Objective To analyze the effect of preoperative nutritional status on the intraoperative un-expected hypothermia in elderly patients with laparoscopic gastrointestinal tumor radical operation and its risk factors.Methods The clinical case data in 282 elderly patients with laparoscopic gastrointestinal tumor radical surgery in the Fourth Affiliated Hospital of Nanjing Medical University from February 2021 to December 2023 were analyzed retrospectively.The mini nutritional assessment short form(MNA-SF)was adopted to e-valuate the preoperative nutritional status of the patients.The intraoperative unexpected hypothermia occur-rence were statistically analyzed.The univariate and multivariate logistic regression was used to analyze the in-fluencing factors.Results Among 282 patients,104 cases(36.88％)had unexpected hypothermia during op-eration.The incidence rate of intraoperative unexpected hypothermia in the patients with complicating malnu-trition or malnutritional risk was significantly higher than that in the patients with normal nutritional status(P＜0.05).The multivariate logistic regression analysis showed that the age ≥70 years old,body mass index(BMI)＜18.5 kg/m2,progressive weight loss appearance before surgery,preoperative MNA-SF score＜12 points,CO2 pneumoperitoneum time＞4 h and complicating hypoalbuminemia were the independent risk fac-tors for intraoperative unexpected hypothermia occurrence in the elderly patients with laparoscopic gastroin-testinal tumor radical operation(P＜0.05),while the use of heating device for initiatively maintaining tem-perature during surgery was the protective factor for avoiding intraoperative unexpected hypothermia occur-rence(P＜0.05).Conclusion The elderly patients with poor nutritional status undergoing laparoscopic gas-trointestinal tumor radical surgery are more likely to develop unexpected hypothermia.There are many influ-encing factors,so close attention should be paid to.

Aim To investigate the role of TNF-αin propofol-induced neuronal apoptosis and long-term cog-nitive impairment in neonatal rats .Methods Seven-day-old SD rats were randomly divided into 3 groups:Control group ( n =12 ) , P ( single ) group ( n =6 ):propofol 50 mg · kg -1 was injected intraperitoneally (ip.)once;P(repeated) group(n=6):propofol 50 mg · kg -1 was injected ip.once daily, and for seven times. Hippocampal TNF-αlevel was measured 2 hours after propofol anesthesia , there were two time points(n=6) in Control group as control levels (post-natal day 7 for P ( single ) group and postnatal day 13 for P ( repeated ) group ) .In another experiment , 7-day-old rats were randomly divided into 5 groups:Con-trol group; P ( single ) group; P ( repeated ) group; P ( single ) +ETN group: ETN ( etanercept ) 0.4 mg · kg -1 was injected intracerebroventricularly 30 min be-fore propofol administration; P ( repeated ) +ETN group:ETN 0.4 mg· kg -1 was injected intracerebrov-entricularly 30 min before the 1st and 4th administration of propofol , which was injected ip .for seven times , once daily .Hippocampal neuronal apoptosis was detec-ted at postnatal day 7 [ P ( repeated ) and P ( repeated )+ETN groups not involved at this time point ] , 13, 21 and 35 , cognitive function was measured at postnatal day 36 to 41 using Morris water maze test .Results Propofol with different exposure times could increase hippocampal TNF-αlevels(P<0.05,P<0.01);in P ( single ) group, active caspase-3 positive neurons in hippocampal pyramidal cell layer were much greater than control level only at postnatal day 7 ( P<0.05 ) , there were no changes of escape latency or platform crossing times compared with control ( P>0.05 );in P ( repeated ) group, active caspase-3 positive neurons were more significantly increased at postnatal day 13, 21 and 35 than those in control group ( P<0.01 ) , es-cape latency was increased or platform crossing times were decreased more significantly than control in Morris water maze test ( P <0.01 ); after etanercept was ad-ministered intracerebroventricularly , there were no sig-nificant changes of active caspase-3 positive neurons , escape latency and platform crossing times after propo-fol anesthesia compared with control ( P>0.05 ) .Con-clusion TNF-αmediates hippocampal neuronal apop-tosis and long-term cognitive impairment induced by propofol in neonatal rats , and long-term cognitive im-pairment may be related with persistent neuronal apop-tosis.

Objective To compare the impacts of four different intravenous anesthetic agents on middle cerebral artery blood flow velocity(V‐MCA) during the anesthesia induction period .Methods Totally 80 cases were randomly divided into four groups (n=20) ,maintenance drugs of anesthesia were propofol 2 .00 mg/kg ,etomidate 0 .30 mg/kg ,midazolam 0 .15 mg/kg and dezocine 0 .20 mg/kg respectively ,the bispectral index (BIS) value was dropping to below 50 ,the endotracheal intubation and mechanical ventilation were performed .The transcranial Doppler (TCD) monitoring was adopted to monitor and record middle cerebral artery mean flow velocity (Vm‐MCA) ,mean arterial pressure (MAP) ,heart rate (HR) ,systolic blood pressure (SBP) ,diastolic blood pressure (DBP) in the four groups before induction after entering operation room (T0 ) ,at1 min before intubation (T1 ) ,immediate intubation (T2 ) ,at 1 min after intubation (T3 ) ,3 min after intubation (T4 ) ,5 min after intubation (T5 ) .Results Except for the midazolam group ,Vm‐MCA at T1 in the other three groups were significantly lower that that in the T0 group (P< 0 .05);Vm‐MCA ,SBP ,DBP after intubation in the midazolam group and the etomidate group were significantly increased compared with the basic values ,while the difference between the propofol group and the dezocine group had no statistical significance (P>0 .05) .Con‐clusion midazolam and etomidate are weaker than propofol and dezocine in the aspect of inhibiting the middle cerebral arterial blood flow fluctuations caused by intubation .

Objective To compare landiolol and esmolol for treatment of intraoperative arrhythmia in dogs.Methods Experiment Ⅰ Eighty-eight KM mice (44 males, 44 females) , aged 4-6 weeks, were studied.The median lethal dose (LD50) and median effective dose (ED50) of landiolol and esmolol were determined using the sequential method.Treatment index (TI) was calculated.Experiment Ⅱ Eighteen dogs (9 males, 9 females), aged 8-12 months, weighing 7-10 kg, were equally and randomly divided into 3 groups: model group (group M) , landiolol group (group L) and esmolol group (group E).Intraoperative arrhythmia model was established by using gastrointestinal surgery combined with epinephrine.When sustained ventricular arrhythmias occurred, normal saline 0.5 ml/kg, landiolol 8.3 mg/kg and esmolol 10.0 mg/kg were given intravenously in C, L and E groups, respectively.The duration of arrhythmias was recorded.If bradycardia occurred (decrease in heart rate [HR] ≥ 25％ of the baseline value) , isoprenaline 0.05 mg/kg and atropine 0.03 mg/kg were injected intravenously.The occurrence of bradycardia after the initial administration of landiolol and esmolol, and the accumulated dose of landiolol and esmolol consumed when bradycardia occurred were recorded.Isoprenaline and atropine-induced improvement in bradycardia was recorded.Results Compared with esmolol, the LD50 and TI of landiolol were significantly increased (P＜0.01), and no significant change was found in ED50 of landiolol (P＞0.05).The duration of arrhythmias was significantly shorter in L and E groups than in group C, and in group L than in group E (P＜0.01).After the initial administration of landiolol and esmolol, the incidence of bradycardia was 0 and 100％, respectively, and the accumulated dose of landiolol and esmolol consumed when bradycardia occurred was (30± 13) mg/kg.Atropine could not effectively treat bradycardia, while isoprenaline could treat bradycardia.Compared with group L, the time for HR to rise and the duration for HR returning to the baseline value were significantly prolonged in group E (P＜0.05).Conclusion Compared with esmolol, landiolol provides faster improvement in intraoperative arrhythmia, weaker negative chronotropic effect, and higher safety;isoproterenol produces better efficacy in treating landiololinduced bradycardia in dogs.

ObjectiveTo explore the effects and underlying mechanisms of acid sensing ion channels (ASICs) on pain behavior in a rat model of post-incision pain.MethodsFifty-eight adult male Sprague Dawley rats were used in this study,four rats were used for immunofluorescence test,thirty rats were employed for pain behavior test,and twenty-four rats were used for Western blot.Rats used for pain behavior test and Western blot were randomly divided into 3 groups:control group ( C group),incision pain model group ( I group) and amiloride group (A group).Plantar skin of rats in A group were infiltrated with 20 μl(200 μg)amiloride solution.Paw withdrawal mechanical threshold(PWMT) and paw withdrawal thermal latency(PWTL) of all rats in pain behavior test was tested at 24 h preoperative,2 h,4 h,8 h,12 h,24 h postoperative.Western blot was tested at 4 h postoperative.ResultsImmunofluorescence test displayed ASIC3 was expressed in plantar skin of all rats.The basal level of PWMT and PWTL of all rats in three groups was C group( (23.15 ± 5.10) g,( 11.32 ± 1.21 ) s),I group ( (23.26 ± 5.69) g,( 11.75 ± 2.01 ) s),A group ( (23.63 ± 4.96 ) g,( 11.47 ± 1.96) s) respectively,which was no significantly difference (P ＞ 0.05 ).PWMT and PWTL of I group and A group was significantly lower than that of C group at all time points postoperative (P ＜ 0.05) ; PWMT and PWTL of A group was at 2 h( ( 13.75 ±3.25)g,(9.96±1.32)s),4h((14.05±3.75)g,(9.17±2.11)s),8 h((9.75 ±2.74)g,(8.11 ±1.22)s)postoperative,which was significantly higher than that of I group (P ＜ 0.05 ).Compared with that of C group,the level of pERK1/2 expression was significantly increased in I group at 4 h postoperative (P ＜ 0.05 ),which could be inhibited by amiloride local infiltration (P ＜ 0.05 ).ConclusionASIC3 can mediate incision pain in a rat model of post-incision pain,through pERK1/2 signaling pathway,which can be inhibited by amiloride.

ObjectiveTo investigate the role of the benzodiazepine receptor in the amnesic effect of propofol,etomicdate and ketamine in mice.MethodsTwo hundred and eighty-eight Kunming mice of both sexes weighing 18-23 g were randomly divided into 9 groups( n =32 each):gruup normal saline + normal saline (group NN); group normal saline+ fat emulsion (group NF); group flumazenil + normal saline (group FN); group normal saline + propofol (group NP) ; group flumazenil + propofol (group FP) ;group nomal saline + etomidate (group NE) ; group flumazenil + etomidate (group FE); group normal saline + ketamine (group NK) and group flumazenil + ketamine (group NK).Normal saline 10 ml/kg was given IP at 10 min before the tests,and normal saline 10 ml/kg,fat emulsion 10 ml/kg,propofol 25 mg/kg,etomidate 3 mg/kg and ketamine 20 mg/kg at 5 min before the tests in groups NN,NF,NP,NE and NK respectively.Flumazenil 1 mg/kg was given IP at 10 min before the tests,and normal saline 10 ml/kg,fat emulsion 10 ml/kg,propofol 25 mg/kg,etomidate 3 mg/kg and ketamine 20 mg/kg at 5 min before the tests in groups NN,NF,NP,NE and NK respectively.Darkness-avoiding test,platform-mounting test and Morris water maze test were performed to assess the cognition function.The latency of response and number of error were recorded in each test.ResultsPropofol,etomidate and ketamine significanfly shortened the duration of latency of response in platform-mounting test as compared with group NN.Etomidate also significantly increased the number of error in platform-mounting test as compared with group NN,while ketamine prolonged the duration of latency of response in Morris water maze test as compared with group NN.Flumazenil significantly counteracted the above action of the 3 intravenous anesthetics.ConclusionBenzodiazepine receptor may play an important role in the amnesic effect induced by propofol,etomidate and ketamine.

Objective To investigate the role of neurokinin-1 receptor (NK-1R) in the anti-nociceptive effect of enflurane, isoflurane and sevoflurane in mice. Methods Three hundred and twenty Kunming mice of both sexes weighing 20-25 g were randomly divided into4 groups (n =80 each): group normal saline (group NS);group enflurane (group E); group isoflurane (group I) and group sevoflurane (group S). Normal saline (NS) 1.0ml/kg, erflurane 0.5 ml/kg, isoflurane 0.4 ml/kg and sevoflurane 2.0 ml/kg were injected intraperitoneally in NS,E,I and S groups respectively. Each group was further divided into 4 subgroups receiving intrathecal NS 5 μl and Sar-SP (NK-IR agonist) 20, 40 and 80 ng respectively at 5 min after intraperitoneal injection of inhalation anesthetics. The anti-nociceptive effect of the inhalation anesthetics was assessed by tail flick latency (TFL) (the latency for removal of the tail from the path of heat source) and paw-licking time (PLT) after intraplantar formalin injection. Results lntraperitoneal enflurane, isoflurane and sevoflurane significantly prolonged TFL and shortened PLT. Intrathecal Sar-SP 20, 40 and 80 ng significantly shortened TFL dose-dependently but had no significant effeet on PLT as compared with control subgroup. Conclusion NK-1R is involved in the anti-nociceptive effect of enflurane, isoflurane and sevofluran on thermal pain but not chemical and inflammatory pain.

Objective To investigate the effects of propofol injected into rostral ventromedial medulla (RVM) on nociceptive responses and examine whether GABA_A resceptor is involved in the mechanism. Methods Sixty-four pathogen free SD rats of both sexes aged 2-3 months weighing 250-300 g were randomly divided into 4 groups ( n = 16 each): group I control (group C) ; group Ⅱ propofol (group P) ; group Ⅲ bicuculline (group B) and group Ⅳ B + P (group BP) . The animals were anesthetized with intraperitoneal 1% pentobarbital 50 mg/kg. Their heads were fixed with stereotactic apparatus. An tracar was inserted into RVM for microinjection of propofol and/or bicuculline. The noxious responses were evaluated by hot plate test (response latency was measured) and formalin test (intraplantar injection of 2.0% formalin 100 μl) . Pain was scored (0 = no pain, 3 = severe pain) . Results Both hot plate test and formalin test showed that hyperalgesia was induced by microinjection of propofol into RVM. In hot plate test hyperalgesia induced by injection of propofol (4μg/0.4μl) into RVM was antagonized at 20 min after microinjection of bicuculline (10 ng/0.4μl) into RVM. In formalin test pain scores were significantly lower at 1, 5,10,20,30,40,50 and 60 min after intraplantar formalin injection in group BP than in group P.Conclusion GABA_A receptor in RVM partially mediates propofol-induced hyperalgesia.

Aim To observe the effects of promethazine on the analgesia,hypnosis,amnesia and therapeutic index of isoflurane.Methods The experiments were designed to study promethazine on the analgesic effect of isoflurane by hot-plate test and writhing test,and to study the effect of promethazine on the sleeping time of isoflurane by the method of righting reflex,and the amnesia of isoflurane by Morris water maze,and the ED_(50),LD_(50) by sequential method in mice.Results The result of hot-plate test and writhing test indicated that promethazine could enhance the analgesic effect of isoflurane(P＜0.05 or P＜0.01);through the experiment of righting reflex, sleeping time of isoflurane in mice was extended by promethazine(P＜0.01);in Morris water maze experiment, the average latency in the combination of promethazine and isoflurane was longer than that of the promethazine group or isoflurane group(P＜0.05 or P＜0.01), while aiming to the residence time, the combination of the two was shorter than that in the third quadrant(P＜0.01 or P＜0.05),the TCPP of the group of isoflurance was more than that of the combination group;promethazine could decrease the ED_(50) of isoflurance(P＜0.01),but it did not obviously affect its LD_(50)(P＞0.05).Conclusion Promethazine can not only reinforce the effect of isoflurance on analgesia,hypnosis and amnesia, but also boost the therapeutic index of isoflurance.

Objective To investigate the effects of propofol on P2X7 receptor activition and IL-1β production induced by endotoxin in murine RAW264.7 macrophages. Methods RAW264.7 macruphages were treated with LPS (1 μg/ml) for 4 h to induce the production and release of IL-1β, and pretreated with BBG (specific P2X7 receptor antagonist) 1 μmol/L or propofol 1-100 μmol/L for 20 min before LPS stimulation, and IL-1β release was measured using ELISA kit. Whole-cell patch clamp technique was used to record the P2X7-gated currents induced by 1 mmol/L ATP, the cells were exposed to propofol with 1-1 000 -μmol/L for 4 min, and the IC_(50) level of propofol was achieved. Western blot technique was used to measure the production of pro-lL-1β protein and IL-1β protein intracellularly after LPS treatment for 4 h under different concentrations of propofol. Results IL-1β was released from RAW264.7 macrophages after LPS stimulation, which was decreased by propofol, and the IC_(50) level of propefol was (24±3) μmol/L. P2XT-gated currents were inhibited by propofol, and the IC_(50) level was (33±5) μmol/L. Pro-IL-1β protein intracellularly was up-regulated after LPS stimulation, and propofol with 3-100 μmol/L decreased the up-regulation of pro-IL-1β intracellularly induced by LPS. Conclusion Propefol could inhibit IL-1β release from RAW264.7 macrophages treated by LPS, which is mediated by inhibiting P2X7 receptor activition and decreasing the production of pro-IL-1β intracellularly.