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Objective To investigate the effect of nalmefene on the cerebral ischemia-reperfusion (I/R) injury in rats.Methods Forty-eight male Sprague-Dawley rats, aged 3-4 months, weighing 220260 g, were randomly allocated to control group (group C), sham operation group (group S), cerebral I/R group (group I/R), or nalmefene group (group N) using a random number table, with 12 rats in each group.Cerebral I/R was induced by occlusion of bilateral common carotid arteries for 20 min followed by reperfusion.Group C received no treatment.Group S underwent 20 min exposure of bilateral common carotid arteries and then received suture.In group N, nalmefene 0.1 mg/kg was injected intraperitoneally immediately after reperfusion.At 6, 24 and 72 h of reperfusion, venous blood samples were collected for determination of the concentrations of S-100β protein and neuron-specific enolase (NSE) in plasma by enzyme-linked immunosorbent assay.After the last blood sampling, the rats were sacrificed, and brains were removed for determination of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) contents in brain tissues by enzyme-linked immunosorbent assay.Results Compared with group C, the plasma S-100β protein and NSE concentrations at each time point of reperfusion, and TNF-α and IL-1βcontents in brain tissues were significantly increased in S and I/R groups (P＜0.01).Compared with group S, the plasma S-100β protein and NSE concentrations at each time point of reperfusion, and TNF-α and IL-1β contents in brain tissues were significantly increased in group I/R (P＜0.01).Compared with group I/R, the plasma S-100β protein and NSE concentrations at each time point of reperfusion, and TNF-α and IL-1β contents in brain tissues were significantly decreased in group N (P ＜ 0.01).Conclusion Nalmefene can mitigate cerebral I/R injury in rats.
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Objective To evaluate the effect of intraperitoneal desferroxmine on the postoperative cognitive function of aged rats.Methods Twenty-four male Sprague-Dawley rats,aged 15-18 months,weighing 490-550 g,were randomly divided into 3 groups (n =8 each) using a random number table:control group (group C),operation group (group O),and desferroxmine group (group D).Exploratory laparotomy was performed after anesthesia in O and D groups.In group D,desferroxmine was injected intraperitoneally (100 mg/kg per time,each time lasting for 12 h) for 7 consecutive days,starting from 7 days before operation,while the equal volume of normal saline (100 ml/kg) was given in group O.All the rats underwent Morris water maze test at 3 days after operation,and the escape latency and frequency of crossing the original platform were recorded.The rats were then sacrificed and the hippocampus was removed for detection of ferritin expression.Results Compared with group C,the escape latency was significantly prolonged,the frequency of crossing the original platform was decreased,and ferritin expression was up-regulated in group O,and no significant changes were found in each parameter mentioned above in group D.Compared with group O,the escape latency was significantly shortened,the frequency of crossing the original platform was increased,and ferritin expression was down-regulated in group D.Conclusion Intraperitoneal desferroxmine 100 mg/kg (injected for 7 consecutive days) before operation can improve the postoperative cognitive function of aged rats.
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Objective To evaluate the effect of deferoxamine on learning and memory ability in aged rats.Methods Forty-two healthy male Sprague-Dawley rats,aged 18 months,weighing 450-550 g,were randomly divided into 2 groups (n =21 each) using a random number table:normal saline group (group N) and deferoxamine group (group D).In group D,deferoxamine 150 mg/kg was injected intraperitoneally once a day for 6 consecutive days,while the equal volume of normal saline was given instead in group N.Morris water maze test was conducted at 2 h after each injection on that day,lasting for 6 days.The escape latency,swimming speed,time of staying at the original platform quadrant and time spent in the central region were recorded.Hippocampal ferritin expression was detected by Western blot before the first administration and at 2 h after 3rd and 2nd administration.Results Compared with group N,the escape latency was significantly shortened,and the percentage of the time of staying at the original platform quadrant and time spent in the central region was increased,the expression of hippocampal ferritin was down-regulated,and no significant change was found in the swimming speed in group D.Conclusion Deferoxamine can enhance the learning and memory ability in aged rats,and reduced iron deposition in hippocampi is involved in the mechanism.
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Objective To evaluate the effect of ulinastatin on brain injury induced by lipopolysaccharide (LPS) in mice.Methods Ninety adult male C57 mice,aged 3-4 months,weighing 200-300 g,were randomly divided into 3 groups (n =30 each) using a random number table:control group (C group),LPS group and ulinastatin group (U group).Group U received intraperitoneal injection of ulinastatin 10 000 U/kg,while group L received the equal volume of normal saline,and 10 min later brain injury was produced with LPS 1 μg/g injected into the cerebral ventricle.Ten animals were chosen and blood samples were taken for determination of plasma concentrations of S100β protein and neuron-specific enolase (NSE) at 1,3 and 7 days after LPS injection.Then the animals were sacrificed and hippocampal tissues were obtained for determination of interleukin-1β (IL-1 β) and tumor necrosis factor-α (TNF-α) contents and IL-1β mRNA and TNF-α mRNA expression.Results Compared with C group,the plasma concentrations of S100β protein and NSE and contents of IL-1β and TNF-α were significantly increased at 1,3 and 7 days after LPS injection,and IL-1β mRNA and TNF-α mRNA expression was up-regulated at 1 and 3 days after LPS injection in LPS and U groups.Compared with group LPS,the plasma concentrations of S100β protein and NSE and contents of IL-1β and TNF-α were significantly increased,and IL-1β mRNA and TNF-α mRNA expression was down-regulated at 1 and 3 days after LPS injection in group U.Conclusion Ulinastatin can attenuate brain injury induced by LPS in mice,and the mechanism is related to inhibited inflammatory responses.
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Objective To investigate the effect of surgical trauma on the cognitive function and activation of microglias in hippocampus in rats of different ages.Methods Seventy-two male Sprague-Dawley rats,aged 3-4months,were randomly allocated into 2 groups:adult control group (n =30) and adult surgery group (n =42).Seventy-two male Sprague-Dawley rats,aged 18-20 months,were randomly allocated into 2 groups:aged control group (n =30) and aged surgery group (n =42).The rats were anesthetized with 5% chloral hydrate 4-6 ml/kg and underwent exploratory laparotomy in surgery groups,while normal saline 1 ml/kg was injected intraperitoneally in control groups.Morris water maze test was performed at 1-7 days after surgery.Fear conditioning test was performed 1 day after surgery to evaluate the space and fear memory abilities.The animals were sacrificed on 1st,3rd and 7th days after surgery and hippocampi were removed for measurement of OX42 expression in microglias by immunohistochemistry.Results Compared with adult control group,the percentage of freezing time in total time was significantly decreased,and OX42 expression in microglias was up-regulated on 1st day after surgery (P ＜ 0.05),and no significant change was found in the escape latency and the number of crossing the original platform in adult surgery group (P ＞ 0.05).Compared with aged control group,the escape latency was significantly prolonged,the number of crossing the original platform was decreased,the percentage of freezing time in total time was decreased,and OX42 expression in microglias was up-regulated on 1st and 3rd days after surgery in aged surgery group (P ＜0.05).Conclusion Surgical trauma decreases fear memory ability,but exerts no effect on the space memory ability in adult rats.Surgical trauma decreases the space and fear memory abilities in aged rats,which maybe related to activation of microglias in hippocampus.
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Objective To evaluate the effect of surgical trauma on the cognitive function and expression of hepcidin and ferroportin 1 (FP1) in hippocampus in aged rats.Methods One hundred male Sprague-Dawley rats,aged 18 months,weighing 400-500 g,were randomly divided into 2 groups with 50 rats in each group:control group (group C) and surgical trauma group (group ST).The rats were anesthetized with chloral hydrate,but underwent no operation in group C.The rats Were anesthetized with chloral hydrate and underwent 30 min of modified exploratory laparotomy in group ST.Ten rats were chosen from each group at 24 h after operation and the cognitive function was assessed using Morris water-maze test for 6 consecutive days.Ten rats were sacrificed on 1st,3rd,5th and 7th days after beginning of Morris water-maze test and brains were removed for determination of hepcidin and FP1 expression in hippocampus by PCR and Western blot.Results Compared with group C,the escape latency was significantly prolonged,the time of staying at the original platform quadrant and frequency of crossing the original platform were decreased on 3rd,4th and 5th days after beginning of Morris water-maze test,and the expression of hepcidin was up-regulated and the expression of FP1 was down-regulated at each time point in group ST (P ＜ 0.05).Conclusion Surgical trauma can decrease the cognitive function in aged rats and the mechanism may be related to up-regulation of hepcidin expression and down-regulation of FP1 expression in hippocampus.
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Objective To investigate the effect of dexamethasone on the postoperative cognitive function in rats.Methods One hundred and eighty Sprague-Dawley rats,aged 18-20 months,weighing 400-600 g,were randomly allocated into 3 groups (n =60 each)∶ control group (C group),surgery group (S group) and dexamethasone group (D group).In groups S and D,the rats were anesthetized with 5％ chloral hydrate 4-6 ml/kg and underwent abdominal surgery.The rats in group D received intraperitoneal injection of dexamethasone 10 mg/kg at the beginning of anesthesia,while the rats in group C underwent no surgery and received intraperitoneal injection of normal saline 1 ml/kg instead.Six rats in each group were chosen at 3 h and 7 days after surgery and sacrificed,and their brains were immediately removed for detection of the expression of OX42 (a specific marker for activation of microglia) in hippocampus.Another 6 rats in each group were chosen at 3 h,and 1,3 and 7 days after surgery and sacrificed,and their brains were immediately removed for detection of the expression of IL-1β mRNA and TNF-α mRNA in hippocampus.Cognitive function was assessed by Morris water maze test and fear conditioning test.Results Compared with group C,the escape latency was prolonged,the frequency of crossing the original platform was decreased,the postoperative freezing time was shortened,and the expression of OX42 after surgery and IL-1β mRNA and TNF-α mRNA at 3 h and 1 and 3 days after surgery was up-regulated in groups S and D (P ＜ 0.05 or 0.01).Compared with group S,the escape latency was shortened,the frequency of crossing the original platform was increased,the postoperative freezing time was prolonged,and the expression of OX42 at 3 h after surgery and IL-1β mRNA and TNF-α mRNA at 3 h and 1 and 3 days after surgery was down-regulated in group D (P ＜ 0.05 or 0.01).Conclusion Dexamethasone can inhibit the over-activation of microglia and reduce the inflammatory response,thus improving cognitive function in rats.
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AIM: To study the effects of tumor necrosis factor-α (TNF-α) on the transcriptional activity of nuclear factor-erythroid 2-related factor 2 (Nrf2) in pulmonary microvascular endothelial cells. METHODS: Rat pulmonary micro-vascular endothelial cells (PMVECs) were cultured by lung tissue block pasted methods, and identified immunocytochemically using Ⅷ factor-related antigen. The cells were treated with different doses TNF-α (prepared in serum-free medium) for 4 h. Subcellular localization and levels of Nrf2 in PMVECs were observed with immunocytochemical methods. Nuclear extract were obtained to assayed transcriptional activity of Nrf2 with EMSA. Total RNA were isolated to assay the mRNA expression of Nrf2 by RT-PCR. RESULTS: The protein level of Nrf2 in the nuclei and transcriptional activity increased dose-dependently in PMVECs after treated with TNF-α at concentrations of 2.5, 5.0 or 10.0 μg/L. However, the protein level of Nrf2 in nuclei and transcriptional activity decreased dose-dependently in PMVECs after treated with TNF-α at concentrations of 20 or 40 μg/L. No different mRNA expression of Nrf2 in PMVECs treated with TNF-α at all concentration above was observed. CONCLUSION: Transcriptional activity of Nrf2 increases in PMVECs treated with low or moderate doses of TNF-α and decreases in PMVECs treated with high doses of TNF-α.
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Objective To explore the effect of isofluranee on receptor for advanced glycation end products (RAGE) expression of hippocampus and learning and memory function in rats. Methods 24-month Sprague-Dawley male rats (n=45) and 4-month Sprague-Dawley male rats (n=45) were randomly divided into six groups with 15 rats each group. Group C1 (aged control group),group C2(adult control group) breath 30% oxygen and air mixed gas; Group S1(single inhalation of isoflurane aged group),Group S2(single inhalation of isoflurane adult group)were anesthetized with 1.5% isoflurane,breath 30% oxygen and air mixed gas for 2h;Group R1(Repeated inhalation of isoflurane aged group), group R2(Repeated inhalation of isoflurane adult group) were anesthetized with 1.5% isoflurane,breath 30% oxygen and air mixed gas 2h a day for three days. Eight rats randomly selected from each group were killed and their hippocampus were immediately isolated for detection of RAGE expression by immunohistochemistry and RT-PCR after accomplished treatment 24h. The remained rats' learning and memory function were assessed using Morris water-maze test. Results The results of Morris water-maze test showed that the times of acerossing the original platform and the time consumption of staying the original platform quadrant was shorter in group S1 and group R1,but the escape latency was longer than group C1(escape latency C1 (9.42± 2.63)s,S1(13.20±3.85)s,R1(17.20±3.44)s, F=12.773, P<0.05). In the group R2,the escape latency was longer but the times of accrossing the original platform and the time consumption of staying the original plat-form quadrant was shorter than group C2 (times of accrossing the original platform C1(7.30±2.40), S1(3.90± 2.42),R1(3.44±2.40), F=7.448, P<0.01).To contrast with the group C2,there were no significant differ-enees in spatial probe test in the group S2(P>0.05). The levels of mRNA and protein of RAGE in hippocampus was significantly higher in group S1 and group R1 than group C1(RAGE mRNA expression C1(0.11±0.02),S1 (0.56±0.09), R1(0.73±0.14), F=179.447, P<0.01). To contrast with the group C2, there were no differ-ences found in the levels of mRNA and protein of RAGE in group S1(P>0.05), but it was higher in the group R2 (RAGE mRNA express C2(0.22±0.04), R2 (0.41±0.08), F=40. 209, P < 0. 01). Conclusion Isoflurane can reduce learning and memory function in both aged and adult rats, but aged rats are particularly significant im-pacted. This effect may be induced by the increase of RAGE expression in hippocampas.
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Objective To investigate the effects of isoflurane on receptor for advanced glycation endproducts (R(A)GE) expression in the hippocampus in rats. Methods Forty-five male 4-month-old and 45 male 24-month-old rats were used in this study. The animals were divided into 2 age groups ( n = 45 each): the aged group (group O) and the adult group (group A). Each group was further divided into 3 subgroups ( n = 15 each):Ⅰ control subgroup (group OC,AC) inhaled 30% O2 in air; 1 single isoflurane inhalation subgroup (group OS,AS) inhaled 1.5 % isoflurane for 2 h and Ⅲ repeated isoflurane inhalation subgroup (group OR, AR) inhaled 1.5 % isoflurane 2 h per day for 3 days. One day after isoflurane inhalation, learning and memory function was assessed using Morris water maze test in 8 animals in each subgroup. The rest of each subgroup were killed and their hippocampi were immediately isolataed for detection of RAGE mRNA and protein expression by RT-PCR and immuno-histochemistry. Results The cognitive function was impaired after signle or repeataed isoflurane anesthesia as compared with control animals in both aged and adult groups. The expression of RACE mRNA and protein in hippocampus was significantly increased after either single or repeated isoflurane anesthesia in aged group but only after repeated isoflurane anesthesia in adult gpoup. There was no significant difference in RAGE mRNA and protein expression in the hippocampus between control and single isoflurane inhalation animals in adult group. Conclusion Isoflurane can reduce learning and memory function in both aged and adult rats by increasing RAGE expression in hippocampus especially in aged rats.
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Objective To investigate the effects of inhalation of different concentrations of isoflurane on the expression of cytochrome c ( Cyt c) in hippocampus in aged rats.Methods Sixty-three aged male SD rats (20 months) weighing 500-600 g were randomly divided into 3 groups(n=21each):control group inhaling 30%O2 for 2h (group C) and 2 isoflurane groups anesthetized with 0.75 % and 1.5 % isoflurane in 30 % O2 for 2 h respectively (group Ⅰ1 and Ⅰ2 ).Arterial blood samples were obtained from 5 rats at 30 min, 1 and 2 h of anesthesia for blood gas analysis. Eight animals were killed at 24 h after anesthesia in each group.Their hippocampi were immediately removed for determination of Gyt c expression by immuno-histochemistry and Western blot analysis.Cognitive function was assessed by Morris water maze test the day before experiment and once a day for 6 consecutive days starting from the 1st postoperative day.Results The Cyt c expression in hippocampus was significantly increased in Ⅰ1 and Ⅰ2 groups in a concentration-dependent manner as compared with group C.The escape latency was significantly prolonged and the frequency of crossing the original platform and the duration of staying at the original platform quadrant were decreased in group Ⅰ1 and Ⅰ2 compared with group C.Conclusion Inhalation of isoflurane anesthesia can decrease cognitive function through up-regulating the Gyt c expression in hippocampus in aged rats.
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BACKGROUND: Not only can auditory evoked potential (AEP) reflect electric activities of cerebral cortex and subcortex, but also have dose-effect relationship with many sorts of anesthesia agents; it is a relatively good index for monitoring anesthesia depth at present.OBJECTIVE: To analyze target controlled infusion propofol by auditory evoked potentials index during anaesthesia.DESIGN: Patients with operations were taken as objects in the randomized controlled trial.SETTING: Department of Anesthesia of Southwest Hospital of the Third Military Medical UniversityPARTICIPANTS: A total of 16 patients, with selective simply laparoscopic cholecystectomy, admitted to Department of Anesthesia of Southwest Hospital from October to November 2003, were selected and randomly divided into normal control group and auditory evoked potential index monitoring group with 8 in each group. The baseline information of the patients, such as gender, age, weight and operating time etc., was similar between the two groups (P ＞ 0.05).METHODS: Same anesthesia induction method was conducted on the patients in both groups; anesthesia was maintained with propofol (10 g/L) according to ALARIS P6003 pump calculation in the two groups; age, weight and target concentration of propofol (4 mg/L) was regulated according to clinical experience, while, in auditory evoked potential monitoring group,the concentration value of propofol in effective site was regulated by maintaining auditory evoked potential index between 15 and 30. Non-invasive blood pressure, heart rate and AAI were monitored at the moment of reposing for 10 minutes after entering operating room (T0), eyelash reflex disappearing after anaesthesia induction (T1), trachea intubation (T2), 3 minutes after intubation (T3), boring abdomenal holes (T4), 30 minutes after aeroperitonia steady (T5), observer's assessment of alertness and sedation (OAA/S) ≥4 at the end of operation (T6).MAIN OUTCOME MEASURES: ① Comparison of dosages of anaesthetia agents between the two groups. ② Changes of hemodynamics and auditory evoked potential index at each phase point. RESULTS: According to intention to treat analysis, all the 16 patients entered results analysis. ①Comparison of dosages of anesthesia agents between the patients in each two: The actual dosage of propofol in auditory evoked potential monitoring group was significantly lower than that in normal control group [(247.25±37.11), (337.38±36.72) mg, P ＜ 0.05], while the dosages of fentanyl and vecuronium bromide were no differences between two groups (P ＞ 0.05). ② Changes of hemodynamics and auditory eyoked potential index at each phase points of the two groups: Changes of hemodynamics at each phase points were similar between the two groups (P ＞ 0.05). Compared with T0 phase, there was no significant difference in auditory evoked potential index between the two groups in T1, T2 and T3 phases (P ＞ 0.05), however, in T4 and T5 phases, auditory evoked potential index in auditory evoked potential monitoring group was remarkably higher than that in normal control group (28.50±6.19, 21.25±4.06; 28.00±5.66,20.75±3.41; P ＜ 0.05). All patients had no awareness during the operation. CONCLUSION: Auditory evoked potential index is a new indicator for monitoring anesthesia depth, which can be helpful to regulate and control depth of anesthesia so as to avoid awareness and recall during general anesthesia.
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Objective To clarify the effective location of propofol in central nervous system (CNS) by detection of the c-jun expression after propofol-induced anesthesia in rats. Methods Wistar rats were randomly divided into 6 groups: normal control (C), low-dose propofol group (50 mg/kg, P 1), middle-dose propofol group (100 mg/kg, P 2), high-dose propofol group (150 mg/kg, P 3), stimulation with tail broken group (S 1), and propofol + stimulation with tail broken group (S 2). The expressions of nucleoprotein JUN in the CNS were detected by immunohistochemisty. Results Rather weakly stained nucleoprotein JUN positive neurons were observed in the supraoptic nucleus, lateral septal nucleus, and lateral habenular nucleus in the control group. In groups P 1, P 2, and P 3, the expressions of nucleoprotein JUN were increased significantly as compared with those in the control group. The expressions were mainly located in the accumbent nucleus, lateral septal nucleus, periventricular hypothalamic nucleus, ventral lateral geniculalaten nucleus, dorsal lateral geniculate nucleus, supraoptic nucleus, suprachiasmatic nucleus, anteroventral preoptic nucleus, nucleus of the solitary tract, supramammillary nucleus, basolateral amygdaloid nucleus, paraventricular thalamic nucleus, lateral habenula nucleus, and islands of Calleja. The expressed positive neuron number was positively correlated with the doses of propofol. Conclusion Propofol anesthesia has the determined sites of action in rat CNS.
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Objective To investigate the variation of fentanyl concentration and the gene expression and activity of rat intestinal cytochrome P450 3A1 in anhepatic phase. Methods The experiment was comprised of 2 steps. Step 1: The rats were randomly divided into experimental group (group A2, underwent occlusion of the hepatic portal) and control group (group A1), with 10 rats in each group. Fentanyl blood concentration was analyzed by LC/MS/MS. Step 2: The rats were randomly divided into group B1 (control), group B2 and group B3 (the rats underwent devascularization of the hepatic portal for 30 or 60 min). The levels of CYP3A1 in rat small intestine were assessed with RT-PCR and the enzymic activity of CYP3A1 was detected by fluorometry. Results Fentanyl concentration in anhepatic phase dropped more slowly in group A2 than group A1 (P
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Objective To study the possible mechanisms of aprotinin in the protection of platelets. Methods Cytosolic free calcium concentration ([Ca 2+ ]i) was determined in calcium fluorescent indicator Fura 2/AM loaded washed human platelets by using dual wavelength spectrofluorophotometer. The mean value of resting [Ca 2+ ]i and the changes of [Ca 2+ ]i response to thrombin and aprotinin were observed. Results In the presence of extracellular Ca 2+ at the dose of 1 mmol/L, the resting level of [Ca 2+ ]i in platelets of human was (151.840?28.719) nmol/L. Thrombin stimulated the rise in [Ca 2+ ]i in the presence of Ca 2+ at the dose of 1 mmol/L, and the effects were inhibited by aprotinin in a concentration dependent manner ( P
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0.05). ② The depth of anesthesia: the value of AEP index in AEP index group was significantly higher than that in control group ( P
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Objective To investigate the clinical value of aprotinin blood anesthesia in the radical excision of esophageal carcinoma. Methods A total of 90 patients with esophageal carcinoma undergoing radical excision were divided into two groups according to using aprotinin or not. Patients in experiment group (group A, 40 patients) were injected with 1 112 EPU aprotinin followed by constant pumped infusion of 278 EPU/h until 2 h after operation. Patients in the control group (group B, 50 patients) were treated with constant pumped infusion of 0.9% saline. The venous blood was collected for blood routine examination, thromboelastography(TEG) and normal coagulable function test at the following time points: before induction, at 2 h and 4 h after the beginning of operation, at the end of operation and at 12 h after operation. The changes of TEG and normal coagulable state were monitored during the whole surgical process. The intraoperative volume of hemorrhage, perioperative transfusion rate and average volume of transfusion in the two groups were compared. Results The preoperative coagulable state in experiment group was kept relatively stable during the operation. Volume of intraoperative hemorrhage, perioperative transfusion rate and average volume of blood transfusion in experiment group were significantly lower than those in the control group. Conclusion Aprotinin blood anesthesia can stabilize the coagulable state, reduce the volumes and rates of hemorrhage and transfusion, and hence can find wide application in the radical excision of esophageal carcinoma.
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Objective To assess the protective effect of remifentanil on cultured human hepatocytes against anoxia-reoxygenation injury. Methods Cultured hepatocytes were divided into 5 groups: group C receiving normoxia as control; groups AR, R, CH, R+CH receiving 15-hour xypoxia followed by 5-hour reoxygenation (group R receiving 5 ng/ml remifentanil, group CH 10 ?mol/L chelerythrine, group R+CH 5 ng/ml remifentanil and 10 ?mol/L chelerythrine before reoxygenation). The content of MDA in the hepatocyte mitochondria were measured. The rate of apoptotic cells was measured by flow cytometry. The expression of protein kinase C mRNA was measured by RT-PCR. Results Anoxia-reoxygenation caused dramatic increase in the content of MDA, the rate of apoptotic cells and the expression of protein kinase C mRNA. The three indexes mentioned above of groups R and CH were between that of groups C and AR (P
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Objective To clarify the effective location of propofol in central nervous system (CNS). Methods Forty-two Wistar rats were ramdomized into control group,50 mg/kg propofol,100 mg/kg propofol,150 mg/kg propofol,tail shearing,propofol followed by tail shearing (n=7 in each group). The NOS expressions in the CNS were recorded by NADPH-d histochemistry after anesthesia by intraperitoneal injection of propofol. Results Rather widely stained NOS positive neurons were observed in the control group. In propofol groups,the NOS expressions were decreased significantly as compared with the control group,mainly located in ACB,LS,Pe,VLG,Den,SO,SCh,AVPO,Sol,SuM,BL,PV,LHb and Icj,showing a negative dose-effect relation with propofol. Conclusion Propofol has the determined sites of action in CNS and the decrease of NO synthesis by the inhibition of NOS may play a role in propofol-induced general anesthesia.
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Objective To investigate the advantage and safety of penehyclidine hydrochloride as the antagonist of muscle relaxant in aged patients with myocardial ischemia. Methods Sixty cases over 60 years old with myocardial ischemia in ECG were randomized to receive 15 ?g/kg atropine+40 ?g/kg neostigmine (group A),sole 20 ?g/kg penehyclidine hydrochloride (group B),20 ?g/kg penehyclidine hydrochloride +40 ?g/kg neostigmine (group C). Vital signs of antagonism were observed before and after the changes of antagonism. Results All cases had an uneventful anesthesia and operation. After antagonists were administered,heart rate and heart rate variation index increased,respiration became shallow and faster in group A. The heart rate in group B only increased mildly and the muscle tone returned very slowly as the increasing of BIS. The signs were the most desirable such as mildly lower heart rate,the minimal heart rate variation index,faster recover of muscle tone without re-relaxation,slow and deep respiration,and slowly recovered BIS. Conclusion Penehyclidine hydrochloride combined with neostigmine is suitable to reverse the muscle relaxant in aged with myocardial ischemia.