Hydrocodone is More Effective than Morphine or Oxycodone in Suppressing the Development of Burn-Induced Mechanical Allodynia.
BACKGROUND
Pain is the most frequent complaint of burn-injured patients. Opioids are commonly used in the course of treatment. However, there is a lack of rodent studies that examine the differential effects of various opioids on burn pain.


OBJECTIVE
This study compared the ability of morphine, oxycodone, and hydrocodone to suppress the development of burn-induced mechanical allodynia and reduce pain sensitivity.


METHODS
Mice were examined for their baseline pain sensitivity thresholds using the von Frey Filaments test. Then, they were subjected to burn or sham injury and treated orally with morphine, oxycodone, hydrocodone (20 or 40 mg/kg), or saline twice daily throughout the study. They were retested on days 4, 7, 11, 14, 21, and 28 postburn.


RESULTS
In the sham animals, morphine produced significant opioid-induced hyperalgesia (OIH). Development of OIH was minimal for hydrocodone and was not observed for oxycodone. Secondary mechanical allodynia was observed beginning four days after the burn injury and intensified with time. All opioids produced comparable antinociceptive effects. Hydrocodone was effective in suppressing the development of burn-induced mechanical allodynia and fully treated the burn-induced increase in pain sensitivity. In contrast, morphine and oxycodone had only minimal effects on the development of burn-induced mechanical allodynia and only partially treated the burn-induced increase in pain sensitivity.


CONCLUSIONS
This study demonstrated that hydrocodone is effective in suppressing the development of burn-induced mechanical allodynia, while both morphine and oxycodone had minimal effects. These findings underscore the need for additional studies on the differences among various opioids using clinically relevant pain models.
Behavioral and Cellular Neuroscience, Department of Psychology, Texas A&M University, College Station, Texas.|Interdisciplinary Program in Neuroscience, Texas A&M Institute for Neuroscience (TAMIN), College Station, Texas, USA.
Michael A
MA
Emery
Behavioral and Cellular Neuroscience, Department of Psychology, Texas A&M University, College Station, Texas.|Interdisciplinary Program in Neuroscience, Texas A&M Institute for Neuroscience (TAMIN), College Station, Texas, USA.
M L
ML
Shawn Bates
Behavioral and Cellular Neuroscience, Department of Psychology, Texas A&M University, College Station, Texas.|Interdisciplinary Program in Neuroscience, Texas A&M Institute for Neuroscience (TAMIN), College Station, Texas, USA.
Paul J
PJ
Wellman
Behavioral and Cellular Neuroscience, Department of Psychology, Texas A&M University, College Station, Texas.|Interdisciplinary Program in Neuroscience, Texas A&M Institute for Neuroscience (TAMIN), College Station, Texas, USA.
Shoshana
S
Eitan
D000701:Analgesics, Opioid / Q000627:therapeutic use; D000818:Animals; D002056:Burns / Q000150:complications / Q000188:drug therapy*; D004305:Dose-Response Relationship, Drug; D006853:Hydrocodone / Q000008:administration & dosage / Q000627:therapeutic use*; D006930:Hyperalgesia / Q000188:drug therapy; D008297:Male; D008810:Mice, Inbred C57BL; D009020:Morphine / Q000008:administration & dosage / Q000627:therapeutic use*; D010098:Oxycodone / Q000008:administration & dosage / Q000627:therapeutic use*; D010146:Pain / Q000188:drug therapy; D010147:Pain Measurement / Q000187:drug effects; D017288:Pain Threshold / Q000187:drug effects
D000701:Analgesics, Opioid; D006853:Hydrocodone; D009020:Morphine; D010098:Oxycodone