title: Changes of somatosensory evoked potential accompanying ischaemia and hypoxia in cats.
abstract: Changes of evoked potential accompanying haemorrhagic hypotension and hypoxia were investigated on cats to evaluate the usefulness of SEP as a monitor in an intensive care unit (ICU), and the following results were obtained. Positive-negative diphasic potential was elicited at posterior sigmoid gyrus(PSG) by contralateral superficial radial nerve stimulation. This potential was recorded at the restricted area of the posterior border of PSG and regarded as primary somatosensory evoked potential. In the initial stage of haemorrhagic hypotension, both positive and negative components of SEP occasionally increased in amplitude. In profound hypotension in which CBF fell to less than the critical level of 30 ml 100 g-1 min-1, the latency was retarded and the amplitude was decreased. At CBE less than 10 ml 100 g-1 min-1, SEP disappeared. Within the range of CBF between 10 and 30 ml 100 g-1 min, a close correlation was noted between CBF and SEP amplitude. Transient increase of SEP amplitude was also observed during hypoxia induced by inhalation of nitrogen gas. (3) In normal state SEP was decreased in amplitude by conditioning stimulation of the nucleus lateralis posterior (LP nucleus) of the thalamus. This might be explained by the fact that intracortical inhibitory interneurons were activated by stimulation of LP nucleus. After haemorrhagic hypotension and hypoxia, however, the inhibitory effect on SEP elicited by LP nucleus stimulation attenuated or disappeared. Because of the initial impairment of the inhibitory interneurons by ischaemia and hypoxia, the amplitude of SEP might increase transiently. In conclusion, the authors thought that SEP might be less useful than EEG in ICU, because of its insensible change to hypoxia and ischaemia.
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D002415:Cats; D004569:Electroencephalography; D005073:Evoked Potentials, Somatosensory; D002534:Hypoxia, Brain / Q000503:physiopathology*; D013787:Thalamic Nuclei / Q000502:physiology