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AJP - Heart and Circulatory Physiology, Vol 268, Issue 3 1045-H1052, Copyright © 1995 by American Physiological Society
ARTICLES |
S. Seki and K. T. MacLeod
Department of Cardiac Medicine, National Heart and Lung Institute, University of London, United Kingdom.
Single, enzymatically isolated guinea pig ventricular myocytes were exposed to 3-min periods of anoxia with glucose-free Tyrode solution containing 1 mM sodium dithionite (Na2S2O4) and were then reoxygenated for 10 min. The myocytes were exposed to rapid applications of 10 mM caffeine during the control, anoxic, and reoxygenation periods. Intracellular Ca2+ concentration ([Ca2+]i) was measured ratiometrically using indo 1 with simultaneous measurements of cell length. The effects of anoxia on Ca2+ were compared with those of hypoxia and metabolic inhibition. The amplitude of the electrically stimulated (Ca transient) and caffeine-evoked Ca2+ (Caff-Ca) transients decreased during anoxia and recovered after reoxygenation. Diastolic [Ca2+]i did not change during 3 min of anoxia but rose progressively after prolonged anoxia and remained at this higher level on reoxygenation. During metabolic inhibition the Ca transients decreased, while the Caff-Ca transients showed no change in amplitude. During hypoxia the Ca transients decreased. Anoxia slowed the time to peak of the Ca transient, the time to 50% relaxation, and the time to 90% relaxation. The decline of indo 1 fluorescence on rapid caffeine application was slowed during anoxia, metabolic inhibition, and hypoxia and partially recovered after reoxygenation.
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