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Effects of Propofol on H-reflex in Humans

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Background Depression of spinal cord motoneuron excitability has been proposed to contribute to surgical immobility. The H-reflex, which measures alpha-motoneuron excitability, is depressed by volatile anesthetics, whereas the action of propofol is unknown. The objective of this study was to determine the effects of propofol anesthesia on the H-reflex. Methods In 13 patients (group 1), H-reflex was measured before (T0), 3 min after (T1), and 10 min after (T2) a 2-mg/kg bolus dose of propofol, followed by an infusion of 10 mg x kg(-1) x h(-1). Ten patients (group 2) were studied when propofol was given via a programmable pump set to a propofol blood concentration of 6 microg/ml, and 10 patients (group 3) were studied with the pump set to 9 microg/ml. Latencies and amplitudes of H-reflexes (H0, H1, H2) and M-responses (M0, M1, M2) of the soleus muscle were recorded, and H/M ratios (H0/M0, H1/M1, H2/M2) were calculated. Results In group 1, H-reflex amplitudes and the H/M ratio were diminished after induction with propofol (H0 vs. H1, P = 0.033; H0/M0 vs. H1/M1, P = 0.042). After 10 min of propofol infusion, the H2/M2 ratio was still decreased versus H0/M0 (P = 0.031). In group 2, no difference was detected. In group 3, propofol depressed H-reflex amplitudes at T2 (H0 vs. H2, P < 0.01), and amplitudes were also lower at T2 than at T1 (H1 vs. H2, P < 0.01). In this group, the H/M ratio decreased from T0 to T2 (H0/M0 vs. H2/M2, P < 0.002). Conclusions During steady state conditions using propofol as the sole agent, a depression of the H-reflex is observed only at a high blood concentration of 9 microg/ml. The authors suggest that immobility during propofol anesthesia is not caused by a depression of spinal motoneuron circuit excitability.
Title: Effects of Propofol on H-reflex in Humans
Description:
Background Depression of spinal cord motoneuron excitability has been proposed to contribute to surgical immobility.
The H-reflex, which measures alpha-motoneuron excitability, is depressed by volatile anesthetics, whereas the action of propofol is unknown.
The objective of this study was to determine the effects of propofol anesthesia on the H-reflex.
Methods In 13 patients (group 1), H-reflex was measured before (T0), 3 min after (T1), and 10 min after (T2) a 2-mg/kg bolus dose of propofol, followed by an infusion of 10 mg x kg(-1) x h(-1).
Ten patients (group 2) were studied when propofol was given via a programmable pump set to a propofol blood concentration of 6 microg/ml, and 10 patients (group 3) were studied with the pump set to 9 microg/ml.
Latencies and amplitudes of H-reflexes (H0, H1, H2) and M-responses (M0, M1, M2) of the soleus muscle were recorded, and H/M ratios (H0/M0, H1/M1, H2/M2) were calculated.
Results In group 1, H-reflex amplitudes and the H/M ratio were diminished after induction with propofol (H0 vs.
H1, P = 0.
033; H0/M0 vs.
H1/M1, P = 0.
042).
After 10 min of propofol infusion, the H2/M2 ratio was still decreased versus H0/M0 (P = 0.
031).
In group 2, no difference was detected.
In group 3, propofol depressed H-reflex amplitudes at T2 (H0 vs.
H2, P < 0.
01), and amplitudes were also lower at T2 than at T1 (H1 vs.
H2, P < 0.
01).
In this group, the H/M ratio decreased from T0 to T2 (H0/M0 vs.
H2/M2, P < 0.
002).
Conclusions During steady state conditions using propofol as the sole agent, a depression of the H-reflex is observed only at a high blood concentration of 9 microg/ml.
The authors suggest that immobility during propofol anesthesia is not caused by a depression of spinal motoneuron circuit excitability.

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