The comparison of predictive performance in bispectral index prediction during target effect-site controlled infusion of propofol using different blood effect-site equilibration rate constants in the same pharmacokinetic model / 대한마취과학회지

BACKGROUND: Blood-brain equilibration rate constant (k(e0)) is derived from either pharmacokinetic and pharmacodynamic modeling (k(e0_model)) or a model-independent observed time to peak effect (k(e0_tpeak)). Performance in bispectral index (BIS) prediction was compared between k(e0_model) and k(e0_tpeak) for microemulsion or long chain triglyceride (LCT) propofol. METHODS: Time to peak effect (t(peak), time to a maximally reduced BIS value) of microemulsion propofol after an intravenous bolus (1 mg/kg) was measured in 100 patients (group A(micro)). An observed t(peak) of 1.6 min for LCT propofol was obtained from an earlier study. Another 40 patients received a target controlled infusions of microemulsion propofol (k(e0_model) = 0.187/min, group B(micro) = 20) or LCT propofol (k(e0_model) = 0.26/min, group B(LCT) = 20) and remifentanil. The k(e0_tpeak)'s in group B(micro) and B(LCT) were calculated using the observed t(peak) value obtained from group A(micro) and 1.6 min, respectively. Effect-site concentrations of propofol were recalculated using the amounts of propofol infused over time and k(e0_tpeak)'s. Predicted BIS values calculated by sigmoid Emax equations with k(e0_model) and k(e0_tpeak) were compared with observed BIS values during induction and emergence for both formulations of propofol. RESULTS: Observed t(peak) of microemulsion propofol was 1.68 min. The median performance errors of BIS in group B(micro) were -1.83% (-24.8 to 18.9, k(e0_model)) and -2.42% (-26.1 to 36.2, k(e0_tpeak)), while 8.01% (-20.5 to 30.1, k(e0_model)) and 7.37% (-27.0 to 49.1, k(e0_tpeak)) in group B(LCT). The median absolute performance errors of BIS in group B(micro) were 11.87% (2.2-31.1k(e0_model)) and 14.38% (-0.6 to 44.6, k(e0_tpeak)), while 17.31% (5.54-36.0, k(e0_model)) and 18.28% (-0.1 to 56.0, k(e0_tpeak)) in group B(LCT). CONCLUSIONS: The k(e0_model) showed better performance in BIS prediction than the k(e0_tpeak).

Effect of the Heme Oxygenase Inhibitor on the Hypoxic Ischemic Brain Injury in the Neonatal Rat / 대한마취과학회지

BACKGROUND: The heme oxygenase system catalyzes the conversion of heme to free iron, carbon monoxide and bilirubin. This study was purposed to evaluate the effect of the heme oxygenase inhibitor, Tin protoporphyrin IX (SnPPIX) on the hypoxic ischemic brain injury in a neonatal rat. METHODS: Seven-day old Sprague-Dawley rat pups were used. The rats were divided into two groups; control group (n = 9) and SnPPIX group (n = 6). SnPPIX 50 micromol/kg and the dissolvent were administered respectively intraperitoneally. For hypoxic ischemic brain injury, the right common carotid artery was ligated with 5-0 silk and the rats were put in the moisturized hypoxic gas chamber for 150 minutes. Lipid/N-acetyl aspartate and Lipid/Creatine ratio of 1H magnetic resonance spectroscopy were evaluated on the 1st day and the 7th day after hypoxic ischemic brain injury. All rats were sacrificed 2 weeks after hypoxic ischemic brain injury for morphological study. RESULTS: There were no statistically significant differences between two groups in the result of MRS and Lip/Cr and Lip/NAA ratio on 1th day and 7th day after hypoxic ischemic brain injury. In addition, there was no significant difference in the gross morphological evaluation on the 14th day. CONCLUSIONS: Our results suggest that the pretreatment of the Tin protoporphyrin IX does not affect the degree of brain damage which is caused by apoptosis in the model of hypoxic ischemic brain injury in a neonatal rat.