Antagonists at the L-type voltage sensitive calcium channel (L-VSCC) potent
iate anesthetic potency in experimental models, suggesting that it may be a
target site for IV anesthetics. Nimodipine is a 1,4-dihydropyridine antago
nist of L-VSCC which crosses the blood-brain barrier. We tested the hypothe
sis that premedication with oral nimodipine in healthy patients would reduc
e the induction dose of propofol, independently of its effects on the cereb
ral circulation. Sixty ASA physical status I or II patients (18-60 yr), und
ergoing knee arthroscopy or minor urological surgery, were randomized to re
ceive either nimodipine 60 mg or placebo, orally 1-2 h before induction. No
ninvasive mean blood pressure, heart rate, and time-averaged mean velocity
in the middle cerebral artery by using transcranial Doppler ultrasonography
were obtained before and 5 min after the induction of anesthesia. Propofol
1% was administered by an infusion pump at a rate of 10 mL/min. Both group
s of patients had a reduction in mean blood pressure after the induction (P
< 0.01), but there were no significant differences between the groups. The
induction dose of propofol was 2.19 mg/kg (95% confidence interval [CI]: 1
.97-2.42) in the nimodipine group, compared with 2.16 mg/kg (95% CI: 1.98-2
.34) in the control group, P = 0.8. Time-averaged mean velocity remained un
changed after the induction of anesthesia in both patients receiving nimodi
pine premedication (51% CI: 43-59 cm/s to 52% CI: 46-58 cm/s, P = 0.6) and
those receiving placebo (50% CI: 43-58 cm/s to 53% CI: 45-59 cm/s, P = 0.3)
. Premedication with oral nimodipine 60 mg does not reduce the induction do
se of propofol compared with placebo, casting doubt on the hypothesis that
propofol has an anesthetic action at L-VSCC. Implications: Premedication wi
th oral nimodipine 60 mg does not reduce the induction dose of propofol com
pared with placebo, casting doubt on the hypothesis that propofol has an an
esthetic action at L-type voltage sensitive calcium channels.