Abstract
In the isolated electrically stimulated right ventricular papillary muscles the onset of hypoxic contracture occurred 7 +/- 1.2 min and reached maximum 29.2 +/- 4.6 min after the onset of hypoxia. Switching off of the stimulation and diltiazem (10(-6) M) or tetrodotoxin (3 X 10(-6) M) administration delayed the development of the hypoxic contracture and decreased its maximum level. The protective action of diltiazem was noted only in the presence of rhythmical stimulation. It was concluded that, in addition to the influx of Ca ions through calcium channels, the influx of Na ions through sodium channels was important in the development of hypoxic contracture.
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