Increase of TOI during ECPR might reflect an improvement in cerebral blood flow, while decrease of TOI after ECPR might reflect oxygen utilization by the brain tissue as a result of neuronal cell survival. NIRS may be useful for monitoring cerebral hemodynamics and oxygen metabolism during CPR.

The metabolites of prostacyclin (PGI2) and thromboxane A₂ (TxA₂), 6-keto-PGFι_α and thromboxane B₂ (TXB2), were investigated during reperfusion (RP) following warm (37 °C, 60 min, n = 9) or cold (15 °C, 120 min, n = 11) ischemia induced by cold (4 ° C) or normothermic (30 °C) K⁺ cardioplegia (CP) in isolated canine hearts subjected to global ischemia and RP. 6-Keto-PGF_1α flux was significantly higher (p < 0.025) in the warm group at 1, 5, and 10 min of RP (4,202 ± 1,412, 2,475 ± 1,875, and 1,255 ± 633 pg/g·min, mean ± SD) compared to those in the cold group (1,504 ± 1,245, 434 ± 641, and 370 ± 329 pg/g·min). TxB₂ flux was small in amount compared to 6-keto-PGF_1α in both groups. Regarding the coronary hemodynamics, the cold group alone showed statistically significant relationships of coronary sinus blood flow to TxB₂ level and TxB₂/6-keto-PGF_1α ratio in coronary sinus blood. Also, coronary vascular resistance showed linear relations to these two parameters of the metabolites. In a supplementary experiment only with cold ischemia for 180 min, 6-keto-PGF_1α was released at each coronary flush-out by CP and the incremental amount showed a gradual increase during ischemia. These results indicated that significant production and release of PGI₂ occurred during ischemia and RP following CP arrest and these related to the degree of myocardial damage while the response of TxA₂ seemed less significant. The role of PGI₂ release during RP following cardioplegic arrest was discussed.