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Effect of Hyperoxia on Neurogenic Plasma Protein Extravasation in the Rat Dura Mater


  • Sigrid Schuh-Hofer MD,

  • Wiebke Siekmann,

  • Nikolas Offenhauser MD,

  • Uwe Reuter MD,

  • Guy Arnold MD

  • Charité Universitätsmedizin Berlin, Campus Mitte, Department of Neurology, Berlin, Germany (Drs. Schuh-Hofer, Siekmann, Offenhauser, Reuter, and Arnold).

  • Krankenhaus Sindelfingen, Department of Neurology, Sindelfingen, Germany (Dr. Arnold).

Address all correspondence to Dr. Sigrid Schuh-Hofer, MD; Department of Neurology, Charité Universitätsmedizin, Berlin, Germany.


Objective.—We aimed to study the effect of normobaric hyperoxia on neurogenic inflammation of the rat dura mater.

Background.—Inhalation of 100% oxygen is a first-line therapy for the treatment of acute cluster headache (CH). However, the mechanisms underlying the antinociceptive effect of oxygen are poorly understood. Sumatriptan, which is also effective in aborting CH attacks, is known to inhibit neurogenic inflammation of the dura mater. We hypothesized that hyperoxia reduces dural plasma protein extravasation in the model of electrically stimulating the rat trigeminal ganglion.

Methods.—Unilateral stimulation of the trigeminal ganglion was performed in anesthetized male Sprague-Dawley rats. We assessed plasma protein extravasation (PPE) in the ipsilateral dura mater under normoxic (group 1) and hyperoxic conditions (group 2: pO2 200 mmHg; group 3: pO2 300 mmHg; group 4: pO2 400 mmHg). The study results were compared to the effect of sumatriptan (300 μg/kg) on dural PPE.

Results.—Under normoxic conditions, the calculated extravasation ratio was 1.72 ± 0.2. Hyperoxic treatment (groups 2, 3, 4) significantly attenuated dural PPE. At oxygen levels of 400 mmHg, the PPE ratio was 1.14 ± 0.2 (P < .01). After IV application of sumatriptan (300 μg/kg), PPE was nearly abolished (PPE ratio: 1.06 ±0.17).

Conclusion.—Our findings demonstrate that hyperoxia is able to inhibit dural PPE. Hyperoxia may play an anti-inflammatory role in neurogenic inflammation, but further studies are needed to clarify whether this effect is either caused by prejunctional mechanisms or by modulation of the vascular permeability at postcapillary venules.