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Am J Physiol Lung Cell Mol Physiol 276: L81-L89, 1999;
1040-0605/99 $5.00
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Vol. 276, Issue 1, L81-L89, January 1999

Effect of halothane on intracellular calcium oscillations in porcine tracheal smooth muscle cells

Christina M. Pabelick1, Y. S. Prakash1, Mathur S. Kannan2, Keith A. Jones1, David O. Warner1,3, and Gary C. Sieck1,3

Departments of 1 Anesthesiology, and 3 Physiology and Biophysics, Mayo Clinic and Foundation, Rochester 55905; and 2 Department of Veterinary PathoBiology, University of Minnesota, St. Paul, Minnesota 55108

The effect of halothane on intracellular Ca2+ concentration ([Ca2+]i) regulation in porcine tracheal smooth muscle cells was examined with real-time confocal microscopy. Both 1 and 2 minimum alveolar concentration (MAC) halothane increased basal [Ca2+]i when Ca2+ influx and efflux were blocked, suggesting increased sarcoplasmic reticulum (SR) Ca2+ leak and/or decreased reuptake. In beta -escin-permeabilized cells, heparin inhibition of inositol 1,4,5-trisphosphate-receptor channels blunted the halothane-induced increase in [Ca2+]i. Both 1 and 2 MAC halothane decreased the frequency and amplitude of ACh-induced [Ca2+]i oscillations (which represent SR Ca2+ release through ryanodine-receptor channels), abolishing oscillations in ~20% of tracheal smooth muscle cells at 2 MAC. When Ca2+ influx and efflux were blocked, halothane increased the baseline and decreased the frequency and amplitude of [Ca2+]i oscillations, inhibiting oscillations in ~70% of cells at 2 MAC. The fall time of [Ca2+]i oscillations and the rate of fall of the [Ca2+]i response to caffeine were both increased by halothane. These results suggest that halothane abolishes agonist-induced [Ca2+]i oscillations by 1) depleting SR Ca2+ via increased Ca2+ leak through inositol 1,4,5-trisphosphate-receptor channels, 2) decreasing Ca2+ release through ryanodine-receptor channels, and 3) inhibiting reuptake.

airway; volatile anesthetic; muscarinic receptor; sarcoplasmic reticulum


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