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AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 1 201-R206, Copyright © 1989 by American Physiological Society
ARTICLES |
M. V. Westfall and M. M. Sayeed
Department of Physiology, Loyola University Stritch School of Medicine, Maywood, Illinois 60153.
To determine whether cellular Ca2+ regulation is altered in bacteremic rat skeletal muscle, 45Ca2+ uptake was measured in soleus muscles 12 h after an intraperitoneal bacterial (Escherichia coli) injection. Some rats received diltiazem (2.4 mg/kg iv) 10 h after bacterial injection to determine whether calcium blockers could inhibit changes in Ca2+ regulation. Cellular exchangeable Ca2+ was measured in soleus muscles incubated for 5 min to 4 h in Krebs-Ringer bicarbonate (KRB) media (pH 7.4) containing 45Ca2+ (1.5 muCi/ml) and subsequently "washed" in La3+-containing, Ca2+-free KRB media. Bacteremia had no effect on steady-state exchangeable Ca2+, but it significantly reduced the time required to reach half-maximal uptake compared with controls. Diltiazem treatment returned the half-maximal Ca2+ uptake toward control values in bacteremic rat muscles. Depolarization of soleus muscles with high K+ (60 mM) transiently increased Ca2+ uptake in control and bacteremic rat muscles, although the increase was significantly greater (P less than 0.05) in bacteremic rat muscles. The altered skeletal muscle Ca2+ regulation may be due to excessive stimulation of Ca2+ messenger systems, sarcolemmal Ca2+ channels, and/or Ca2+ release from the sarcoplasmic reticulum in response to bacteremia.
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