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With the rapid development of general anesthesia technology and the occurrence of new types of inhalation and intravenous anesthetics,safety and comfort requirements of general anesthesia become increas-ingly higher. Therefore,emergence agitation and its adverse consequences gradually receive more and more atten-tion . Thus the etiology and prevention of emergence agitation is an important issue in pediatric anesthesia at pres-ent. In recent years, some achievement has been made in emergence agitation following general anesthesia in children. This article will summarize the related factors,possible mechanisms and prevention strategics of pediat-ric emergence agitation.
ABSTRACT
Objective To evaluate the effects of isoflurane postconditioning on mitochondrial permeability transition pore (mPTP) in brain tissues of neonatal rats with hypoxic-ischemic brain injury.Methods One hundred and twenty 7-day-old Sprague-Dawley rats,weighing 12-16 g,were randomly divided into 4 groups (n =30 each) using a random number table:sham operation group (group S),isoflurane group (group I),hypoxicischemic brain injury group (group HIBI),and hypoxic-ischemic brain injury + isoflurane postconditioning group (group HI).To establish hypoxic-ischemic brain injury model in the neonatal rats,the left common carotid artery ligation was carried out,and then the rats were exposed to 8％ O2 + 92％ N2 at 37 ℃ for 2 h in HIBI and HI groups.The rats inhaled 1.5 ％ isoflurane for 30 min after the model was established in group HI.The rats only inhaled 1.5％ isoflurane for 30 min in group I.At 24 h after the model was established,10 rats taken out randomly in each group were sacrificed and brains were removed to detect mPTP opening.At 7 days after the model was established,the survival rate was recorded in the rest rats.The rats were then sacrificed and brains were removed and the right and left cerebral hemispheres were weighed separately,and the ratio between left/right cerebral hemispheres was calculated.The density of normal neurons in ventral posterior inferior thalamic nucleus and hippocampal CA3 region in the left and right cerebral hemispheres were measured and the ratios of the density of normal neurons in the left to right cerebral hemisphere were calculated.Results There was no significant difference in the survival rate between the four groups (P ＞ 0.05).Compared with group S,the ratios of the density of normal neurons in the left to right cerebral hemisphere,weight of left cerebral hemisphere,and ratio between left/right cerebral hemispheres were significantly decreased,and mPTP opening was increased in group HIBI (P ＜ 0.05),and no significant changes were found in the parameters mentioned above in group I (P ＞ 0.05).Compared with group HIBI,the ratios of the density of normal neurons in the left to right cerebral hemisphere,weight of left cerebral hemisphere,and ratio between left/right cerebral hemispheres were significantly increased,and mPTP opening was decreased in group HI (P ＜ 0.05).Conclusion The mechanism by which isoflurane postconditioning reduces hypoxic-ischemic brain injury may be related to inhibition of mPTP opening in brain tissues of neonatal rats.
ABSTRACT
Objective To evaluate the effects of isoflurane postconditioning on long-term cognitive function of neonatal rats with hypoxic-ischemic brain injury (HIBI).Methods Sixty 7-day-old Sprague-Dawley rats,weighing 12-16 g,were randomly divided into 4 groups (n =15 each) using a random number table:sham operation group (group Ⅰ),isoflurane postconditioning group (group Ⅱ),cerebral hypoxia-ischemia group (group Ⅲ),and isoflurane postconditioning after cerebral hypoxia-ischemia group (group Ⅳ).Brain ischemia was induced by permanent ligation of the left common carotid artery followed by inhalation of 8 ％ O2-92 ％ N2 for 2 h at 37 ℃ in Ⅲ and Ⅳ groups.In Ⅰ and Ⅱ groups,the left common carotid artery was only isolated but not ligated.The rats inhaled 1.5％ isoflurane in 30％ O2-70％ N2 for 30 min starting from 2 h of hypoxia in Ⅱ and Ⅳ groups.The rats were exposed to 30％ O2-70％ N2 for 30 min in Ⅰ and Ⅲ groups.Morris water maze test was carried out at 30-35 days after HIBI.The escape latency,swimming speed,swimming distance,the number of times the animals crossing the platform quadrant,the percentage of time spent in the platform quadrant and the percentage of swimming distance in the platform quadrant were recorded.The animals were sacrificed after Morris water maze test.The density of normal neurons in ventral posterior inferior thalamic nucleus and hippocampal CA3 region in left and right cerebral hemisphere was measured and the ratio of the density of normal neurons in the left to right cerebral hemisphere was calculated.Results Compared with group Ⅰ,the escape latency was significantly prolonged at 30-34 days after HIBI in group Ⅲ and at 31 and 34 days after HIBI in Ⅳ group,the number of times the animals crossing the platform quadrant,percentage of time spent in the platform quadrant,percentage of swimming distance in the platform quadrant,and ratio of the density of normal neurons in the left to right cerebral hemisphere were decreased at day 35 after HIBI in group Ⅲ,no significant changes were found in the number of times the animals crossing the platform quadrant,percentage of time spent in the platform quadrant,and percentage of swimming distance in the platform quadrant,and the ratio of the density of normal neurons in the left to right cerebral hemisphere was decreased at day 35 after HIBI in group Ⅳ,and no significant changes were found in the parameters mentioned above in group Ⅱ.Compared with group Ⅲ,the escape latency was significantly shortened at 31-34 days after HIBI,and the number of times the animals crossing the platform quadrant,percentage of time spent in the platform quadrant,percentage of swimming distance in the platform quadrant,and ratio of the density of normal neurons in the left to right cerebral hemisphere were increased at day 35 after HIBI in group Ⅳ.There was no significant difference in the swimming speed and swimming distance at day 35 after HIBI between groups.Conclusion Isoflurane postconditioning can improve long-term cognitive function of neonatal rats with HIBI.
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Objective To investigate whether intranasal dexmedetomidine prevents the emergency delirium after sevoflurane-based anesthesia (ASA) in children.Methods Ninety children (ASA I,2 to 7years) undergoing elective tonsillectomy with or without adenoidectomy,were randomly divided into group D1 (intranasal dexmedemidine 1.0 μg/kg),group D2 (intranasal dexmedemidine 0.5 μg/kg),and group NS (intranasal normal saline).Anesthesia was induced with sevoflurane (30 min after intranasal administration) and maintained with sevoflurane in 50/50％ O2/N2O.Heart rate (HR),blood pressure (BP),and hemoglobin oxygen saturation (SpO2) were monitored before intranasal administration to 2 hours after extubation.Time of operation and extubation were recorded.Pediatric anesthesia emergence delirium (PAED) scale,Modified Children's Hospital of Eastern Ontario Pain Scale (m-CHEOPS) Pain scale and the adverse effects were observed.Results The PAED scales of group D1 and Group D2 were significantly lower than group NS.No significant differences were found in hemodynamic and respiratory variables,pain scale,time of extubation and adverse effects among three groups.Conclusions Intranasal dexmedetomidine decreased the severity of emergence delirium after sevoflurane-based anesthesia in children without prolonging the time to extubate and affect hemodynamics and respiratory variables.