Moskvin A N, Zhilyaev S Yu, Sharapov O I, Platonova T F, Gutsaeva D R, Kostkin V B, Demchenko I T
I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, 44 M. Torez Prospekt, 194223 St. Petersburg, Russia.
Neurosci Behav Physiol. 2003 Nov;33(9):883-8. doi: 10.1023/a:1025996721736.
Studies on conscious rats with inhibition of NO synthase were used to assess the dynamics of brain blood flow and EEG traces during hyperbaric oxygenation at 4 or 5 atm. Oxygen at a pressure of 4 atm induced cerebral vasoconstriction in intact animals and decreased blood flow by 11-18% (p < 0.05) during 60-min exposure to hyperbaric oxygenation. Paroxysmal EEG activity and oxygen convulsions did not occur in rats at 4 atm of O2. At 5 atm, convulsive activity appeared on the EEG at 41 +/- 1.9 min, and blood flow decreased significantly during the first 20 min; blood flow increased by 23 +/- 9%, as compared with controls, (p < 0.01) before the appearance of convulsions on the EEG. Prior inhibition of NO synthase I (NOS I) and NO synthase III (NOS III) with N(omega)-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg) or inhibition only of NOS I with 7-nitroindazole (7-NI, 50 mg/kg) prevented the development of hyperoxic hyperemia and paroxysmal spikes on the EEG during hyperbaric oxygenation at 5 atm. These results show that hyperbaric oxygen induces changes in cerebral blood flow which modulate its neurotoxic action via nitric oxide synthesized both in neurons and in cerebral vessels.
对一氧化氮合酶受抑制的清醒大鼠进行研究，以评估在4个或5个大气压的高压氧疗过程中脑血流量和脑电图的动态变化。4个大气压的氧气在完整动物中诱导脑血管收缩，在60分钟的高压氧疗暴露期间血流量减少11 - 18%（p < 0.05）。在4个大气压的氧气环境下，大鼠未出现阵发性脑电图活动和氧惊厥。在5个大气压时，脑电图在41±1.9分钟出现惊厥活动，在前20分钟血流量显著下降；与对照组相比，在脑电图出现惊厥之前血流量增加了23±9%（p < 0.01）。预先用N(ω)-硝基-L-精氨酸甲酯（L-NAME，30毫克/千克）抑制一氧化氮合酶I（NOS I）和一氧化氮合酶III（NOS III），或仅用7-硝基吲唑（7-NI，50毫克/千克）抑制NOS I，可防止在5个大气压的高压氧疗过程中出现高氧性充血和脑电图上的阵发性尖峰。这些结果表明，高压氧诱导脑血流量变化，通过神经元和脑血管中合成的一氧化氮调节其神经毒性作用。
