Acute and chronic nociceptive phases observed in a rat hind paw ischemia/reperfusion model depend on different mechanisms.
Complex regional pain syndrome type 1 (CRPS1) may be evoked by ischemia/reperfusion, eliciting acute and chronic pain that is difficult to treat. Despite this, the underlying mechanism of CRPS1 has not been fully elucidated. Therefore, the goal of this study is to evaluate the involvement of inflammation, oxidative stress, and the transient receptor potential ankyrin 1 (TRPA1) channel, a chemosensor of inflammation and oxidative substances, in an animal model of chronic post-ischemia pain (CPIP). Male Wistar rats were subjected to 3 h hind paw ischemia/reperfusion (CPIP model). Different parameters of nociception, inflammation, ischemia, and oxidative stress were evaluated at 1 (acute) and 14 (chronic) days after CPIP. The effect of a TRPA1 antagonist and the TRPA1 immunoreactivity were also observed after CPIP. In the CPIP acute phase, we observed mechanical and cold allodynia; increased levels of tumor necrosis factor-α (hind paw), ischemia-modified albumin (IMA) (serum), protein carbonyl (hind paw and spinal cord), lactate (serum), and 4-hydroxy-2-nonenal (4-HNE, hind paw and spinal cord); and higher myeloperoxidase (MPO) and N-acetyl-β-D-glucosaminidase (NAGase) activities (hind paw). In the CPIP chronic phase, we detected mechanical and cold allodynia and increased levels of IMA (serum), protein carbonyl (hind paw and spinal cord), and 4-HNE (hind paw and spinal cord). TRPA1 antagonism reduced mechanical and cold allodynia 1 and 14 days after CPIP, but no change in TRPA1 immunoreactivity was observed. Different mechanisms underlie acute (inflammation and oxidative stress) and chronic (oxidative stress) phases of CPIP. TRPA1 activation may be relevant for CRPS1/CPIP-induced acute and chronic pain.
Grupo Multidisciplinar de Saúde, Programa de Pós-Graduação em Atenção Integral à Saúde, Universidade de Cruz Alta (UNICRUZ), 98020-290, Cruz Alta, RS, Brazil.
J Z
JZ
Klafke
Departamento de Saúde, Curso de Biomedicina, Faculdade de Educação e Cultura de Vilhena, 76980-000, Vilhena, RO, Brazil.
M A
MA
da Silva
Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica, Departamento de Química, Universidade Federal de Santa Maria (UFSM), 97105-900, Santa Maria, RS, Brazil.
M F
MF
Rossato
Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense (UNESC), Avenida Universitária, 1105, room 21, building S, 88806-000, Criciúma, SC, Brazil.
S Dal Toé
SD
de Prá
Programa de Pós-Graduação em Biomedicina do Instituto de Ensino e Pesquisa da Santa Casa de Belo Horizonte, Departamento de Biomedicina e Medicina (IEPBH), Belo Horizonte, MG, Brazil.
F K
FK
Rigo
Departamento de Saúde (Farmácia), Universidade Federal do Sergipe (UFS), 49400-000, Lagarto, SE, Brazil.
C I B
CI
Walker
Programa de Pós-Graduação em Farmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal de Santa Maria (UFSM), 97105-900, Santa Maria, RS, Brazil.
G V
GV
Bochi
Programa de Pós-Graduação em Farmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal de Santa Maria (UFSM), 97105-900, Santa Maria, RS, Brazil.
R N
RN
Moresco
Laboratório de Bioquímica Clínica, Departamento de Análises Clínicas e Toxicológicas, Universidade Federal de Santa Maria (UFSM), 97105-900, Santa Maria, RS, Brazil. ferreiraj99@gmail.com.|Programa de Pós-Graduação em Farmacologia, Departamento de Farmacologia, Universidade Federal de Santa Catarina (UFSC), Block "D"/CCB, Trindade, 88040-900, Florianópolis, SC, Brazil. ferreiraj99@gmail.com.
J
J
Ferreira
Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense (UNESC), Avenida Universitária, 1105, room 21, building S, 88806-000, Criciúma, SC, Brazil. gabitrev@hotmail.com.
G
G
Trevisan
D000118:Acetylglucosaminidase / Q000378:metabolism; D059787:Acute Pain / Q000209:etiology / Q000378:metabolism*; D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D059350:Chronic Pain / Q000209:etiology / Q000378:metabolism*; D003080:Cold Temperature; D006614:Hindlimb / Q000098:blood supply*; D006930:Hyperalgesia / Q000209:etiology / Q000378:metabolism; D019344:Lactic Acid / Q000097:blood; D008297:Male; D059225:Nociception; D018384:Oxidative Stress; D009195:Peroxidase / Q000378:metabolism; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D012019:Reflex Sympathetic Dystrophy / Q000209:etiology / Q000378:metabolism*; D015427:Reperfusion Injury / Q000150:complications; D012709:Serum Albumin / Q000378:metabolism; D000074025:TRPA1 Cation Channel; D050052:TRPC Cation Channels / Q000037:antagonists & inhibitors* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D000447:Aldehydes; D012709:Serum Albumin; D000074025:TRPA1 Cation Channel; D050052:TRPC Cation Channels; C480976:Trpa1 protein, rat; D014409:Tumor Necrosis Factor-alpha; D019344:Lactic Acid; D009195:Peroxidase; D000118:Acetylglucosaminidase; C027576:4-hydroxy-2-nonenal
4-HNE; Allodynia; CRPS 1; HC-030031; Neuropathy; Pain