Simultaneous, real-time measurement of nitric oxide and oxygen dynamics during cardiac ischemia–reperfusion of the rat utilizing sol–gel-derived electrochemical microsensors

Abstract In this study, we simultaneously measured nitric oxide (NO) and oxygen (O 2 ) dynamics in the myocardium during myocardial ischemia–reperfusion (IR) utilizing sol–gel modified electrochemical NO and O 2 microsensors. In addition, we attempted to clarify the correlation between NO release in the ischemic period and O 2 restoration in the myocardium after reperfusion, comparing a control heart with a remote ischemic preconditioning (RIPC)-treated heart as an attractive strategy for myocardial protection. Rat hearts were randomly divided into two groups: a control group ( n  = 5) and an RIPC group ( n  = 5, with RIPC treatment). Myocardia that underwent RIPC treatment (182 ± 70 nM, p p O 2 ) in the RIPC group significantly increased and was restored to pre-ischemic levels (92.6 ± 36.8%); however, the p O 2 of the control group did not increase throughout the reperfusion period (5.7 ± 7.5%, p  = 0.001). Myocardial infarct size measurements revealed a significant decrease in cell death in the myocardium region of the RIPC group (41.44 ± 6.42%, p  = 0.001) compared with the control group (60.05 ± 10.91%). As a result, we showed that the cardioprotective effect of RIPC could be attributed to endogenous NO production during the ischemic period, which subsequently promoted reoxygenation in post-ischemic myocardia during early reperfusion. Our results suggest that the promotion of endogenous formation during an ischemic episode might be helpful as a therapeutic strategy for protecting the myocardium from IR injury. Additionally, our NO and O 2 perm-selective microsensors could be utilized to evaluate the effect of drug or treatment.