Intradermal administration of magnesium sulphate and magnesium chloride produces hypesthesia to mechanical but hyperalgesia to heat stimuli in humans.
BACKGROUND
Although magnesium ions (Mg2+) are known to display many similar features to other 2+ charged cations, they seem to have quite an important and unique role in biological settings, such as NMDA blocking effect. However, the role of Mg2+ in the neural transmission system has not been studied as sufficiently as calcium ions (Ca2+). To clarify the sensory effects of Mg2+ in peripheral nervous systems, sensory changes after intradermal injection of Mg2+ were studied in humans.


METHODS
Magnesium sulphate, magnesium chloride and saline were injected into the skin of the anterior region of forearms in healthy volunteers and injection-induced irritating pain ("irritating pain", for short), tactile sensation, tactile pressure thresholds, pinch-pain changes and intolerable heat pain thresholds of the lesion were monitored.


RESULTS
Flare formation was observed immediately after magnesium sulphate or magnesium chloride injection. We found that intradermal injections of magnesium sulphate and magnesium chloride transiently caused irritating pain, hypesthesia to noxious and innocuous mechanical stimulations, whereas secondary hyperalgesia due to mechanical stimuli was not observed. In contrast to mechanical stimuli, intolerable heat pain-evoking temperature was significantly decreased at the injection site. In addition to these results, spontaneous pain was immediately attenuated by local cooling.


CONCLUSIONS
Membrane-stabilizing effect and peripheral NMDA-blocking effect possibly produced magnesium-induced mechanical hypesthesia, and extracellular cation-induced sensitization of TRPV1 channels was thought to be the primary mechanism of magnesium-induced heat hyperalgesia.
Ushida
Takahiro
T
Multidisciplinary Pain Center, Aichi Medical University, 21 Karimata, Yazako, Nagakute, Aichi 480-1195, Japan. ushidat-koc@umin.ac.jp
Iwatsu
Osamu
O
Shimo
Kazuhiro
K
Tetsunaga
Tomoko
T
Ikeuchi
Masahiko
M
Ikemoto
Tatsunori
T
Arai
Young-Chang P
YC
Suetomi
Katsutoshi
K
Nishihara
Makoto
M
D000328:Adult; D000700:Analgesics / Q000009:adverse effects; D002121:Calcium Channel Blockers / Q000009:adverse effects; D004311:Double-Blind Method; D006358:Hot Temperature / Q000009:adverse effects; D006801:Humans; D006930:Hyperalgesia / Q000139:chemically induced* / Q000503:physiopathology; D006987:Hypesthesia / Q000139:chemically induced* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000009:adverse effects; D007271:Injections, Intradermal; D015636:Magnesium Chloride / Q000009:adverse effects*; D008278:Magnesium Sulfate / Q000009:adverse effects*; D009420:Nervous System / Q000187:drug effects / Q000378:metabolism; D009619:Nociceptors / Q000187:drug effects / Q000378:metabolism; D010147:Pain Measurement / Q000187:drug effects; D017288:Pain Threshold / Q000187:drug effects* / Q000502:physiology; D010812:Physical Stimulation; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000378:metabolism; D011984:Sensory Receptor Cells / Q000187:drug effects / Q000378:metabolism; D012684:Sensory Thresholds / Q000187:drug effects / Q000502:physiology; D050916:TRPV Cation Channels / Q000187:drug effects / Q000378:metabolism; D055815:Young Adult
D000700:Analgesics; D002121:Calcium Channel Blockers; D018836:Inflammation Mediators; D016194:Receptors, N-Methyl-D-Aspartate; D050916:TRPV Cation Channels; C494482:TRPV1 protein, human; D015636:Magnesium Chloride; D008278:Magnesium Sulfate