Magnesium is the second most abundant intracellular cation and plays an integral role in several biological processes. It influences membrane potentials via modulatory effects on sodium and potassium currents and serves as a cofactor for protein synthesis, nucleic acid stabilization, and neuromuscular function.1 Magnesium also acts as a calcium-channel antagonist and has inhibitory effects on the CNS, including antagonism of the TV-methyl-D-aspartate glutamate receptor and suppression of catecholamine release from the adrenal medulla and adrenergic nerve endings.1,2
The administration of MgSO4 has been associated with volatile and injectable anesthetic–sparing effects, augmentation of neuromuscular blockade, and attenuation of postoperative pain in human patients.3–5 A volatile anesthetic–sparing effect of MgSO4 has been found for human patients anesthetized with desflurane.6,7 Injectable anesthetic– and analgesic-sparing effects of MgSO4 have been reported for several agents, including propofol, fentanyl, remifentanil, and midazolam.8–10 Postoperative administration of MgSO4 decreases opioid consumption and pain scores in a variety of human surgical patients.11–13 In particular, the propofol-sparing effect of Mg has been reported for several studies14–16 of humans in which an infusion of Mg was used to decrease dose requirements of propofol during surgery and at the time of anesthetic induction. In dogs undergoing ovariohysterectomy, dose requirements of halothane and thiopental were decreased following anesthetic premedication and intraoperative infusion of MgSO4.17 The anesthetic- and analgesic-sparing properties of Mg have been attributed primarily to its antagonism of the N-methyl-D-aspar tate receptor2; thus, Mg may potentiate the effect of other agents (including volatile anesthetics, propofol, and ketamine) that act on the same receptor.18–20
On the basis of the proposed anesthetic-sparing mechanism of Mg and the reports of its volatile anesthetic– and propofol-sparing effects in humans, the objective of the study reported here was to evaluate the effects of IV administration of MgSO4, alone and in combination with propofol, on the MACNM in sevoflurane-anesthetized dogs. The MACNM was used as an endpoint that corresponds to the lack of any motor movement in response to a noxious stimulation.21–23 The hypothesis was that MgSO4 would decrease the MACNM of sevoflurane and potentiate the MAC-sparing effect of propofol.
Supported by the Companion Animal Fund of the University of Tennessee.
Presented in abstract form at the annual American College of Veterinary Anesthesia and Analgesia meeting during the 20th International Veterinary Emergency and Critical Care symposium, Indianapolis, September 2014.
Constant rate infusion
Minimum alveolar concentration
Minimum alveolar concentration preventing motor movement
Minimum alveolar concentration preventing motor movement measured at baseline
Minimum alveolar concentration preventing motor movement measured after treatment
End-tidal partial pressure of carbon dioxide
End-tidal partial pressure of sevoflurane
SAS, version 9.4, SAS Institute Inc, Cary, NC.
Sevoflo, Abbott Laboratories, North Chicago, Ill.
DRE Premier XP, DRE Veterinary, Louisville, Ky.
Datex-Ohmeda S/5, Planar Systems, Beaverton, Ore.
Air Liquide Healthcare, Scott Medical Products, Plumsteadville, Pa.
ProtectIV Johnson & Johnson, North Brunswick, NJ.
Hospira Inc, Lake Forest, Ill.
PropoFlo, Abbott Laboratories, North Chicago, Ill.
K-Mod 107, Allegiance Healthcare Corp, Waukegan, Ill.
Bair Hugger, Arizant, Healthcare Inc, Saint Paul, Minn.
TOF Watch SX, Organon Ltd, Dublin, Ireland.
Grass Instrument Co, Warwick, RI.
Medfusion 2010i, Medox Inc, Wilmington, NC.
COBAS c501, Roche Diagnostics, Indianapolis, Ind.
2695 separations module, Waters Corp, Milford, Mass.
2475 fluorescence detector, Waters Corp, Milford, Mass.
Empower Software, Waters Corp, Milford, Mass.
Parafilm, Sigma-Aldrich Corp, St Louis, Mo.
Waters XBridge C18, Waters Corp, Milford, Mass.
PROC MIXED, SAS, version 9.4, SAS Institute Inc, Cary, NC.
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