Abstract:
Hypoxaemia consequent to inspired carbon monoxide (CO), and to other causes, often does not injure the brain cortex. At least five types of brain and heart protective cardiovascular response to hypoxaemia have been reported. The underlying mechanism is unknown. The present study was designed to test the hypothesis that the reaction to inspired CO involves the amygdala as this structure is thought to be central to stress responsivity; involvement would support the additional hypothesis that the somatic response to CO-hypoxaemia is regulated. Eighteen ewes were randomly allocated to control and two CO groups. The CO groups were exposed to 1% CO for 120 min and killed either 5 or 15 days later. This exposure caused isolated white matter brain injury and a transient increase in protein-kinase C (gamma) activity in the pyramidal neurons in the nuclei of the central and basal–lateral amygdala and in the neurons of the audio-cortex (p < 0.05). This was associated with evidence of a sympathetic response. It would seem reasonable to hypothesise both that the amygdala is important in the processes by which the hypoxaemic effects of CO on the brain are prevented, delayed and/or mitigated and that these processes are regulated.
