title: High-intensity swimming exercise reduces neuropathic pain in an animal model of complex regional pain syndrome type I: evidence for a role of the adenosinergic system.
abstract: This study investigated the involvement of the adenosinergic system in antiallodynia induced by exercise in an animal model of complex regional pain syndrome type I (CRPS-I). Furthermore, we analyzed the role of the opioid receptors on exercise-induced analgesia. Ischemia/reperfusion (IR) mice, nonexercised and exercised, received intraperitoneal injections of caffeine (10mg/kg, a non selective adenosine receptor antagonist), 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (0.1mg/kg, a selective adenosine A receptor antagonist), ZM241385 (3mg/kg, a selective adenosine A receptor antagonist), adenosine deaminase inhibitor erythro-9-(2-hydroxy-3nonyl) adenine [(EHNA), 5mg/kg, an adenosine deaminase inhibitor] or naloxone (1mg/kg, a nonselective opioid receptor antagonist). The results showed that high-intensity swimming exercise reduced mechanical allodynia in an animal model of CRPS-I in mice. The antiallodynic effect caused by exercise was reversed by pretreatment with caffeine, naloxone, DPCPX but it was not modified by ZM241385 treatment. In addition, treatment with EHNA, which suppresses the breakdown of adenosine to inosine, enhanced the pain-relieving effects of the high-intensity swimming exercise. This is the first report demonstrating that repeated sessions of high-intensity swimming exercise attenuate mechanical allodynia in an animal model of CRPS-I and that the mechanism involves endogenous adenosine and adenosine A receptors. This study supports the use of high-intensity exercise as an adjunct therapy for CRPS-I treatment.
authors.affiliation: Laboratório de Neurobiologia da Dor e Inflamação, Departamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Campus Universitário - Trindade, Florianópolis, SC, Brazil.
authors.forename: D F
authors.initials: DF
authors.lastname: Martins
authors.forename: L
authors.initials: L
authors.lastname: Mazzardo-Martins
authors.forename: F
authors.initials: F
authors.lastname: Soldi
authors.forename: J
authors.initials: J
authors.lastname: Stramosk
authors.forename: A P
authors.initials: AP
authors.lastname: Piovezan
authors.forename: A R S
authors.initials: AR
authors.lastname: Santos
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives; D000241:Adenosine / Q000502:physiology*; D058916:Adenosine A1 Receptor Antagonists / Q000494:pharmacology; D058917:Adenosine A2 Receptor Antagonists / Q000494:pharmacology; D058892:Adenosine Deaminase Inhibitors / Q000494:pharmacology; D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D005081:Exercise Therapy; D006930:Hyperalgesia / Q000150:complications / Q000503:physiopathology / Q000628:therapy; D008297:Male; D051379:Mice; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009437:Neuralgia / Q000150:complications / Q000628:therapy*; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D012019:Reflex Sympathetic Dystrophy / Q000150:complications / Q000628:therapy*; D013550:Swimming; D014227:Triazines / Q000494:pharmacology; D014230:Triazoles / Q000494:pharmacology; D014970:Xanthines / Q000494:pharmacology
chemical_list: D058916:Adenosine A1 Receptor Antagonists; D058917:Adenosine A2 Receptor Antagonists; D058892:Adenosine Deaminase Inhibitors; D009292:Narcotic Antagonists; D014227:Triazines; D014230:Triazoles; D014970:Xanthines; C097270:ZM 241385; D009270:Naloxone; D002110:Caffeine; C010192:9-(2-hydroxy-3-nonyl)adenine; C051360:1,3-dipropyl-8-cyclopentylxanthine; D000225:Adenine; D000241:Adenosine