Objective:To study whether hypoxia and reoxygenation (H/R)injury induces the necrosis of cardiomyocyte via regulation of programmed necrosis (necroptosis). Methods:Neonatal rats ventricular myocytes were isolated from neonatal Sprague–Dawley rats. The incubated cells were subjected to reoxygenation (4 h)after hypoxia (2 h). The effect of H/R injury on the necrosis of cardiaomyocytes was determined by PI (propidium iodide)staining. Wsetern blot and Co-IP were performed to test the protein expression of receptor interacting protein (RIP)1 and 3,the formation of RIP1/RIP3 complex Ⅱ,and the ubiquitination level of RIP1 and RIP3. Results:When subjected to reoxygenation (4 h) after hypoxia (2 h),the protein expression levels of RIP1 and RIP3 were significantly increased compared with those of control. Besides,H/R injury also promoted the formation of RIP1/RIP3 complex Ⅱ and upregulated the ubiquitination of RIP1 and RIP3. Conclusion:Hypoxia and reoxygenation injury could induce the necrosis of cardiomyocytes,which may be involved in regulation of RIP1/RIP3 dependent programmed necrosis signaling pathway.