Intrathecal midazolam reduces isoflurane MAC and increases the apnoeic threshold in rats

Abstract

The purpose of this study was to examine the anaesthetic requirement of intrathecal midazolam in a dose-response fashion in isoflurane-anaesthetized, tracheostomized rats, and to evaluate the apnoeic threshold after each intrathecal midazolam dose. Intrathecal midazolam,5,10,20, and 30 I~g, was administered

Addition of midazolam to continuous postoperative epidural bupivacaine infusion reduces requirement for rescue analgesia in children undergoing upper abdominal and flank surgery

“…Neurotoxicity studies of central midazolam in animals have yielded conflicting results. Six studies have found neurotoxicity associated with neuraxial midazolam [18][19][20][21][22][23] whereas 7 others have reported no adverse effect associated with its use [24][25][26][27][28][29][30]. The studies documenting neurotoxicity have a number of limitations that have raised several questions regarding the validity of the results obtained.…”

Brachial plexus block with midazolam and bupivacaine improves analgesia

“…19 Studies in animals have revealed no neurotoxic effects of intrathecally administered midazolam. [20][21][22] More recently, Tucker and associates demonstrated that the administration of intrathecal midazolam causes potentiation of the analgesic effect of intrathecal fentanyl in labouring patients. 23 The administration of intrathecal midazolam, 2 mg, did not increase the occurrence of neurologic or urologic symptoms.…”

MAC reduction after intrathecal coadministration of GABA A agonist and glutamate antagonist in rats

“…The GABA A receptor has been considered a main target site of volatile anesthetics [5,6], and it has been reported that intrathecal administration of midazolam, which enhances GABA activity by activation of a GABA-benzodiazepine ionophore complex, reduce the MAC for isoflurane in rats [9]. However, to our knowledge, there are no reports of reduction in MAC by intrathecal administration of a specific GABA A agonist.…”

“…GABA and glutamate are major neurotransmitters in spinal cord inhibitory and excitatory circuits, and it has been reported that volatile anesthetics can act on both receptors [5][6][7][8]. Furthermore, it has been shown that intrathecal administration of a GABA A receptor agonist or a glutamate receptor antagonist reduces the minimum alveolar anesthetic concentration (MAC; the anesthetic concentration that prevents movement in response to supramaximal stimulation in 50% of animals) of volatile anesthetics [9][10][11]. Therefore it is hypothesized that one or both of these receptors may be involved in the mechanism by which volatile anesthetics produce immobility.…”