title: The effects of amifostine and dexamethasone on brain tissue lipid peroxidation during oxygen treatment of carbon monoxide-poisoned rats.
abstract: The mechanisms of injury of, and methods of treating patients with, carbon monoxide (CO) poisoning are poorly understood. Besides the hypoxic degenerative effects of CO, reoxygenation injury may play an important role. Amifostine (Ami), which is most often used in radiotherapy for its tissue protective characteristics, may offer benefits. In this study, investigators evaluated the effectiveness of various treatments in a CO-poisoned rat model. A total of 36 Wistar rats were randomly assigned to 1 of 6 groups (n=6 each), including control and poisoned groups exposed to CO at 2000 ppm (v/v) for 1 h, followed by various 1-h treatments: group C (control), group COair (ambient air), group CO-NBO (normobaric 100% oxygen), group CO-HBO (hyperbaric oxygen with 3 atmospheres absolute [3 ATA]), group CO-NBO-Ami (normobaric oxygen with intraperitoneal [i.p.] injection of amifostine 250 mg/kg body weight [bw]), and group CO-70O (70% O2 and 5% CO2 with dexamethasone 10 mg/kg bw, i.p.). Blood gas analysis, carboxyhemoglobin determination, brain tissue lipid peroxidation, and glutathione peroxidase (GSHPx), superoxide dismutase (SOD), lactate dehydrogenase (LDH), and creatine kinase (CK) activities were evaluated. Carboxyhemoglobin concentration in the air-treated group was 44+/-2%; it decreased to the control level with all oxygen treatments. Brain tissue GSH-Px and SOD measurements did not change. The activity of LDH in group CO-HBO and the activities of LDH and CK in group CO-70O were similar to those of group C. Lipid peroxides were high in ambient air and normobaric oxygen, but HBO, amifostine with oxygen, or 70% O2 reduced these to control levels (P<.05).
authors.affiliation: Department of Anesthesiology and Reanimation, University of Pamukkale School of Medicine, Denizli, Turkey.
authors.forename: Habip
authors.initials: H
authors.lastname: Atalay
authors.forename: Hülya
authors.initials: H
authors.lastname: Aybek
authors.forename: Mehmet
authors.initials: M
authors.lastname: Koseoglu
authors.forename: Suleyman
authors.initials: S
authors.lastname: Demir
authors.forename: Hakan
authors.initials: H
authors.lastname: Erbay
authors.forename: Ali Zahit
authors.initials: AZ
authors.lastname: Bolaman
authors.forename: Aslihan
authors.initials: A
authors.lastname: Avci
mesh_terms: D004999:Amifostine / Q000494:pharmacology*; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D001930:Brain Injuries / Q000097:blood / Q000473:pathology / Q000628:therapy*; D002249:Carbon Monoxide Poisoning / Q000097:blood / Q000473:pathology / Q000628:therapy*; D003402:Creatine Kinase / Q000097:blood; D003907:Dexamethasone / Q000494:pharmacology*; D004195:Disease Models, Animal; D006931:Hyperbaric Oxygenation; D007770:L-Lactate Dehydrogenase / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D003907:Dexamethasone; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D004999:Amifostine