Effect of hypoxia and hyperoxia on cortical oxidative metabolism in relation to cerebral blood flow autoregulation

Our earlier studies have shown that local cortical blood flow (CoBF) in the rabbit has been autoregulated in a narrow range of mean arterial blood pressure (MABP) and autoregulation of cortical oxygen tension (bPO2) has been maintained in a wider range (75-110 mmHg) than that of CoBF. In the present studies, bPO2, NAD/NADH redox state, and CoBF were measured under the various conditions of hypoxia and hyperoxia to discuss the critical level of cortical oxidative metabolism and autoregulation of CoBF in relation to oxidative metabolism. New Zealand white rabbits were anesthetized with pentobarbital sodium intraperitoneally and paralyzed with gallamine triethiodide intravenously. They were ventilated artificially maintaining normal blood gas analysis. NAD/NADH redox state was measured with a compensated fluorometer with a reflectance device to correct for hemodynamic artefacts and bPO2 was monitored continuously with the polarographical method. They were measured simultaneously. CoBF was monitored with the thermal diffusion cerebral blood flow monitor of Flowtronics. Hypoxia and hyperoxia were produced by decreasing or increasing the inspired oxygen concentration. Arterial blood samples were obtained for blood gas determination before and during the episode of hypoxia or hyperoxia. A definite reduction of NADH began at a 50% decrease of PaO2. It corresponded to 70 mmHg of PaO2. Below 50% decrease of PaO2, NADH was reduced largely. This was statistically significant (p less than 0.01). Although, the oxidation of NADH occurred in the moderate hyperoxic state, no oxidation of NADH occurred more than 6.1% of full scale even in the condition of higher PaO2.(ABSTRACT TRUNCATED AT 250 WORDS)