Abstract
Purpose
To determine if 100% oxygen (O2) inhalation induces ischemic tolerance to focal cerebral ischemia and if the effect is induced via O2 free radical formation.
Methods
Experiment 1: 36 rats were randomly assigned to four groups (n = 9 each): Group A, control rats inhaled air for 24 hr; Groups B, C and D animals inhaled 100% O2 for six hours, 12 hr and 24 hr respectively. Experiment 2: 32 rats were randomly assigned to four groups (n = 8 each): Groups E and F rats received normal saline (5 mL·kg−1 intraperitoneally) and then inhaled air (Group E) or 100% O2 (Group F) for 24 hr; Groups G and H animals received 10% dimethylthiourea (500 mg·kg−1 intraperitoneally) and then inhaled 100% O2 (Group G) or air (Group H) for 24 hr. Twenty-four hours after the treatments, the right middle cerebral artery was occluded in all rats for 120 min. The neurologic deficit scores (NDS) and brain infarct volumes were evaluated at 24 hr after reperfusion.
Results
Experiment 1: the infarct volume and NDS of Group D were smaller than in controls (P = 0.004 and 0.042 respectively). The infarct volume was reduced by 47% in Group D. There was no statistical difference among Groups A, B and C. Experiment 2: the infarct volume and NDS in Group F were less than in controls (Group E;P = 0.001 and 0.036 respectively). The infarct volume was reduced by 60% in Group F There was no difference among Groups E, G and H.
Conclusion
Our study demonstrates that preconditioning with 100% O2 for 24 hr can induce ischemic tolerance via formation of O2 free radicals in transient focal cerebral ischemia in rats.
Résumé
Objectif
Déterminer si l’inhalation d’oxygène à 100 % (O2) induit une tolérance ischémique à une ischemic cérébrale focale et si l’effet est causé par la formation de radicaux libres d’O2.
Méthode
Essai 1: 36 rats ont été répartis au hasard en quatre groupes (n = 9 chacun): Groupe A, les rats témoins ont inhalé de l’air pendant 24 h; Groupes B, C et D, les animaux ont inhaié de l’O2 à 100 % pendant six heures, 12h et 24 h, respectivement. Essai 2: 32 rats répartis au hasard en quatre groupes (n = 8 chacun): Groupes E et F, les rats ont reçu une solution saline (une dose intrapéritonéale de 5 mL·kg−1) et ont ensuite inhalé de l’air (Groupe E) ou de l’O2 à 100% (Groupe F) pendant 24 h; Groupes G et H, les animaux ont reçu du diméthyithiourée à 10 % (dose intrapéritonéale de 500 mg·kg−1) et ont ensuite inhalé de l’O2 à 100 % (Groupe G) ou de l’air (Groupe H) pendant 24 h. Vingt-quatre heures après ie traitement, nous avons procédé à l’occlusion de l’artère cérébrale moyenne droite chez tous les rats pendant 120 min. Les scores de déficit neurologique (SDN) et ies volumes de l’infarctus cérébral ont été évalués 24 h après la reperfusion.
Résultats
Essai 1: te volume de l’infarctus et le SDN du Groupe D ont été plus faibles que ceux du Groupe témoin (P = 0,004 et 0,042 respectivement). Le volume de l’infarctus a été réduit de 41 % dans le Groupe D. Il n’y avait pas de différence statistique entre les Groupes A, B et C. Essai 2: le volume de l’infarctus et le SDN du Groupe F ont été plus faibles que ceux du Groupe témoin (Groupe E; P = 0,001 et 0,036 respectivement). Le volume de l’infarctus a été réduit de 60 % dans le Groupe F. Les Groupes E, G et H étaient comparables.
Conclusion
Le préconditionnement avec de l’O2 à 100% pendant 24 h peut induire une tolérance ischémique par la formation de radicaux libres d’O2 pendant une ischémie cérébrale focale chez les rats.
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This work was supported in part by the National Natural Science Foundation of China (Grant 30170907 to Dr. Xiong).
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Zhang, X., Xiong, L., Hu, W. et al. Preconditioning with prolonged oxygen exposure induces ischemic tolerance in the brain via oxygen free radical formation. Can J Anesth 51, 258–263 (2004). https://doi.org/10.1007/BF03019107
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DOI: https://doi.org/10.1007/BF03019107