Nmr spectroscopy studies of severe hypokalemia in the isolated rat heart. Peterson, E. W., K. G. Chen, N. Elkins, R. B. Hutchison, and J. I. Shapiro. The Giles Filley Research Laboratory and Departments of Medicine and Radiology, Webb Waring Lung Institute and University of Colorado School of Medicine
APStracts 2:0260H, 1995.
The effects of acute tissue potassium depletion on cellular energy metabolism are poorly understood. To examine this issue, we performed the following studies in an isovolumic isolated perfused heart preparation. Perfusion of isolated hears with media lacking potassium (K = 0 mmol/l) for thirty minutes resulted in the development of ventricular fibrillation as well as rapid decreases in creatine phosphate and adenosine triphosphate as well as increases in inorganic phosphate. During reinstitution of normal perfusate potassium, hearts did not resume normal contractions, and no increases in tissue ATP were observed. However, some normalization of PCr and Pi were noted during reinstitution of normal perfusate. Perfusion with media containing K = 2 mmol/l caused significant but less dramatic decreases in tissue ATP concentrations than with K = 0 mmol/l media. Reduction of perfusate calcium from 1.2 mmol/l (normal) to 0.6 mmol/l in the setting of K = 0 mmol/l attenuated the fall in ATP seen with K = 0 mmol/l media. Conversely, increasing perfusate calcium to 2.4 mmol/l in the setting of K = 2 mmol/l media markedly worsened the fall in tissue ATP seen with K = 2 mmol/l media. In this subgroup (K = 2 mmol/l, Ca = 2.4 mmol/l), ventricular fibrillation developed approximately half of the time. However, no differences in the rate of ATP fall were observed between those hearts that fibrillated and those that did not. During perfusion with K = 0 mmol/l media, NMR visible tissue potassium concentrations fell rapidly and dramatically. Significant but less severe reductions in NMR visible potassium were seen during perfusion with K = 2 mmol/l media. With K = 2 mmol/l perfusate, the rate of cellular potassium loss was influenced by perfusate calcium concentration. Examining cardiac mitochondria following perfusion with K = 0 mmol/l media, evidence for calcium loading as well as respiratory dysfunction were noted. Summarizing these data, reductions in perfusate potassium caused dramatic reductions in tissue ATP and NMR visible potassium concentrations. The abnormal energy metabolism which results from acute cellular potassium depletion appears to be due, at least in part, to impaired energy production by cardiac mitochondria which become calcium loaded. 

Received 16 March 1995; accepted in final form 1 June 1995.
APS Manuscript Number H256-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  6 July 1995.