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Objective:To analyze the research hotspots and development trend of the application of artificial intelligence to the field of anesthesia using bibliometrics, and to provide reference for further research.Methods:Based on the results of the literature search on artificial intelligence and anesthesia in the Web of Science database, Citespace5.5.R2 and VOSviewer1.6.16 softwares were used to draw the knowledge map of scientific research cooperation networks, keywords and citations and implement bibliometric analysis.Results:A total of 298 studies were included, and the number of publications and citation frequency in the early period were maintained at a very low level for a long time, and both showed an increasing trend year by year after 2017.These studies came from 45 countries/regions, among which the United States had the highest publications.Harvard University was the institution with the highest number of papers.The author with the highest publications was Matava Clyde, who worked at the Toronto Hospital for Sick Children.Research on the application of artificial intelligence to the field of anesthesia had mainly focused on artificial intelligence algorithms, event prediction, anesthesia control and pain management.Conclusions:The application of artificial intelligence to the field of anesthesia has gradually attracted the attention of the academic community in the past five years, and the number of publications and citation frequency have increased drastically.The academic achievements in this field in China still have a gap compared with the world advanced level, and more in-depth researches can be conducted in the future for the hot directions.
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Objective To investigate the effects of desflurane on the delayed rectifier potassium current (Ik ) in acutely dissociated rat parietal cortical neurons. Methods Wistar rats between 10- and 14-day old of both sexes were used. The parietal cortical neurons were acutely dissociated enzymatically. The extracellular fluid saturated with 0.3,0.6 and 0.9 mmol/L desflurane was added to the culture dish, then the effects of different concentrations of desflurane on Ik were investigated by using the whole-cell patch-clamp technique in acutely dissociated rat parietal cortical neurons. Results IK was inhibited by desflurane in a concentration-dependent manner ( P ＜0.01). The V1/2 of the activation and inactivation curves and the slop factor had no change after giving 0.6 mmol/L desflurane (P ＞ 0.05). Conclusion Desflurane inhibits delayed rectifier potassium channels of parietal cortical neurons of rats in a concentration-dependent manner, and has no effect on the activation and inactivation of delayed rectifier potassium channels, indicating that the change in the excitability of the channel is not involved in the mechanism of inhibitory effect of desflurane, and the other reasons may be involved in the mechanism.
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Objective To investigate the effects of propofol on Ca2+ -induced mitochondrial dysfunction after focal cerebral ischemia-reperfusion(IR) injury in rats. Methods Eighty-four male Wistar ratsweighing 250-300 g were randomly divided into 4 groups (n= 21 each):group Ⅰ sham operation (group S); group Ⅱ IR; group Ⅲ CaCl2 and group Ⅳ propofol (group P). In group Ⅱ - Ⅳ focal cerebral IR was induced by 2 h middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion. Neurological function was assessed at 2 h of ischemia and scored (0= no deficit, 5 = death). The animals were decapitated at the end of 24 h reperfusion. Left parietal and frontal cortex were immediately isolated and mitochondria were extracted. In group Ⅲ and Ⅳ mitochondria were incubated with 200 μmol/L CaCl2 for 5 min at 37 ℃, and were pretreated with propofol 200 μmol/L in group Ⅳ for 2 min before CaCl2. Morphological changes of mitochondria were examined by electron microscopy. Mitochondrial permeability transition pore (MPTP) activity was detected by ultraviolet visible absorption spectroscopy.Results Mitochondrial ultrastructure was normal in group Ⅰ . Significant mitochondrial swelling, disrupted cristae and membrane rupture were observed in group Ⅲ. Propofol significantly attenuated the Ca2+ -induced changes. The MPTP activity was significantly increased in group Ⅱ and Ⅲ as compared with group Ⅰ but were significantly decreased in group Ⅳ (propofol group). The decrease in MPTP activity was attenuated in group Ⅳ as compared with group Ⅲ. Conclusion Propofol can improve mitochondrial dysfunction induced by Ca2+ after focal cerebral IR by inhibiting MPTP opening in rats.
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Objective To investigate the effect of ketamine on hippocampal uncoupling protein 2 (UCP 2) expression after forebrain ischemia-reperfusion (I/R) in rats and the mechanism of protective effect of ketamine on brain. Method Forty-five male Wistar rats weighing 250～300 g were randomly divided into 3 groups, with 15 animals in each group. Forebrain I/R was estabhshed by occlusion of bilaleral carotid artery combined with hy-potemion,EFG in a sustained low rate of 7 Hz, 30～40 μVθ rhythm was the success signs of forebrain I/R. Con-trol group (C) :sham operation was performed; I/R group (Ⅰ): bilateral common carotid arteries were clamped for lOmin combined with hypotension [MAP:(40±5) mmHg] induced by exsanguinations, then saline (1 mg/kg) was injected into the lateral cerebral ventricle using microsyringe; ketamine group (K):ketamine (1 mg/kg) was injected into the lateral cerebral ventricle using microsyringe after I/R. The animals were decapitated, the brain was immediately removed,and the hippocampal tissues were dissociated at 6 h after reperfusion. The cerebral I/R injury was observed with light microscope, the levels of UCP 2 mRNA expression in hippocampus were detected by using semi-quantitative RT-PCR technique (n=7), coronal sections including hippocampal tissue were obtained for detection of UCP 2 protein expression by immuno-histochemistry (IH) method (n=8). The RT-PCRR and IH data were expressed as the mean±SD, the statistical signiticance was determined by one-way ANOVA. Results The UCP 2 mRNA expression was (1.06±0.02) in group Ⅰ and (1.18±0.06)in group K increased significantly compared with that in group C(0.91±0.02) (P<0.05), there were more UCP2 mRNA expression in group K increased than that in group Ⅰ(P<0.05). The expression of UCP 2 protein was (31.56±4.01) in group Ⅰ and (44.61±4.96) in group K, increased significantly compared with that in group C (17.91±5.49) (P<0.05),there were more UCP 2 protein expression in group K than that in group Ⅰ (P<0.05). Conclusions Ketamine can attenuate the cerebral I/R injury in rats, the underlying mechanism may be related to the up-regulartion of the expression of hippocampal UCP 2 mRNA and UCP 2 protein.