Benzodiazepine receptor-dependent modulation of neutrophil (PMN) free amino- and alpha-keto acid profiles or immune functions |
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| Authors: | Mühling J Gonter J Nickolaus K A Matejec R Welters I D Wolff M Sablotzki A Engel J Krüll M Menges T Fuchs M Dehne M G Hempelmann G |
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| Institution: | (1) Department of Anaesthesiology, Intensive Care Medicine, Pain Therapy, University Hospital, Justus Liebig University, Giessen, Germany;(2) Dr. Ing. Herbert Knauer GmbH, Berlin, Germany;(3) Clinics of Anaesthesiology and Intensive Care Medicine, Martin Luther University, Halle-Wittenberg, Germany;(4) Department of Internal Medicine/Infectious Diseases, Charité, Medical School of Humboldt University, Berlin, Germany |
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| Abstract: | Summary. We have examined the effects of midazolam, Ro 5-4864 (agonist for  peripheral p] benzodiazepine receptors BR]), PK 11195 (antagonist for pBR), flumazenil (antagonist for central BR), naloxone (antagonist for opiate receptors) and the combination of midazolam and Ro 5-4864, PK 11195, flumazenil or naloxone on intracellular amino- and  -keto acids and the immune function markers superoxide anion (O2–), hydrogen peroxide (H2O2) and released myeloperoxidase (MPO) activity in neutrophils (PMN). Only midazolam and Ro 5-4864 led to significant changes in the dynamic PMN free amino- and -keto acid pools. Concerning PMN immune function markers, midazolam and Ro 5-4864 significantly decreased O2– and H2O2 formation and released MPO. When midazolam and Ro 5-4864 were applied together they appeared to act additively. Pre-incubation with PK 11195 partially neutralized the midazolam effects whereas flumazenil or naloxone showed no effects. We therefore believe that pBR are involved in the signal transmission of anesthetic-induced cellular metabolic changes in PMN. |
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| Keywords: | : Benzodiazepine receptors – Neutrophil – Amino acids –  -Keto acids –" target="_blank">gif" alt="agr" align="BASELINE" BORDER="0">-Keto acids – Immune function |
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