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Effects of nimodipine and dexamethasone on low‐level co 2 laser‐induced release of 51 chromium from canine 2c5 gliosarcoma cells
Author(s) -
van Kooten David W.,
Maciunas Robert J.,
Carver Robert S.
Publication year - 1994
Publication title -
lasers in surgery and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.888
H-Index - 112
eISSN - 1096-9101
pISSN - 0196-8092
DOI - 10.1002/lsm.1900150409
Subject(s) - nimodipine , gliosarcoma , laser , irradiation , chemistry , dexamethasone , pharmacology , biophysics , glioma , cancer research , calcium , biology , medicine , organic chemistry , physics , nuclear physics , optics
Low‐energy penumbral irradiation of surgical lasers may produce undesirable effects on surrounding tissues. This study used a 51 Cr cell labeling technique to determine if gliosarcoma cells could be therapeutically protected prior to their exposure to low‐power laser irradiation. Canine 2C5 gliosarcoma cells with intra‐cellular 51 Cr were treated with nimodipine and/or dexamethasone and then exposed to low‐power levels of CO 2 laser. The 51 Cr was released from the cells in a dose‐dependent fashion following exposure to laser energy. Correlative analysis of the data indicated that a strong direct relationship between laser fluence and 51 Cr release did exist for controls and drug‐treated groups with coefficients of correlation r ≥ +0.90 and coefficients of determination r 2 ≥ 0.82. However, comparison of the data from the drug‐treated and control groups found that there was no significant difference between them ( P >.05). Therefore, no protective or detrimental effects were observed with the use of nimodipine and/or dexamethasone on the gliosarcoma cells as tested in this system. Further investigation is necessary in order to define the mechanisms by which low‐power level lasers affect these cells. These effects do not appear to be mediated through localization of mechanisms to the cell membranes or their constituent Ca 2+ channels. © 1994 Wiley‐Liss, Inc.