Roles of cerebral perfusion pressure and neurotransmitters in changes of evoked potentials induced by hypoxia

Abstract

AIM: We studied the effects of hypoxia on excitability of the brain with evoked potentials and membrane transmitter release. METHODS: Dogs were anesthetized with pentobarbital sodium and artificially ventilated. (1) In a hypoxia group, somatosensory evoked potential (SEP) and auditory brain-stem response (ABR) were measured to study the brain behavior in response to sensory input during hypoxia. Electric stimulation for SEP and acoustic stimulation for ABR were generated in a fixed sequence, i.e., once for SEP and 4 times for ABR, and one ensemble of SEP data and 4 ensembles of ABR data were stored for 500 msec. We averaged 20 ensembles of SEP data and 80 ensembles of ABR data every 10 seconds. After room air ventilation (control period), dogs were exposed to a 5%O2-95%N 2 gaseous mixture for 5 min (hypoxic period) and returned to room air (recovery period). ABR and SEP (EPs) were monitored throughout the periods. (2) In a barostat group, systemic arterial pressure was clamped at 120 mmHg to artificially stabilize cerebral peffusion pressure (CPP), because the hydrodynamics influence edema spreading and tissue impedance. Other procedures were the same as used in the hypoxia group. (3) In an/n vivo voltammetry (IW) group, neurotransmitter metabolitcs were measured throughout the control, hypoxic and recovery periods. RESULTS: In the hypoxia group, amplitude of EPs showed transient increase in response to hypoxia, accompanied by an increase in CPP. This phenomenon preceded a decrease in amplitude. In the barostat group, the amplitude also increased during the hypoxic period, though CPP was maintained at the same level as the control period. This finding suggests that the volume conductor properties are not involved in the transient increase in amplitude of EPs in response to hypoxia. In the IVV group, 5-HIAA transiently increased in response to hypoxia, in the same fashion with the change of EPs. DISCUSSION: The transient increase of neurotransmitter metabolite might be a reflection of enhanced transmitter release associated with a transient increase in membrane excitability. In conclusion, hypoxia transiently enhances membrane excitability, and results in transient increases of amplitude of EPs and neurotransmitter metabolite.