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Life-saving coronary artery bypass and vascular grafting procedures can result in ischaemic reperfusion injury (IRI). The carbon monoxide (CO) releasing molecule oCOm-21 has been shown to provide cardioprotection in an ex vivo model of IRI in normotrophic and hypertrophic rat hearts. oCOm-21 is a novel drug, with literature suggesting that the active product CO can inhibit the Nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome. NLRP3 is activated by sterile inflammatory signals, facilitating inflammasome assembly via NLRP3 and ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain) interactions. Following assembly, the inflammasome cleaves pro-interlukin-1β (IL-1β) into IL-1β, allowing the secretion of the pro-inflammatory cytokine. This study aimed to examine the effect of 1 and 3 μM oCOm-21 on NLRP3 in isolated normotrophic and moderately hypertrophic CYP1A1-Ren2 rat hearts exposed to warm global ischaemia (30 minutes) and reperfusion (60 minutes).