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Chico, CA, United States

Carlile E.L.,Washington State University | Shirachi D.Y.,Chico Hyperbaric Center | Quock R.M.,Washington State University
Life Sciences | Year: 2012

Aims: We studied whether hyperbaric oxygen (HBO 2) treatment, which is known to increase production of nitric oxide (NO) in the brain, might also produce an NO-dependent anxiolytic-like behavioral response. Main methods: Male NIH Swiss mice (20-25 g) were subjected to a 60-min HBO 2 treatment at different absolute atmospheres, and anxiety was assessed using the light/dark exploration test at different time intervals following the cessation of HBO 2 treatment. To ascertain the underlying mechanism of action, other groups of mice were pretreated with the NO synthase inhibitor N G-monomethyl-l-arginine acetate, the NO scavenger 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethyl-1H-imidazolyl-1-oxy-3-oxide (carboxy-PTIO), the soluble guanylyl cyclase-inhibitor 1H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one (ODQ) or the benzodiazepine antagonist flumazenil to determine their influence on the HBO 2-induced anxiolytic-like effect. Key findings: A 60-min HBO 2 treatment at 3.0 absolute atmospheres increased the time spent by mice in the light compartment that lasted up to 90 min following the end of HBO 2 treatment. This anxiolytic effect of HBO 2 was significantly reduced by pretreatment with L-NMMA, carboxy-PTIO, ODQ and flumazenil. Significance: Based on these findings, we conclude that a 60-min HBO 2 treatment is capable of inducing an anxiolytic effect that possibly involves NO, cyclic GMP and the benzodiazepine binding site. © 2011 Elsevier Inc. All rights reserved. Source


Quock L.P.,Washington State University | Zhang Y.,Washington State University | Chung E.,Chungnam National University | Ohgami Y.,Chungnam National University | And 2 more authors.
Brain Research | Year: 2011

Previous research has found that hyperbaric oxygen (HBO2) produces an acute antinociceptive effect that is dependent on nitric oxide (NO). The present study was undertaken to determine whether HBO2-induced acute antinociception might involve a NO-cyclic GMP-protein kinase G-ATP-sensitive potassium (KATP) channel pathway. Male NIH Swiss mice were subjected to a 5-min HBO2 treatment (100% oxygen at 3.5 absolute atmospheres) and antinociception was assessed over the next 6 min still under HBO2 using the acetic acid abdominal constriction test. Pretreatment with 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethyl-1H- imidazolyl-1-oxy-3-oxide (carboxy-PTIO, an NO scavenger), 1H-[1,2,4]-oxadiazolo- [4,3-a]quinoxalin-1-one) (a soluble guanylyl cyclase-inhibitor, Rp-8-(4-chlorophenylthio)-guanosine-3′,5′-cyclic monophosphorothioate (a protein kinase G-inhibitor) or glibenclamide (an ATP-sensitive potassium channel-inhibitor) all led to antagonism of the HBO 2-induced acute antinociception in a dose-dependent manner. These findings suggest that HBO2-induced acute antinociception might be due to activation of a NO-cyclic GMP-protein kinase G-KATP channel pathway. © 2010 Elsevier B.V. All rights reserved. Source


Chung E.,Washington State University | Zelinski L.M.,Washington State University | Ohgami Y.,Washington State University | Shirachi D.Y.,Chico Hyperbaric Center | Quock R.M.,Washington State University
Journal of Pain | Year: 2010

Hyperbaric oxygen (HBO2) therapy is approved by the FDA for limited clinical indications but is reported to produce pain relief in several chronic pain conditions. However, there have been no studies to explain this apparent analgesic effect of HBO2. Research conducted in our laboratory demonstrates that 4 daily 60-minute HBO2 treatments at 3.5 absolute atmospheres induced an unparalleled antinociceptive response that consists of 1) an early phase that lasted at least 6 hours after the HBO 2 treatment before dissipating; and 2) a late phase that emerged about 18 hours after the early phase and lasted for up to 3 weeks. The early phase was sensitive to antagonism by acutely intracerebroventricular (i.c.v.)-administered opioid antagonist naltrexone and the nitric oxide synthase (NOS)-inhibitor L-NAME. The late phase was inhibited by treatment with i.c.v. naltrexone or L-NAME during the 4 daily HBO2 treatments but was not antagonized by either naltrexone or L-NAME following acute pretreatment 2 weeks after HBO2 treatment. These experimental results implicate a novel mechanism that is activated by HBO2, resulting in an antinociceptive response of unusually long duration that is of potential interest in the clinical management of pain. Perspective: Hyperbaric oxygen treatment of mice can induce a 2-phase antinociceptive response of unusually long duration. Nitric oxide and opioid receptors appear to initiate or mediate both phases of the antinociceptive response. Further elucidation of the underlying mechanism may potentially identify molecular targets that cause long-lasting activation of endogenous analgesic systems. © 2010 by the American Pain Society. Source


Ohgami Y.,Washington State University | Ohgami Y.,Chungnam National University | Elstad C.A.,Washington State University | Chung E.,Washington State University | And 4 more authors.
Anticancer Research | Year: 2010

Background: Artemisinin selectively kills cancer cells which have more intracellular free iron than do normal cells. Hyperbaric oxygen (HBO 2) may be beneficial in the treatment of cancer. The hypothesis of this study was that HBO2 enhances anticancer activity of artemisinin. Materials and Methods: After pretreatment with 12 μM holotransferrin, Molt-4 human leukemia cells were cultured in 10 μM artemisinin and exposed for 90 min to one of three different conditions: control, room air control, and HBO2. Cell growth was determined for 48 h after exposure. Results: Differences in growth were noted after 6 h of incubation. After 48 h of incubation, growth of cells treated with artemisinin alone or HBO2 alone was 85% of that of cells grown under artemisinin-free control conditions. Combined artemisinin and HBO2 treatment resulted in an additional 22% decrease in growth. Conclusion: Combined HBO2 and artemisinin exposure may be an effective anticancer chemotherapeutic strategy. Source

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