RESUMO
The use of a surfactant solution during oil and gas field development might improve the recovery rate of oil reservoirs. However, the serious emulsification of the produced liquid will bring challenges to the subsequent treatment process and storage and transportation. It is urgent to understand the coalescence mechanism of crude oil under the action of surfactant solution. This research investigates the coalescence mechanism of numerous oil droplets under liquid flow perturbation. The model was established to study the coalescence process of multiple oil droplets. The effects of the number of oil droplets under homogeneous conditions, the size of oil droplets, and the distance between oil droplets under non-homogeneous conditions on the coalescence process were analyzed. Meanwhile, the change rules of the completion time of oil droplet coalescence were drawn. The results show that the smaller the size of individual oil droplets under non-homogeneous conditions, the longer the coalescence completion time is, and when the size of individual oil droplets reaches the nanometer scale, the time for coalescence of oil droplets is dramatically prolonged. Compared to static circumstances, the time it takes for oil droplets to coalesce is somewhat shorter under gravity. In the fluid flow process, in the laminar flow zone, the coalescence time of oil droplets decreases with the increase of the liquid flow rate. However, in the turbulent flow zone, the coalescence time of oil droplets increases with the increase in the liquid flow rate. The coalescence time is in the range of 600~1000 ms in the flow rate of 0.05~0.2 m/s. In the presence of surfactants, the oil content in the emulsion system increases under the influence of pumping flow. The change in oil content rate with various surfactants is less impacted by flow rate, owing to the stable emulsion structure created by the extracted fluid within the reservoir. The study findings presented in this research provide technical assistance for effective crude oil storage and transportation.
RESUMO
BACKGROUND: Although immunomodulatory effects of anesthetics have been increasingly recognized, their underlying molecular mechanisms are not completely understood. Toll-like receptors (TLRs) are one of the major receptors to recognize invading pathogens and danger signals from damaged host tissues to initiate immune responses. Among the TLR family, TLR2 and TLR4 recognize a wide range of ligands and are considered to be important players in perioperative pathophysiology. Based on our recent finding that volatile anesthetics modulate TLR4 function, we tested our hypothesis that they would also modulate TLR2 function. METHODS: The effect of anesthetics isoflurane, sevoflurane, propofol, and dexmedetomidine on TLR2 activation was examined by reporter assays. An anesthetic that affected the activation was subjected to in silico rigid docking simulation on TLR2. To test our prediction that sevoflurane and a TLR1/TLR2 ligand Pam3CSK4 would compete for the same pocket of TLR2, we performed Pam3CSK4 competitive binding assay to TLR2 using HEK cells stably transfected with TLR2 (HEK-TLR2) with or without sevoflurane. We examined the effect of different anesthetics on the functions of human neutrophils stimulated with TLR2 ligands. Kruskal-Wallis test and Mann-Whitney U test were used for statistical analysis. RESULTS: We observed that the attenuation of TLR1/TLR2 activation was seen on sevoflurane exposure but not on isoflurane, propofol, or dexmedetomidine exposure. The attenuation of TLR2/TLR6 activation was not seen in any of the anesthetics tested. The rigid docking simulation predicted that sevoflurane and Pam3CSK4 bound to the same pocket of TLR1/TLR2 complex. The binding of Pam3CSK4 to HEK-TLR2 cells was impaired in the presence of sevoflurane, indicating that sevoflurane and Pam3CSK4 competed for the pocket, as predicted in silico. The stimulation of neutrophils with Pam3CSK4 induced L-selection shedding but did not affect phagocytosis and reactive oxygen species production. L-selectin shedding from neutrophils was attenuated only by sevoflurane, consistent with the result of our reporter assays. CONCLUSIONS: We found that TLR1/TLR2 activation was attenuated by sevoflurane, but we found no evidence for attenuation by isoflurane, propofol, or dexmedetomidine at clinically relevant concentrations. Our structural analysis and competition assay supported that sevoflurane directly bound to TLR2 at the interphase of the TLR1/TLR2 complex. Sevoflurane attenuated neutrophil L-selectin shedding, an important step for neutrophil migration.
