Effects of propofol on H-reflex in humans

Background: Depression of spinal cord motoneuron excitability has been prop osed to contribute to surgical immobility. The H-reflex, which measures alp ha -motoneuron excitability, is depressed by volatile anesthetics, whereas the action of propofol is unknown. The objective of this study was to deter mine the effects of propofol anesthesia on the H-reflex. Methods: In 13 patients (group 1), H-reflex was measured before (T-0), 3 mi n after (T-1), and 10 min after (T-2) a 2-mg/kg bolus dose of propofol, fol lowed by an infusion of 10 mg . kg(-1) . h(-1). Ten patients (group 2) were studied when propofol was given via a programmable pump set to a propofol blood concentration of 6 mug/ml, and 10 patients (group 3) were studied wit h the pump set to 9 mug/ml. Latencies and amplitudes of H-reflexes (H-0, H- 1, H-2) and M-responses (M-0, M-1, M-2) of the soleus muscle were recorded, and H/M ratios (H-0/M-0, H-1/M-1, H-2/M-2) were calculated. Results: In group 1, H-reflex amplitudes and the H/M ratio were diminished after induction with propofol (H-0 vs. H-1, P = 0.033; H-0/M-0 vs. H-1/M-1, P = 0.042). After 10 min of propofol infusion, the H-2/M-2 ratio was still decreased versus H-0/M-0 (P = 0.031). In group 2, no difference was detect ed. In group 3, propofol depressed H-reflex amplitudes at T-2 (H-0 vs. H-2, P < 0.01), and amplitudes were also lower at T-2 than at T-1 (H-1 vs. H-2, P < 0.01). In this group, the H/M ratio decreased from T-0 to T-2 (H-0/M-0 vs. H-2/M-2, P = 0.002). Conclusions: During steady state conditions using propofol as the sole agen t, a depression of the H-reflex is observed only at a high blood concentrat ion of 9 mug/ml. The authors suggest that immobility during propofol anesth esia is not caused by a depression of spinal motoneuron circuit excitabilit y.