a flow-dependent phenomenon.
Under long term anoxia and upon reoxygenation, ventricle and conotruncus suddenly ceased contracting, whereas a residual activity persisted in the atrium. This observation suggests that populations of pacemaker cells, more resistant to anoxia, could preferentially use glycolytically derived energy, and/or working cells could become uncoupled, inducing conduction disturbances culminating in atrioventricular block. During reoxygenation, atrial contractile activity recovered more rapidly than the ventricular and conotruncal activities, which suggests that the potentialities of recovery along the heart tube is not homogeneous. Such a functional hierarchy regarding the resistance to and recovery from anoxia deserves particular interest and is being investigated in our laboratory. You will be glad to come across purchase alegra costing you very little money.
The values of atrioventricular and ventricular Pv found in this work under normoxia are quite comparable with the conduction velocity determined electrophysiologically at the same developmental stage in the atrioventricular canal (10 to 15 mm/s) and in the ventricle (30 to 60 mm/s).