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AJP - Heart and Circulatory Physiology, Vol 249, Issue 3 620-H628, Copyright © 1985 by American Physiological Society
ARTICLES |
J. Krivokapich, C. R. Watanabe and K. I. Shine
We investigated the effects of anoxia and ischemia on thallium (201Tl) exchange using isolated rabbit interventricular septa. Anoxia for 20 or 40 min caused a decrease in 201Tl tissue uptake due to an increased efflux of 201Tl with a smaller increase in 201Tl influx. Between 40 and 60 min of anoxia, the increased efflux of 201Tl was reversed and the increase in 201Tl influx was absent. After 60 min of reoxygenation, septa made anoxic for 20-60 min recovered at least 95% of the Tl lost. Mechanical recovery, however, was still significantly depressed. Reperfusion after total ischemia for 20-60 min was followed by resumption of 201Tl uptake despite continued mechanical dysfunction. Efflux rates during reperfusion after ischemia were significantly different from preischemic values but not in a predictable way. This unpredictability complicates interpretation of clinical 201Tl redistribution studies. These results represent important differences from those reported previously using 42K [Am. J. Physiol. 232 (Heart Circ. Physiol. 1): H85-H94 and H564-H570, 1977]. Anoxia did not increase the influx of 42K. Also, 60 min of ischemia resulted in progressive losses of 42K. This implies there are different sensitivities and/or mechanisms for Tl compared with K uptake. Our results are consistent with 201Tl uptake by severely damaged and nonviable cells.
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