Direct observation of the "oxygen paradox" in single rat ventricular myocytes.

By phase contrast microscopy with video length tracking, we followed the sequence of morphological changes in individual isolated rat ventricular myocytes during anoxia followed by reoxygenation. Cells appeared normal during early anoxia. After a duration of anoxia T1, which varied from 17-47 minutes in different cells, each cell abruptly contracted an average of 33% in length to an inert rectangular form presumed to be a rigor state. Cells which were reoxygenated before the onset of rigor showed normal morphology and an unchanged extent of shortening on field stimulation, compared to control. Cells that were reoxygenated after a time in the rigor state, T2, either partially recovered to a shortened rectangular form capable of stimulated twitches or rounded up rapidly to a disordered hypercontracture form. The distribution of T1 was the same for cells which recovered and which hypercontracted. In contrast, the outcome of reoxygenation depended markedly on T2: all cells that were reoxygenated after less than 10 minutes of rigor recovered function, whereas all cells that spent more than 20 minutes in rigor hypercontracted when reoxygenated. The hypercontracture appears to be the cellular analog of the "oxygen paradox" in whole hearts. Its occurrence is reliably related to duration of rigor state but not to duration of hypoxia, because of marked cellular variability in the time of onset of rigor.