The effects of intravenous succinylcholine on cerebral function and muscle afferent activity following complete ischemia in halothane-anesthetized dogs.

The effects of iv succinylcholine (SCh) on cerebral blood flow (CBF), the electroencephalogram (EEG), muscle afferent activity (MAA), electromyographic activity (EMG), and PaCO2 were tested in six halothane-anesthetized dogs (1.0 MAC) more than 1 h after a 10-min period of complete cerebral ischemia. All dogs received treatments of both iv SCh (1.0 mg.kg-1) and saline placebo in a random sequence. Fasciculations and substantial increases in EMG activity were observed in all dogs following SCh administration. At the onset of fasciculations, there was an increase in MAA to a peak value of 353 +/- 74% of control (mean +/- SE; n = 5 for MAA; n = 6 for all other variables) at the 1-min measurement point. Thereafter, MAA gradually declined toward control values. There were delayed increases in PaCO2 throughout the 45-min study period, achieving values of 106 +/- 1% to 118 +/- 4% of control (an increase in PaCO2 of 2-7 mmHg). Despite the increases in MAA and PaCO2, there were no significant increases in CBF during the study. The control EEG 1-h after complete cerebral ischemia, but immediately before administering the drug treatments, consisted predominantly of a delta rhythm, denoting cerebral dysfunction. In one dog, SCh administration produced transient attenuation of the delta rhythm, a change consistent with cerebral stimulation. In the remaining five dogs, SCh had no effect on the EEG. Treatment with saline placebo did not affect any variable measured. The authors conclude that, in the electrically dysfunctioning brain (e.g., as occurs following resuscitation from complete cerebral ischemia), the cerebral (i.e., CBF and EEG) response to iv SCh is attenuated when compared to the previously reported response in normal brain.