REVERSAL OF OXYCODONE OPIOID-INDUCED RESPIRATORY DEPRESSION IN MICE

Abstract

Opioid use can lead to severe side effects, including opioid-induced respiratory depression (OIRD), which poses a significant risk to patient safety. This thesis explores the potential of CBR2 receptors in mitigating OIRD through mouse models and respiratory measures. The study aims to understand the mechanisms underlying respiratory depression induced by acute oxycodone opioid exposure and investigate the efficacy of CBR2 receptor modulation in reversing this phenomenon. The study involves the acute intraperitoneal (IP) injections of oxycodone in mice and the subsequent administration of a CBR2 receptor antagonist, AM2301, along with 10:10:80. Whole Body Plethysmography (WBP) was used to measure respiratory parameters: respiratory rate, minute volume, and tidal volume. The WBP data measures baseline, post-oxycodone injection, and post-AM2301 mixture injection in the room air and 5% CO2 air. Our results demonstrate that the CBR2 antagonist, AM2301, along with 10:10:80 cannot mitigate opioid-induced respiratory depression by looking at the basal breathing patterns and WBP data. These findings show a need for additional research in managing OIRD, whether exploring prevention paradigms or co-administration of oxycodone and the AM2301 mixture.