The effect of (+)-tubocurarine chloride and of acute hypotension on electrocortical activity of the cat.

1. The effects of I.V. injection of tubocurarine (3 mg/kg) and of acute hypotension upon electrocortical activity of cats under sodium pentobarbitone were analysed. Technical artifacts associated with changes in brain volume were minimized.2. Initially, the superficial cortical response was reduced by tubocurarine either insignificantly or by 34% or less. Cats bled before injection of tubocurarine showed initially a similar reduction but, occasionally, a severe delayed reduction was found. Any fall in the superficial cortical response started during the secondary rise in B.P., many seconds after the B.P. had reached its lowest initial level. By contrast, spontaneous electrocortical activity was reduced approximately when the peak initial fall of B.P. occurred and it started to recover during the secondary rise in B.P. Reduction of the superficial cortical response could still be elicited after spindling had been suppressed by deep barbiturate anaesthesia. The initial thalamocortical afferent component in somatosensory area I, which was evoked by dorsal column stimulation, was less reduced by injection of tubocurarine than were the post-synaptic positive-negative components.3. The depressant effects of injected tubocurarine upon the superficial cortical response and spindle activity were approximated by rapid arterial bleeding.4. The superficial cortical response was reduced following virtual arrest of the cerebral circulation by acute exsanguination or by acute oil embolization. Such reduction most likely does not depend on systemic transport of inhibitory substances to the brain.5. After injection of tubocurarine the rate of outflow from the superior sagittal sinus was variably reduced during the initial fall in B.P., and often showed a variable, secondary increase. A net deficit in cerebral blood flow was usually present during the period of 80 sec after injection.6. The variability in the effects of injected tubocurarine upon electrocortical activity is attributed to the variability of the net deficit in cerebral blood flow.