Objective To study the rate and time-course of the cerebral uptake of propofol during the intravenous continued infusion at a constant rate.Methods Fourteen adult patients were randomly assigned to receive a propofol infusion at a constant of 6 mg?kg -1?h -1(group A) or 12 mg?kg -1?h -1 (group B) for 30-35 min. Blood samples were taken simultaneously from radial artery and jugular venous bulb for measurement of propofol concentrations by high performance liquid chromatography.Results The arterial propofol concentrations(C a) increased progressively during the first 15min after the start of propofol infusion and became stable 15min later.Jugular bulb venous blood propofol concentrations(C ijbv) were increased progressively during the first 30min after the start of propofol infusion in group A and the first 20min in group B, but they were lower than C a at the corresponding interval. 30min after the start of propofol infusion in group A and 20min in group B C ijbv became stable and close to C a. There was significant difference in the accumulated area between the arterial and jugular bulb venous concentration-time curves at the different interval between the two groups before the equilibrium of cerebral uptake was achieved.Conclusions Cerebral propofol uptake is rate- and time-dependent when administered at a constant infusion rate, and there is a hysteresis between the arterial blood concentration and equilibrium of cerebral uptake. Propofol is not metabolized in human brain.

0.05), but there were significant differences in the mean induction time(697 and 313 s, P

AIM:To explore the changes of excitatory amino acids and N-methyl-D-aspartate receptor (NMDAR) in brain undergoing ischemia-reperfusion injury following hepatic portal occlusion (HPO) in vivo.METHODS: The electrolytes and pH of portal vein blood, the content of Glu and Asp in brain, and the expression of NMDAR mRNA were studied with blood-gas analysis, HPLC and semi-quantitative RT-PCR method in two groups(HPO or sham), respectively. Three time points(6 h,12 h and 24h after reperfusion) were included.RESULTS: HPLC measure showed that the content of cortex Glu and Asp in group HPO elevated significantly after reperfusion compared with sham group, the peaks were at 6 h and 24 h Glu:(349?145) ?g?g-1wt,(456?203) ?g?g-1wt vs (238?24) ?g?g-1wt,(225?59) ?g?g-1wt;Asp:(134?50) ?g?g-1wt,(166?50) ?g?g-1wt vs (99?24) ?g?g-1wt,(71?20) ?g?g-1wt.Moreover, semi-quantitative RT-PCR analysis discovered that the expression of NMDAR mRNA increased significantly , the subunit NR1 mRNA was higher in reperfusion 6 h and last to 12 h(1.63?0.06 vs 1.18?0.05; 1.73?0.06 vs 1.17?0.03), the peak of NR2B mRNA was in 12 h (1.75?0.04 vs 1.18?0.05) ,but they did not further increase after reperfusion for 24 h.CONCLUSION: HPO increases the content of Glu and Asp and the expression of NMDAR in brain cortex. The Glu-NMDAR pathway plays a role in the mechanism for the brain injury after HPO. The products of IR injury might be the key factor to cause EAAs acumulation in synapse space.