Poole-Wilson P A
Adv Myocardiol. 1980;2:285-93.
Whereas the changes of calcium influx and net calcium content in the myocardium have been described during ischemia, less is known of the changes that occur during and after hypoxia. In this study calcium uptake was measured with 47Ca2+, a high energy gamma emitter, calcium efflux with both 47Ca2+ and 45Ca2+, and extracellular space with 51Cr-EDTA. The experimental preparation was the isolated but arterially perfused interventricular septum of the rabbit. Temperature was 32 degrees C. Hypoxia in the absence of substrate caused a fall in developed tension and rise in resting tension. After 30 min, recovery on reoxygenation was incomplete. During hypoxia without substrate small changes of the extracellular space were associated with changes of mechanical function. Calcium efflux did not alter. Calcium influx decreased during the initial 30 min, but after 60 min a small increase was evident. The tissue content of 51Cr-EDTA only increased after prolonged hypoxia, suggesting that the increase of calcium influx at this time was due to nonspecific damage to the cell membrane. On reoxygenation calcium efflux was unaltered, but a large incrase of calcium influx occurred without an associated influx of 51Cr-EDTA. The influx of calcium on reoxygenation appears, therefore, to be caused by a relatively specific abnormality of the calcium transport system and not by generalized destruction of the cell membrane.