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Inhibition of nitric oxide synthase on brain oxygenation in anesthetized rats exposed to hyperbaric oxygen
1F. G. Hall Hypo-Hyperbaric Environmental Laboratory, Duke University Medical Center, Durham, North Carolina 27710, USA.
Abstract:
Nitric oxide (NO) production is involved in the development of oxygen toxicity of the central nervous system (CNS) since inhibition of nitric oxide synthase (NOS) significantly protects animals from hyperbaric oxygen (HBO)-mediated convulsions. One potential mechanism for this protection is that NOS inhibition decreases cerebral O2 delivery thereby limiting the PO2 of brain tissues during hyperoxia. To investigate this hypothesis, anesthetized rats were exposed to 7, 100, and 7% O2 under 3 atm abs for 15-min periods. Cortical blood flow (CBF) and O2 tension were measured with a laser-Doppler flowprobe and an O2 electrode, respectively, with and without pretreatment with the NOS doppler, N omega-nitro-L-arginine methyl ester (L-NAME). We found that HBO exposure significantly increased the brain O2 tension whereas changes in CBF were not significant. Compared with control rats, L-NAME administration did not change either brain O2 tension or CBF during the period of the experiment. We conclude that the effects of L-NAME on cortical oxygenation and CBF during HBO exposure in rats do not seem to provide a physiologic explanation for protection from CNS O2 toxicity by the drug.
Insights
Inhibition of nitric oxide synthase (NOS) protects against oxygen toxicity of the central nervous system (CNS). However, this study found that L-NAME did not alter brain oxygen levels or blood flow, questioning this protective mechanism.
Area of Science:
- Neuroscience
- Physiology
- Hyperbaric Medicine
Background:
- Nitric oxide (NO) plays a role in central nervous system (CNS) oxygen toxicity.
- Inhibiting nitric oxide synthase (NOS) protects against hyperbaric oxygen (HBO)-induced convulsions.
- A proposed mechanism involves reduced cerebral oxygen delivery due to NOS inhibition.
Purpose of the Study:
- To investigate if NOS inhibition reduces cerebral oxygen delivery, limiting brain tissue oxygen tension during hyperoxia.
- To determine the physiological basis for the protective effects of NOS inhibition against CNS oxygen toxicity.
Main Methods:
- Anesthetized rats were exposed to hyperbaric oxygen (3 atm abs) with varying oxygen concentrations (7%, 100%).
- Cortical blood flow (CBF) and oxygen tension (PO2) were measured using laser-Doppler flowmetry and an oxygen electrode.
- Rats were pretreated with N-omega-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, to assess its effects.
Main Results:
- Hyperbaric oxygen exposure significantly increased brain oxygen tension.
- Cortical blood flow did not change significantly during hyperbaric oxygen exposure.
- L-NAME administration did not alter brain oxygen tension or cortical blood flow in rats.
Conclusions:
- The protective effect of L-NAME against CNS oxygen toxicity in rats is not explained by reduced cortical oxygenation or altered cerebral blood flow.
- The mechanism by which NOS inhibition protects against hyperbaric oxygen toxicity requires further investigation.