[Electrophysiological studies of acute anoxic hypoxia]

This study was designed to analyse the effects of acute anoxic hypoxia on brainstem auditory evoked potentials (BAEPs) and electroencephalogram (EEG) and identify their sensitivities of response. After ether anesthesia, endotracheal intubation was performed on 20 adult Long-Evans rats. Relaxin was injected to immobilize the rats and a rodent respirator was provided for artificial ventilation. Acute anoxic hypoxia was induced by apnea with abrupt cessation of the respirator. The BAEPs and EEG were monitored and analyzed continuously before, during and after hypoxia. Experimental hypoxia was induced initially for 3 minutes and, after recovery, for another 5 minutes. Elapsed time was recorded as the waves altered or became flat. Characteristic wave changes were observed, which included delta bursts, epileptic discharges and alpha coma activity in the EEG; and decreased amplitude or delayed latency in the BAEPs. In all experiments, EEG flattening (71.80 +/- 7.80 sec) significantly preceded the flattening of the BAEPs (146.90 +/- 7.00 sec; Wilcoxon signed rank test, p less than 0.01). However, recovery after reoxygenation was more rapid in the BAEPs than in the EEG (162.80 +/- 18.90, 208.20 +/- 17.90 sec, Wilcoxon signed rank test, p less than 0.05). BAEP loss began with the later waves. In the EEG, during the recovery period epileptogenic foci (45%), delta bursting (45%) or alpha coma activity (40%) appeared. The isoelectric EEG and BAEPs were reversible in 12 of the 18 rats after 3-minutes of apnea and immediately followed by reoxygenation. The results of this study indicate the functional vulnerability of the various structures of the nervous system in regard to hypoxia.