Is protection from ischaemic-reperfusion injury with adenosine pretreatment reversed by inhibition of ATP sensitive potassium channels?
While adenosine pretreatment protects against necrosis in the rabbit, (1) the expression of this protection depends at least in part upon the actions of K(+)ATP channels during ischaemia, and (2) glibenclamide at higher doses increases infarct size, suggesting either that the K(+)ATP channel is endogenously protective during ischaemia, or that the higher dose has other infarct extending effects.
We conclude that the different calcium ion-induced effects on energy metabolism, structure and function of patients' erythrocytes are due to an augmented membrane leakage of Ca2+ and therefore an accumulated intracellular Ca2+ pool. This will result in an increased energy demand by the Ca2+-stimulated ATPase (calcium pump) to compensate for the dissipated Ca2+ gradient across the plasma membrane. The concomitant haemolysis may be explained by a diminished erythrocyte deformability due to Ca2+ overload.