Lidocaine, MK-801, and MAC
Lidocaine, MK-801, and MAC
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DOI:
10.1213/01.ane.0000260318.60504.a9
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发表时间:
2007-05-01
影响因子:
5.7
通讯作者:
Sonner, James M.
中科院分区:
文献类型:
--
作者:
Zhang, Yi;Laster, Michael J.;Sonner, James M.
BACKGROUND: Previous studies have found that the local anesthetic/sodium channel blocker lidocaine decreased MAC by maximum amounts approximately equal to the decreases produced by dizocilpine (MK-801), a N-methyl-D-aspartate (NNMA) receptor antagonist. Blockade of sodium channels by inhaled anesthetics has been suggested as a possible cause for impairment of transmission through NMDA receptors. We postulated that the net effect of lidocaine and MK-801 on MAC would be the same, albeit by affecting NMDA neurotransmission at different points.,METHODS: We measured the effect of various lidocaine infusions on the MAC of cyclopropane, halothane, isoflurane, and o-difluorobenzene in rats. We also measured the effect of concurrent lidocaine-MK-801 infusion on the MAC of isoflurane and o-difluorobenzene.RESULTS: Our data contradicted our predictions. (a) We found no limit to the effect of lidocaine infusion, in some cases finding that lidocaine, alone, produced immobility; (b) lidocaine infusion did not decrease the MAC of o-difluorobenzene differently from the MAC of other inhaled anesthetics; and (c) the addition of MK-801 equally affected the decrease in MAC produced by lidocaine infusion for isoflurane versus o-difluorobenzene.CONCLUSION: Lidocaine does not primarily decrease MAC by decreasing the release of glutamate from nerve terminals.