The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Effects of propofol on H-reflex in humans.

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.[1]

References

  1. Effects of propofol on H-reflex in humans. Kerz, T., Hennes, H.J., Fève, A., Decq, P., Filipetti, P., Duvaldestin, P. Anesthesiology (2001) [Pubmed]
 
WikiGenes - Universities