Korean J Anesthesiol.
2001 Sep;41(3):337-346. 10.4097/kjae.2001.41.3.337.
Effects of Propofol on the Cytosolic Calcium Concentration of the Astrocytoma Cells
- Affiliations
-
- 1Department of Anesthesiology, Eulji University School of Medicine, Daejeon, Korea.
- 2Departments of Physiology, Sungkyunkwon University School of Medicine, Seoul, Korea.
- 3Departments of Anesthesiology, Sungkyunkwon University School of Medicine, Seoul, Korea.
- 4Departments of Pharmacology, Chonbuk National University Medical School, Jeonju, Korea.
- 5Departments of Anesthesiology, Chonbuk National University Medical School, Jeonju, Korea.
- KMID: 2031887
- DOI: http://doi.org/10.4097/kjae.2001.41.3.337
Abstract
- BACKGROUND
Propofol is a widely-used intravenous anesthetic with a rapid onset, short duration of action and rapid elimination but the molecular mechanisms of action are not completely understood. Not only neurons but astrocytes are potential substrates for anesthetics, specifically for propofol. Intracellular calcium ion ([Ca2 ]i) is known to play a key role in the transduction and propagation of various chemical signals in astrocytes.
METHODS
In the present study, the effects of propofol on the intracellular calcium concentration of astrocytoma cells by using a fura-2 fluorescence spectroscopy was investigated.
RESULTS
In an isotonic standard solution, propofol (50 and 500microM) produced a transient increase in [Ca2 ]i while the intralipid did not change [Ca2 ]i. In several cells (20%), a transient increase in [Ca2 ]i was followed by sustained elevation which was sensitive to depletion of external calcium. A propofol-induced increase in [Ca2 ]i was not altered by an L-type calcium channel blocker (nifedipine 2microM). In cells bathed in a Ca2 -free external solution, a transient increase in [Ca2 ]i was observed. After the pretreatment of cyclopiazonic acid (CPA), an endoplasmic reticulum Ca2 -ATPase blocker, propofol 500microM did not produce any significant increase in [Ca2 ]i. Carbachol, which is known to release calcium from the inositol 1,4,5-triphosphate (IP3)-induced calcium release (IICR) stores, prevented the [Ca2 ]i increase by propofol and vice versa. High concentrations of caffeine (10 mM), which release calcium from the calcium-induced calcium release (CICR) stores, had no effect on [Ca2 ]i.
CONCLUSIONS
From the above results, it is suggested that an increase in [Ca2 ]i by propofol in astrocytoma cells is mainly due to calcium release from the IICR stores.
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