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In vivo microdialysis—A technique for analysis of chemical activators of muscle pain
Author(s) -
McArdle Anne,
Khera Goldie,
Edwards Richard H.T.,
Jackson Malcolm J.
Publication year - 1999
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199908)22:8<1047::aid-mus6>3.0.co;2-q
Subject(s) - microdialysis , hypoxanthine , skeletal muscle , ischemia , in vivo , anesthesia , chemistry , medicine , pharmacology , biochemistry , central nervous system , biology , enzyme , microbiology and biotechnology
The accurate measurement of the chemical activators of pain in skeletal muscle has proved to be a major challenge. This study examined the applicability of microdialysis to the measurement of pain‐producing substances in skeletal muscle using a defined model of ischemia and reperfusion in the rat. Microdialysis probes were placed into muscle of anesthetized rats. Ischemia was induced for 4 h, followed by reperfusion for 1 h. Perfusates were analyzed for hypoxanthine, potassium, prostaglandin (PG) E 2 and histamine. A 20‐fold increase in perfusate hypoxanthine concentration was seen prior to reperfusion (70.1 ± 27.1 μM for ischemic versus 3.7 ± 1.9 μM for control; P < 0.05). An initial increase in PGE 2 concentration was seen during ischemia (7.4 ± 2.0 nM versus 3.4 ± 1.4 nM; P < 0.05) and immediately post‐reperfusion (17.9 ± 5.2 nM versus 4.0 ± 1.1 nM; P < 0.05). Potassium concentration was significantly increased following occlusion and reperfusion. This indicates the applicability of microdialysis to the measurement of pain‐producing substances in muscle during ischemia and reperfusion. Further use will provide novel information on muscle pain both in defined model systems and in clinical situations in humans. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 1047–1052, 1999