Objective To investigate the effect of dexmedetomidine and small dose of ketamine on the hyperalgesia and brain-derived neurotrophic factor (BDNF) mRNA in the spinal cord of rats with neuropathic pain.Methods Forty-five male Sprague-Dawley rats,weighing 240-270 g,were randomly divided into 5 groups (n =9 each):sham operation group (group S),spinal nerve injury (SNI) group,ketamine group (group K),dexmedetomidine group (group D) and dexmedetomidine + ketamine group (group K+ D).The animals were anesthetized with intraperitoneal 10% chloral hydrate 400 mg/kg.SNI was produced by exposing the sciatic nerve and its branches and ligation and transection of tibial nerve and common fibular nerve in groups SNI,K,D and K + D.In S group,the sciatic nerves and its branches were only exposed but not ligated.In groups D,K and K + D,dexmedetomidine 40 μg/kg (2 ml),ketamine 10 mg/kg (2 ml) and mixture of dexmedetomidine 20μg/kg + ketamine 5 mg/kg (2 ml) were injected intraperitoneally,respectively,once a day for 21 consecutive days starting from 24 h after successful SNI surgery.While the equal volume of normal saline 2 ml was injected instead in S and SNI groups.The paw withdrawal threshold to mechanical stimuli (PWT) was measured at 1 day before surgery,and 3,7,14 and 21 days after surgery.Three rats were sacrificed after measurement of pain threshold at 1 day before surgery,and 7 and 21 days after surgery and the lumbar segments (L4-6) of the spinal cord were removed for determination of BDNF mRNA expression in spinal dorsal horn by real time PCR.Results Compared with group S,the PWT was significantly decreased,and the expression of BDNF mRNA in spinal dorsal horn was up-regulated after surgery in groups SNI,K,D and K + D (P ＜ 0.05).The PWT was significantly higher,and the expression of BDNF mRNA in spinal dorsal horn was lower after surgery in groups K,D and K + D than in group SNI,and in group K + D than in groups K and D (P ＜ 0.05).Conclusion The combination of dexmedetomidine and small dose of ketamine produces a synergistic antinociception in rats with neuropathic pain,and direct or indirect inhibition of BDNF mRNA expression in spinal dorsal horn is involved in the underlying mechanism.

Public hospitals play a dominant role in providing medical services.Meanwhile,they are also critical for un-dertaking missions to handle health emergencies.This paper analyzes the necessity,current situation,and existing weaknesses of the health emergency capacity of public hospitals.It also conducts a comparative study of the emergency response mechanisms of foreign medical institutions.This paper aims to explore a well-developed design for health emergency in public hospitals that is suitable for China's medical conditions and to provide a feasible model for promoting high-quality health emergency management.

A case of severe complications is presented that replaced the double J tubeless misguided by zebra guidewire into ileum in a patient with ureteral dermostomy, causing a ureteral ileum fistula.The result suggests improper operation of zebra guidewire could have a risk of ureteral perforation when the ureter is distorted, narrow or with inflammatory lesions.Standardized diagnosis and treatment and correct selection of guidewire can reduce the risk of ureteral perforation.

OBJECTIVE To reveal the role of the basal forebrain(BF)GABAergic neurons in the regulation of isoflurane anesthesia and to elucidate the underlying neural pathways.METHODS The activity of BF GABAer-gic neurons was monitored during isoflurane anesthesia using a genetically encoded calcium indicator in Vgat-Cre mice of both sexes.The activity of BF GABAer-gic neurons was manipulated by chemogenetic and opto-genetic approaches.Sensitivity,induction time and emer-gence time of isoflurane anesthesia were estimated by righting reflex.The electroencephalogram(EEG)power and burst-suppression were monitored by EEG recording.The effects of activation of GABAergic BF-thalamic reticu-lar nucleus(TRN)pathway on isoflurane anesthesia were investigated with optogenetics.RESULTS The activity of BF GABAergic neurons was generally inhibited during isoflurane anesthesia,obviously decreased during the induction of anesthesia and gradually restored during the emergence from anesthesia.Activation of BF GABAergic neurons with chemogenetics and optogenetics promoted behavioral emergence from isoflurane anesthesia,with decreased sensitivity to isoflurane,delayed induction and accelerated emergence from isoflurane anesthesia.Optogenetic activation of BF GABAergic neurons prom-oted cortical activity during isoflurane anesthesia,with decreased EEG delta power and burst suppression ratio during 0.8%and 1.4%isoflurane anesthesia,respectively.Similar to the effects of activating BF GABAergic cell bod-ies,photostimulation of BF GABAergic terminals in the TRN also strongly promoted cortical activation and behav-ioral emergence from isoflurane anesthesia.CONCLU-SION The GABAergic neurons in the BF is a key neural substrate for general anesthesia regulation that facilitates behavioral and cortical emergence from general anesthe-sia via the BF-TRN pathway.