Effects of Non Steroidal Anti-inflammatory Drugs on the Evans Blue Extravasation and Pain Behaviors Evoked by Mustard Oil Induced Visceral Pain in Mice: Comparison with Morphine.
10.4097/kjae.2004.46.5.613
- Author:
Yoo Kyung KIM
1
;
Jin Woo SHIN
;
Jeong Gill LEEM
;
Cheong LEE
Author Information
1. Department of Anesthesiology and Pain Medicine, College of Medicine, University of Ulsan, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
NSAID;
referred hyperalgesia;
visceral pain
- MeSH:
Abdomen;
Adult;
Animals;
Anti-Inflammatory Agents, Non-Steroidal;
Colon;
Evans Blue*;
Foot;
Hair;
Humans;
Hyperalgesia;
Inflammation;
Ketoprofen;
Ketorolac;
Male;
Mice*;
Mice, Inbred ICR;
Morphine*;
Mustard Plant*;
Plasma;
Veins;
Visceral Pain*
- From:Korean Journal of Anesthesiology
2004;46(5):613-619
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Visceral pain is characterized by its spontaneous pain and referred hyperalgesia. Our aim was to examine the inhibitory effects of various NSAIDs on the pain behaviors, both spontaneously and mechanically evoked, and evans blue extravasation induced by intracolonic mustard oil in mice. METHODS: 50 mg/kg of evans blue was injected to adult male ICR mice via tail vein for subsequent determination of plasma extravasation. The animals in the control group were given subcutaneous saline and those in experimental groups were given one of the following drugs: 1, 3, 10 mg/kg of morphine; 10, 100 mg/kg of ketoprofen; 5, 50 mg/kg of ketorolac; 2, 20 mg/kg of DFU (cyclooxygenase-2 inhibitor). Visceral pain-related behaviors were counted for 20 minutes after intracolonic administration of 50 microliter of 1.5% mustard oil. In order to test referred hyperalgesia, before intracolonic administration and 20 min after the administration, the frequency of withdrawal responses to the application of von Frey hairs to the abdomen, foot and tail was tested. The colon was removed post-mortem and evans blue content was measured. RESULTS: Visceral pain-related behaviors were significantly inhibited in the groups administered with 3 and 10 mg/kg of morphine, 50 mg/kg of ketorolac, 100 mg/kg of ketoprofen and 20 mg/kg of DFU (P < 0.05), respectively. Response frequencies to the application of von Frey hairs were decreased in the groups administered with 3 and 10 mg/kg of morphine (P < 0.05) but not any doses of ketorolac, ketoprofen and DFU. Evans blue content was decreased by 100 mg/kg of ketoprofen and 20 mg/kg DFU (P < 0.05) but not in the other groups. CONCLUSIONS: These results suggest that the analgesic effects of NSAIDs on visceral pain could be mainly mediated by peripheral mechanism, reflected by inhibition of the pain behaviors and inflammation but not centrally mediated mechanism reflected by referred hyperalgesia.
