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Objective:To study the pathogenesis and the risk factors of eye injury after non-ocular surgery in the patients underwent general anesthesia, and to provide the reference for its prevention, diagnosis and treatment.Methods:The clinical materials of two patients with eye injury after non-ocular surgery underwent general anesthesia were analyzed and the related literatures were reviewed.Results:A young woman patient underwent laparoscopic hysterectomy with general anesthesia while positioned Trendelenburg, the eyes were being closed naturally without protection, and corneal abrasion of both eyes occurred after operation.The lesion had completely resolved with no sequelae after treatment.An old man underwent cervical posterior laminoplasty with general anesthesia in prone position developed ischemic optic neuropathy (ION) after operation.The vision of the patients partly recovered after symptomatic treatment.Conclusion:Corneal abrasion is the most frequent ophthalmologic complication during general anesthesia, most of the patients have good prognosis.Postoperative visual loss (POVL) is the most severe ophthalmologic complication without effective treatment available, the delicate reasons and mechanisms are not totally clear, prevention outweighs treatment.
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Objective:To study the effect of isoflurane anesthesia on the hippocampal neuroapoptosis in the zincdeficient APP/PS1 transgenic mice,and to clarify its related mechanisms.Methods:The eight-month or ninemonth old APP/PS1 transgenic mice were randomly assigned to four groups (n=24):zinc adequate (ZA) group,the mice were given a standard diet for 2 months;zinc adequate+ isoflurane (ZA+ Iso) group,the mice were given a standard diet for 2 months then exposed to 1.4％ isoflurane for 2 h;zinc-deficient (ZD) group,the mice were given zinc deficient diet for 1 month;zinc deficient with isoflurane (ZD+Iso) group,the mice were given zinc deficient diet for 1 month and then exposed to 1.4％ isoflurane for 2 h.The hippocampus tissue of the mice were obtained 24 h after anesthesia.The immunofluorescence double staining was performed to measure the apoptotic rates of hippocampal neurons.The Western blotting method was used to detect the expression levels of Aβ and Cleaved caspase-3 and the ratio of Bax/Bcl-2.Results:Compared with ZA group,the apoptotic rate of neurons,the ratio of Bax/Bcl-2 and the expression level of Cleaved caspase-3 of the mice in ZA+Iso group were increased 6 h after isoflurane exposure (P＜0.05 or P＜0.01);but no differences were found in the apoptotic rate of neurons and the expression levels of total Aβ,Aβ40 and Aβ42 24 h after isoflurane exposure (P＞0.05).Compared with ZA group,the apoptotic rates of neurons,the ratios of Bax/Bcl-2,the expression levels of Aβ42 and Cleaved caspase-3 of the mice in ZD group and ZD+ Iso group were increased 6 and 24 h after isoflurane exposure (P＜0.05or P＜0.01).Compared with ZD group,the apoptotic rate of neurons,the expression levels of Aβ42,Bax/Bcl-2and Cleaved caspase-3 and the ratio of Bax/Bcl-2 of the mice in ZD+Iso group were elevated significantly 6 and 24 h after isoflurane exposure (P＜0.05 or P＜0.01).Conclusion:1.4％ isoflurane exposure for 2 h can induce the transient elevation of hippocampal neuroapoptosis in the ten-month old APP/PS1 transgenic mice.1.4 ％ isoflurane exposure for 2 h can significantly aggravate the hippocampal neuroapoptosis in the zinc-deficient APP/PS1 transgenic mice,it is probably associated with the hippocampal Aβ aggregation,activation of Bax and Caspase-3 and inhibition of Bcl-2.
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Objective To evaluate the effect of zinc deficiency factor on cognitive function after isoflurane anesthesia in mice with Alzheimer's disease (AD).Methods One hundred and forty-four APP/ PS1 transgenic mice with AD,weighing 22-28 g,aged 8-10 months,were divided into 6 groups (n=24 each) using a random number table:zinc adequate group (group ZA),zinc adequate plus isoflurane anesthesia group (group ZA+Iso),zinc deficiency group (group ZD),zinc deficiency plus isoflurane anesthesia group (group ZD+Iso),zinc treatment group (group ZT) and zinc treatment plus isoflurane anesthesia group (group ZT+Iso).The mice were fed a diet adequate in zinc and deionized water for 2 months in ZA and ZA+Iso groups.The mice were fed a diet low in zinc (0.01‰ zinc) and deionized water for 1 month in ZD and ZD+Iso groups.The mice were fed a diet adequate in zinc and 0.12‰ ZnSO4 · 7H2O water for 2 months in ZT and ZT+Iso groups.The mice underwent 2 h of anesthesia with 1.4％ isoflurane starting from the end of feeding in ZA+Iso,ZD+Iso and ZT+Iso groups.At 24 h after anesthesia,the mice were sacrificed and hippocampal tissues were obtained for determination of the contents of soluble amyloid beta protein 40 (Aβ40) and Aβ42 and insoluble Aβ40 and Aβ42 (using enzyme-linked immunosorbent assay) and expression of total Aβ,Aβ40,Aβ42,tau pSer396,tau pSer262 and tau pThr231 (by Western blot).Morris water maze test was performed at 24 h after anesthesia.Results There was no significant difference in each parameter between group ZA and group ZA+Iso and between group ZT and group ZT+Iso (P＞0.05).Compared with group ZD or group ZT+Iso,the escape latency was significantly prolonged,the space exploration time was shortened,the expression of hippocampal Aβ42,tau pSer396,tau pSer262 and tau pThr231 was up-regulated,and the contents of soluble and insoluble Aβ42 were increased in group ZD+Iso (P＜0.05 or 0.01).Conclusion Zinc deficiency can aggravate the impairment of cognitive function after isoflurane anesthesia in mice with AD,and the mechanism is related to the promotion of hippocampal Aβ aggregation and tau protein phosphorylation.
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Objective:To observe the influence of inhaled anesthetic isoflurane in the neuronal protein damage and aggregation in the APP transgenic mouse hippocampus,and to investigate the intervention effect of trehalose. Methods:Sixty APP transgenic mice aged 12 months were divided into control group,isoflurane group (Iso group) and trehalose group (Tre group)(n=20).The rats in control group were not given any drugs and were put into the anesthetic box with continuonsly entering 2 L·min-1 oxygen for 2 h;the rats in Iso group and Tre group were respectively injected intraperitoneally with 2 mL saline or trehalose (400 μg·kg-1 )30 min before anesthesia,and then inhalated 1.4% isoflurane for 2 h.6 h after anesthesia,the hippocampus tissue of the mice was prepared,and DCFH-DA fluorescence was applied to detect the reactive oxygen species (ROS)level; 24 h after anesthesia, immunohistochemical method and Western blotting method were used to detect the contents of carbonyl compounds and nitrotyrosine and the Aβ1-42 protein expression level in hippocampus;TEM was applied to observe the formation of protein aggregates; TUNEL staining was performed to observe the apoptotic rate of hippocampal neurons. Results:Compared with control group, the ROS level, the expression levels of oxidative protein carbonyl compounds and nitrotyrosine,the expression level of Aβ1-42 protein,and the apoptotic rate of hippocampal neurons in Iso group were significantly increased (P < 0.05);compared with Iso group,the ROS level,the expression levels of oxidative protein carbonyl compounds and nitrotyrosine,the Aβ1-42 protein expression level, and the apoptotic rate of hippocampal neurons in Tre group were significantly decreased (P < 0.05).Conclusion:Isoflurane can induce the protein damage and aggregation,the apoptotic rate of hippocampal neurons,aggravate oxidative stress reaction,increase the apoptotic rate of brain hippocampal neurons in the APP transgenic mice;trehalose can intervene the neurotoxicity induced by inhaled anesthetics.
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Objective To determine the risk factors for postoperative respiratory complications and establish a preoperative risk scoring system.Methods Patients,aged ≥ 18 yr,scheduled for elective surgery or undergoing emergency operation under total intravenous anesthesia or field block anesthesia,were studied.The general data of patients,preoperative SpO2,and conditions of respiratory infection,anemia or cough tests within 1 month before surgery were recorded.The operative sites (thorax,upper abdomen,other sites),duration of operation,type of surgery (emergency operation/elective operation),and methods of anesthesia (general anesthesia/field block) were also recorded.According to the development of respiratory complications within 1-7 days after operation,the patients were divided into either postoperative respiratory complication group or non-postoperative respiratory complication group.The risk factors of which P values were less than 0.05 would enter the multivariate logistic regression analysis to pick out the risk factors for postoperative respiratory complications and to establish a preoperative risk scoring system.Results Two thousand and thirty-seven patients completed the study.A total of 493 patients developed postoperative pulmonary complications,and the incidence was 24.20％.Statistical analysis showed that the risk factors associated with postoperative respiratory complications included age ＞ 50 yr,preoperative SpO2 ≤90％,high ASA physical status,duration of smoking ＞ 1 yr,positive cough tests,respiratory infections at one month before operation,preoperative anemia,upper abdominal and intrathoracic operations,duration of operation ＞ 2 h.A preoperative risk scoring system was established for postoperative respiratory complications based on 6 independent risk factors:preoperative SpO2,anemia,respiratory infections,age,duration of operation and operative sites.The incidence of postoperative respiratory complications was 61.9 ％,52.8 ％ and 17.2 ％ in high-risk,medium-risk and low-risk groups,respectively,and there was significant difference between the three groups (P ＜ 0.01).Area under the ROC curve was 90％ for subsamples and 87％ for the validation subsamples.Conclusion Age ＞ 50 yr,high ASA physical status,duration of smoking ＞ 1 yr,positive cough tests,preoperative SpO2 ≤90％,anemia,respiratory infections at one month before operation,duration of operation ＞ 2 h,upper abdominal and intrathoracic operations are risk factors for postoperative respiratory complications.A preoperative risk scoring system is successfully established for postoperative respiratory complications based on preoperative SpO2,anemia,respiratory infections,age,duration of operation and operative sites.
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Objective To investigate the time-dependent changes in glutamate (Glu) and 7-aminobutyric acid ( GABA) release in the rostral ventromedial medulla in a rat model of incisional pain. Methods Healthy male SD rats weighing 250-300 g were used in this study. Twelve rats in which microdialysis cannulae were implanted in the right rostral ventromedial medulla without neurological deficits were randomly divided into 2 groups ( n = 6 each): group A control and group B incisional pain. In group B an 1 cm long incision was made in the plantar surface of right hindpaw under 1.2% isoflurane anesthesia which was maintained for 5 min. Samples of dialysate were collected before incision (T_0 baseline) and at 3 h, 1 d, 2 d and 3 d after incision was made (T_(1-4)) in both groups for determination of Clu and GABA concentrations (by HPLC). Results In group B Glu and GABA concentrations in the dialysate were significantly increased at 1 d (T_2) and 3 h-3 d (T_(1-4)) respectively as compared with the baseline value at T_0 and were significantly higher than those in group A (control group). Conclusion Incisional pain increases the release of Glu and GABA in the rostral ventromedial medulla which might influence the function of descending pain modulation pathway.
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Objective To investigate the effect of norepinephrine infusion at 0.03-0.3 μg·kg-1 ·min-1 on renal function in patients undergoing kidney transplantation. Methods Thirty-two ASA Ⅲ or Ⅳ patients aged 22-64 yr weighing 44-88 kg undergoing kidney transplantation were studied. Dialysis was performed within 36 h before operation. Blood pressure was fairly stable. Combined spinal-epidural anesthesia (CSEA) was performed. Spinal anesthesia was performed at L2,3 interspace and hyperbaric 0.5% bupivacaine 10-15 mg was injected into the subarachnoid space. The upper level of sensory block measured by pin-prick reached T6. Epidural catheter was placed at T11,12 interspace and 1% ropivacaine was given intermittently. The patients were randomly allocated into preoperative baseline level (increase or decrease amplitude ＜ 10% of baseline level) by dopamine or norepinephrine infusion during operation. Venous blood samples and urine samples were obtained at the end of operation and 12 h after operation for determination of serum concentrations of cystatin C and β2-microglobulin and urine α1- and β2-microglobulin concentrations. Urine was collected and the volume was recorded. Meanwhile the consumption of furosemide administration during the 12 h after operation was recorded. Results The two groups were comparable with respect to age, M/F sex ratio, body weight, the volume of urine and fluid infused, and the consumption of furosemide. There was no significant difference in serum cystatin C and β2-microgiobulin and urine α1- and β2-microglobulin concentratious, urine volume and consumption of furosemide administration between the transplantation without adverse effect on kidney allograft function.
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Objective To evaluate the role of alpha4 beta2 neuronal nicotinic acetylcholine receptor in the inhibition of synaptic long-term potentiation (LTP) by isoflurane in the CA1 area of rat hippocampal slices.Methods Hippocampal slices (400 μm thick) were prepared from the brains of adult male SD rats, 2 months old, weighing 200-250 g, anesthetized with ether and decapitated. The slices were incubated in artificial cerebrospinal fluid (aCSF) at room temperature for at least 2 h before use. Seventy slices were randomly divided into 10 groups ( n = 7 each): Ⅰ LTP group in which the slices were perfused with aCSF; Ⅱ , Ⅲ and Ⅳ group in which the slices were perfused with aCSF containing isoflurane 0.125, 0.25 and 0.5 mmol/L respectively (group Ⅰ1-3 );Ⅴ and Ⅵ group in which the slices were perfused with aCSF containing epibatidine 0.1 and 1.0 μmol/L respectively (group E1.2 ); Ⅶ group epibatidine 0.1 μmol/L + isoflurane 0.25 mmol/L (group E1 + I2 ); Ⅷgroup epibatidine 1.0 μmol/L + isoflurane 0.25 mmol/L (group E2 + I2); Ⅸ group DHβE 0.1 μmol/L (group D); Ⅹ group DHβE 0.1 μmol/L + isoflurane 0.125 mmol/L (group D + I1 ). Population spikes (PS) were recorded for at least 30 min before LTP in each group. For LTP induction, high-frequency stimulation (HFS) was applied to the Schaffer collateral-commissural pathway of hippocampus and maintained for 15 min using a stimulating electrode.The changes in PS amplitude were analyzed at 5, 10, 15, 20, 25, 30, 40, 50 and 60 min after HFS in each group. Results Compared with group LTP, the PS amplitude was significantly decreased after HFS in group I1 ,I2, I3 , D, D + I1 and E1 + I2 ( P ＜ 0.05), while increased after HFS in group E1 .2 ( P ＜ 0.05 ), but no significant change was found after HFS in group E2 + I2 ( P ＞ 0.05). The PS amplitude was significantly decreased after HFS in group D + I1 compared with group I1 (P ＜ 0.05). The PS amplitude was significantly increased after HFS in group E1 + I2 and F2 + I2 compared with group I2 ( P ＜ 0.01 ). Conclusion Isoflurane inhibits LTP induction via inhibiting the activation of alpha4 beta2 nicotinic acetylcholine receptor in rat hippocampus.
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Objective To investigate the effect of isoflurane on the levels of protein kinase A (PKA) and protein kinase C (PKC) in hippocampus in rats. Methods Thirty-six 3-month-old male SD rats weighing 180-220 g were randomly divided into 3 groups ( n = 12 each): group Ⅰ underwent the cognitive function test without being pretreated with isoflurane inhalation (group C); group Ⅱ and Ⅲ inhaled 1.2% isoflurane for 4 h and underwent the cognitive function test 2 days and 2 weeks later respectively (group Ⅰso1,Iso2). Morris water maze was used to assess the cognitive function and the escape latency was recorded. The animals were killed immediately after the test.The hippocampus was isolated for determination of the expression and activities of PKA and PKC.Results The escape latency was significantly longer in group Ⅲ than in group Ⅰ.The expression of PKA and PKC was significantly down-regulated and the activities of PKA and PKC were significantly decreased in group Ⅱand Ⅲ as compared with group Ⅰ . There was no significant difference in the expression and activities of PKA and PKC between group Ⅱ and Ⅲ . Conclusion Four hour 1.2% isoflurane inhalation can decrease cognitive function by inhibiting the levels of PKA and PKC in hippocampus.
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0.05),but it was significantly lower than that in LTP group (P
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Objective To evaluate the effects of patient controlled analgesia(PCEA)on the perioperative changes of circulatory and pulmonary function of elderly with hypertensions after abdominal surgery.Methods Twenty-eight patients of ASAⅡ-Ⅲ aged more than 60 years undergoing uratomy were randomly divided into two groups:control group and PCEA group.Preoperative and postoperative circulatory and pulmonary functions were measured with noninvasion circulatory monitor and pocket lung function meter respectively.Results In control group,the systolic pressure,diastolic pressure,and heart rate increased by 19%,17% and 19%,respectively,as compared with preoperation.The percentage of forced vital capacity(FVC%),percentage of forced expiratory volume in first second to forced vital capacity(FEV1%) and percentage of maximal ventilatory volume(MVV%) of postoperation in control group were significantly decreased compared with preoperation(P
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Objective To investigate the effect of ketamine on the synaptic long-term potentiation(LTP) in the CA1 area of rat hippocampal slices,and to elucidate the mechanisms underlying the effect of ketamine on memory.Methods Hippocampal slices(400 ?m thick) were obtained from the brains of male Sprague-Dawley rats(2 months old) weighing 200-250 g that were decapitated.The slices were incubated in artificial cerebrospinal fluid(ACSF) at room temperature for at least 120 min before use.Forty-nine slices were randomly divided into 7 groups(n=7):control group,ketamine 1,5,10,30,50 and 100 ?mol?L-1 groups.All the slices in each group were perfused with ACSF,ketamine 1,5,10,30,50 or 100 ?mol?L-1,respectively.The slices in each group were performed to record evoked population spikes(PS) using extracellular microelectrode recording technique.Another forty-nine slices were randomly divided into 7 groups(n=7):LTP group,ketamine-LTP 1,5,10,30,50 and 100 ?mol?L-1 groups.All the slices in each group were perfused with ACSF,ketamine 1,5,10,30,50 or 100 ?mol?L-1,respectively.PSs were recorded for at least 30 min before LTP in each group.For LTP induction,high-frequency stimulation(HFS) conditioning pulses(100 Hz?s-1) were applied to the Schaffer collateral-commissural pathway of hippocampus using a bipolar stimulating electrode.The changes in PS amplitude after HFS were analyzed in each group.Results The PS amplitude of the rat hippocampal slices in ketamine 1,5,and 10 ?mol?L-1 groups had no significant difference compared with control group.The PS amplitude in ketamine 30,50 and 100 ?mol?L-1 groups decreased compared with control group(P
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Objective To investigate the analgesic effect of adenosine A1 receptor agonist R( - )-N6-(2-phenylisopropyl)-adenosine (R-PIA) administered into the brainstem medial pontine reticular formation (mPRF) and the underlying mechanism. Methods Sixty male SD rats aged 8-10 weeks weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal 10% chloral hydrate 300 mg?kg-1 .A 24-gauge stainless steel cannula was inserted into mPRF on one side using a stereotaxic apparatus. One week after operation the animals were randomly divided into 12 groups ( n=5 each) : groupⅠcontrol; groupⅡR-PIA 0.5?g; groupⅢR-PIA 1.0?g; groupⅣR-PIA 2.0?g; groupⅤtheophylline (an adenosine receptor antagonist) 5.0?g; groupⅥ8-cyclopentyl-1 ,3-dipropylxanthine (DPCPX, an adenosine A, receptor antagonist) 1.0?g; groupⅦglibenclamide (an ATP-sensitive K+ channel blocker) 5.0?g; groupⅧ4-aminopyridine (4-AP, a voltage dependent K+-channel blocker) 5.0?g; groupⅨtheophylline 5.0?g + R-PIA 2.0?g; groupⅩDPCPX 1.0?g + R-PIA 2.0?g; groupⅪglibenclamide 5.0?g + R-PIA 2.0?g and groupⅫ4-AP 5.0?g + R-PIA 2.0?g. All the drugs were injected into mPRF in 0.3?l of normal saline. In groupⅨ-ⅫR-PIA 2.0?g was administered 15 min after pretreatment with theophylline, DPCPX, glibenclamide or 4-AP. Analgesia was determined using the tailflick latency (TFL) (the time between the onset of the radiant heat stimulus and voluntary tail withdrawal) at 5, 15, 30, 45, 60 and 90 min after R-PIA injection into mPRF. The pain threshold was expressed as percentage of the maximal possible effect ( MPE) : MPE = (TFL after drug - baseline TFL)/( 10.0 -baseline TFL)?100% .Results R-PIA 0.5-2.0?g injected into mPRF produced significant analgesia in a dose-dependent manner. Pretreatment with theophylline or DPCPX completely reversed the analgesic effect of R-PIA while pretreatment with glibenclamide or 4-AP only partially reversed the analgesic effect of R-PIA.Conclusion R-PIA administered into mPRF produces analgesia through activation of both ATP-sensitive and voltage-dependent K+ -channel in mPRF.
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Objective To investigate the effect of propofol on the activation of NF-?B and the expression of Bcl-2 and Caspase-3 gene in cerebral cortex after transient focal cerebral ischemia-reperfusion (I/R) and the possible mechanism. Methods Ninety healthy male Wistar rats aged 3-4 months weighing 250-300g were randomly divided into 3 groups (n=30 each) : group Ⅰ sham operation; group Ⅱ I/R and group Ⅲ propofol + I/R. The animals were anesthetized with intraperitoneal chloral hydrate 300 mg?kg-1. Left common, internal and external carotid arteries (CCA, ICA, ECA) were exposed. Middle cerebral artery occlusion (MCAO) was produced by inserting a nylon thread, 0.26-0.28 mm in diameter and 4.0 cm in length into ICA and advancing it cranially until resistance was felt. After 2 h MCAO the nylon thread was withdrawn to allow reperfusion. In propofol group propofol 100 mg?kg-1 was given IP 10 min before MCAO. The animals were decapitated at 2, 3, 6, 12, 24 and 72 h of reperfusion (n=5 at each time point in each group) . Their brains were immediately removed for determination of translocation of NF-?B in the neurons (by immuno-histochemistry) and expression of NF-?B in cerebral cortex (by Western blotting). The expression of Bcl-2 mRNA and Caspase-3 mRNA in cerebral cortex was determined by in situ hybridization. Neurological deficit was scored and microscopic examination of ischemic cerebral cortex was performed at 24 h of reperfusion. Results In I/R group (Ⅱ) NF-?B was significantly translocated from cytoplasm into the nucleus of the neurons in the ischemic cerebral cortex during 2-24 h of reperfusion while in non-ischemic cortex NF-?B was confined to the cytoplasm. The expression of NF-?B, Bcl-2 mRNA and Caspase-3 mRNA was significantly higher in ischemic cortex than in non-ischemic cortex. Neurologic deficit scores were higher in I/R group than in sham-operation group. Microscopic examination showed congestion and edema of ischemic cerebral cortex and degeneration and necrosis of the neurons in I/R group. In group Ⅲ propofol pretreatment significantly inhibited the translocation of NF-?B, decreased expression of NF-?B and Caspase-3 mRNA and increased Bcl-2 mRNA expression as compared with I/R group (Ⅱ) . Neurologic dificit and histologic damage induced by I/R were significantly ameliorated by propofol pretreatment. Conclusion Propofol pretreatment can inhibit apoptosis of neurons induced by I/R by inhibiting the activation of NF-B, up-regulating Bcl-2 gene and down-regulating Caspase-3 gene.