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Second Department of Anesthesiology Toho University School of Medicine, Tokyo, Japan
To the Editor:
Buvanendran et al. demonstrated that intrathecal magnesium plus fentanyl prolongs spinal analgesia without adverse effects (1). I believe that their result could contribute to pain relief in clinical practice. However, I wish to add the following few points for their consideration.
Magnesium is called "nature’s physiological calcium channel blocker" (2). Calcium channel blocker has antinociceptive effects in rat (3) and morphine potentiation in chronic pain patients (4). Magnesium also possesses a property of N-methyl-D-aspartate (NMDA) receptor antagonist. However, it seems to me that the authors mainly consider the latter in the discussion with regard to the prolongation of spinal analgesia. In this article, the authors postulate that magnesium could potentiate opioid spinal analgesia, and they have reported that intrathecal magnesium potentiates morphine antinociception in rats (5). It is true that NMDA receptor antagonist plays an important role in prevention of central sensitization and pain, but the authors should consider the prolongation of spinal analgesia with magnesium plus fentanyl from these two mechanisms. I think that the prolongation of spinal analgesia could be explained mainly by these two properties.
Why did the authors choose pregnant women as an object of this study? It has been reported that endogenous opioid analgesic system activates during labor and the early postpartum period (6). If the patients were nonpregnant women or men, could such a significant result obtained? The possibility that pregnancy could affect pain threshold and efficacy of fentanyl spinal analgesia cannot be ruled out. Further study is needed in nonpregnant women or men, and it is necessary to determine the optimal dose of magnesium in various cases. Nevertheless, the authors’ result indicates that magnesium may be a useful adjuvant during perioperative pain management.
References
Department of Anesthesiology, Rush Medical College, Chicago, IL
In Response:
It has been well known for almost 50 years that the magnesium ion is a calcium antagonist at neuromuscular junctions (1), and also at synapses in the vertebrate central nervous system (2). However, in 1980, Ault et al (3) demonstrated that the magnesium ion was an antagonist to NMDA receptors. The important difference is that in the classical studies, the magnesium concentration to produce calcium antagonism is very high, 20 mM or greater. On the other hand, NMDA responses in the vertebrate spinal cord can be blocked at concentrations starting at 10 µM (3). Therefore, although we could not measure the concentration of magnesium ion in the CSF of the patients in the present study, as we did in our animal study (4), it can be assumed that the NMDA antagonist effect, which occurs at low magnesium ion concentrations, is a more plausible mechanism for our results than the calcium antagonist effect, which only becomes significant at high magnesium ion concentrations.
The fact that pregnant women were used in this study does not make the magnesium potentiation of fentanyl analgesia a unique case, anymore than any other group of patients that could have been studied (e.g., total knee arthroplasty in arthritic patients). As Dr. Arakawa suggests, a dose-finding study for analgesia for general surgical patients must still be determined.
References
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