Nimodipine premedication and induction dose of propofol.

Anesth Analg

University Department of Anaesthesia, Leicester University and Leicester General Hospital, England.

Published: February 2000

AI Article Synopsis

  • Antagonists at L-type voltage-sensitive calcium channels (L-VSCC) may enhance the effects of anesthesia, leading researchers to explore if nimodipine, an L-VSCC antagonist, could reduce the amount of propofol needed for induction.
  • A study involving 60 healthy patients compared the effects of premedicating with nimodipine versus a placebo before propofol induction for minor surgeries.
  • Results showed no significant difference in induction doses of propofol between the nimodipine and placebo groups, suggesting that nimodipine does not effectively lower the required dose and raising questions about the anesthetic mechanism of propofol at L-VSCC.

Article Abstract

Unlabelled: Antagonists at the L-type voltage sensitive calcium channel (L-VSCC) potentiate anesthetic potency in experimental models, suggesting that it may be a target site for IV anesthetics. Nimodipine is a 1, 4-dihydro- pyridine antagonist of L-VSCC which crosses the blood-brain barrier. We tested the hypothesis that premedication with oral nimodipine in healthy patients would reduce the induction dose of propofol, independently of its effects on the cerebral circulation. Sixty ASA physical status I or II patients (18-60 yr), undergoing knee arthroscopy or minor urological surgery, were randomized to receive either nimodipine 60 mg or placebo, orally 1-2 h before induction. Noninvasive 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 groups 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 unchanged after the induction of anesthesia in both patients receiving nimodipine 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 dose of propofol compared with placebo, casting doubt on the hypothesis that propofol has an anesthetic action at L-VSCC.

Implications: Premedication with oral nimodipine 60 mg does not reduce the induction dose of propofol compared with placebo, casting doubt on the hypothesis that propofol has an anesthetic action at L-type voltage sensitive calcium channels.

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Source
http://dx.doi.org/10.1097/00000539-200002000-00038DOI Listing

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