|Title||Intrathecal veratridine administration increases minimum alveolar concentration in rats.|
|Publication Type||Journal Article|
|Year of Publication||2008|
|Authors||Zhang Y, Sharma M, Eger EI, Laster MJ, Hemmings HC, R Harris A|
|Date Published||2008 Sep|
|Keywords||Anesthesia, Anesthetics, Animals, Dose-Response Relationship, Drug, Immobilization, Inhibitory Concentration 50, Injections, Spinal, Isoflurane, Male, Pulmonary Alveoli, Rats, Rats, Long-Evans, Sodium Channels, Subarachnoid Space, Veratridine|
BACKGROUND: Results from several studies point to sodium channels as potential mediators of the immobility produced by inhaled anesthetics. We hypothesized that the intrathecal administration of veratridine, a drug that enhances the activity or effect of sodium channels, should increase MAC.
METHODS: We measured the change in isoflurane MAC caused by intrathecal infusion of various concentrations of veratridine into the lumbothoracic subarachnoid space of rats. We compared these result with those obtained from intracerebroventricular infusion.
RESULTS: As predicted, intrathecal infusion of veratridine increased MAC. The greatest infused concentration (25 microM) also produced neuronal injury in the hindlimbs of two rats and decreased the peak effect on MAC. A concentration of 1.6 microM produced the largest (21%) increase in MAC. Intraventricular infusion of 1.6 and 6.4 microM veratridine did not alter MAC. Rats given 25 microM died.
CONCLUSIONS: Intrathecal administration of veratradine increases MAC of isoflurane, a finding consistent with a role for sodium channels as potential mediators of the immobility produced by inhaled anesthetics.
|Alternate Journal||Anesth Analg|
|PubMed Central ID||PMC2587212|
|Grant List||P01 GM047818 / GM / NIGMS NIH HHS / United States |
P01 GM047818-14 / GM / NIGMS NIH HHS / United States
R01 GM058055 / GM / NIGMS NIH HHS / United States
1P01GM47818 / GM / NIGMS NIH HHS / United States