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Objective To compare the changes in postoperative pain, complications and clinical effect between gastrodin and remifentanil for controlled hypotension in endoscopic sinus surgery.Methods Eighty patients undergoing endoscopic sinus surgery were enrolled in the study.Patients were randomized into two groups of 40 to receive gastrodin (Group G) or remifentanil (Group R) infusion.Two groups were administered with propofol of 2 mg/kg to induce anaesthesia, which was maintained using sevoflurane.Group R received a continuous infusion of remifentanil titrated between 3 and 4 ng/mL using target-controlled infusion, whereas Group G received an i.v.gastrodin bolus of 2 mg/kg followed by a 20 mg/kg continuous infusion to maintain a mean arterial pressure ( MAP) between 60 and 70 mmHg.Haemodynamic variables, surgical conditions, postoperative pain, and adverse effects, such as postoperative nausea and vomiting ( PONV) and shivering were recorded.Results Controlled hypotension was well maintained in both groups.MAP and heart rate were higher in Group R than Group G after operation(P<0.05).Surgical conditions scores were not different between two groups.Postoperative pain scores were significantly lower in Group G than Group R (P<0.05).Shivering and the use of antiemetic and analgesic drugs were also less frequent in Group G than Group R (P<0.05).Conclusions Both gastrodin and remifentanil when combined with sevoflurane provides adequate controlled hypotension and proper surgical conditions for endoscopic sinus surgery.However, patient administered gastrodin has a more favourable postoperative course with better analgesia and less shivering and PONV.
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Objective To investigate the effects of propofol on neuronal apoptosis in anterior horn of spinal cord in rabbits with spinal cord ischemia-reperfusion (IR) injury. Methods Sixty New Zealand white rabbits aged 4-6 months weighing 2.0-2.5 kg were randomized to receive normal saline (group C), 10% intralipid (group F) and propofol 30 mg/kg (group P1 ), 40 mg/kg (group P2), 50 mg/kg (group P3) and60 mg/kg (group P4 ). 10% intralipid was added to propofol solution to make the fluid infused equal in volume between the 6 groups ( n = 10 each). Spinal cord ischemia was induced by occlusion of abdominal aorta distal to the left renal arteries combined with simultaneous occlusion of bilateral common iliac arteries for 30 min. A catheter was inserted into abdominal aorta close to the site of occlusion via left femoral artery. Normal saline, 10% intralipid or different doses of propofol was infused through the catheter as soon as aorta was clamped at the rate of 12 ml·kg-1·h-1 for 30 min. The aorta and bilateral iliac arteries were then declamped. The L4-6 of spinal cord was removed at 48 h of reperfusion for microscopic examination and the total number of normal motor neurons in the anterior horn of spinal cord was counted. The total number of neurons and apoptosis neurons in the anterior horn of spinal cord was counted by TUNEL and the apoptosis index of neurons was calculated. The expression of caspase-3 in the anterior horn of spinal cord was determined by immunohistochemical technique. Results The number of normal motor neurons was significantly higher, and the apoptosis index and expression of caspase-3 were significantly lower in group P1-4 than in group C and F ( P < 0.05). Compared with group P1, the number of normal motor neurons was significantly increased and the apoptosis index was significantly decreased in group P2-4 and the expression of caspase-3 was down-regulated in group P3 and P4 ( P < 0.05). Compared with group P2, the number of normal motor neurons was significantly increased in group P3 while decreased in group P4, and the apoptosis index was significantly decreased and the expression of caspase-3 was down-regulated in group P3 and P4 ( P < 0.05). Compared with group P3, the number of normal motor neurons was significantly decreased and the apoptosis index was significantly increased and the expression of easpnse-3 was up-regulated in group P4 ( P < 0.05) . Conclusion Propofol 30-60 mg/kg infused through aorta during occlusion can inhibit the neuronal apoptosis and attenuate IR injury to spinal cord dose-dependently in rabbits. The underlying mechanism may be related to the down-regulation of caspase-3 expression.
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BACKGROUND: It is proved that protein of heat shock protein 70 family has protective effects on cells. Ketamine can cause psychiatric symptoms such as illusion and delirium in patients, which can damage neurons of the limbic system in rats. The expression of heat shock protein 70 can be detected in the damaged neurons with immunohistochemical staining.OBJECTIVE: To observe the expression of heat shock protein 70 induced by ketamine in the hippocampus of rats of different ages and probe into the damaging effect on nerves.DESIGN: Randomized controlled trial.SETTING: Department of Anesthesiology and Critical Care Medicine,Huaxi Hospital of Sichuan University.MATERIALS: The experiment was conducted in the laboratory of the Department of Anesthesiology and Critical Care Medicine, Huaxi Hospital of Sichuan University, from January to May 2001. Totally 70 SD rats,weighing 25 to 285 g, of either gender and clean grade, were recruited.Thirty-five adult SD rats were randomly divided into control group and ketamine groups of 20.0, 40.0, 60.0, 80.0, 100.0 and 120.0 mg/kg with 5 rats in each group. The rats in each group were injected intraperitoneally with normal saline and 20.0, 40.0, 60.0, 80.0, 100.0 and 120.0 mg/kg of ketamine, respectively. Another 35 rats aged 0-10, 11-20, 21-30, 31-45,46-60, 61-90 and 91-120 days, 5 rats in each age stage, were given intraperitoneal injection of 80.0 mg/kg ketamine. After 24-hour survival time, the animals were put to death and their brains were removed. 5 μm-thick coronal sections of the hippocampus were cut on a vibratome. The expression of heat shock protein 70 was detected in the hippocampus of rats of different ages with immunohistochemical staining.MAIN OUTCOME MEASURES: Positive cellular percentage, density and grayscale of heat shock protein 70 in the rats' hippocampus.of different doses of ketamine on the expression of heat shock protein in rat hippocampus: In control group, the cellular density of heat shock protein 70 expression induced by 20.0, 40.0, 60.0, 80.0, 100.0 and 120.0 mg/kg of ketaminewas0, 8.12±1.82, 27.07±5.98, 45.35±5.84, 78.51±7.34,74.16±8.17 and 60.84±6.27, respectively. It indicated that when ketamine was under 80.0 mg/kg, the cellular density of heat shock protein 70 in creased significantly with the dose increase (P ＜ 0.01). When ketamine was over 80.0 mg/kg, the cellular density significantly decreased with the dose tamine in the hippocampus of rats of different ages: The density of positive nerve cells of heat shock protein 70 in young rats aged under 20 days was 0; the density of young rats aged 21-30 days, 31-45 days, 46-60 days and 61-90 days was 34.17±6.18, 55.42±4.80, 78.51±7.34 and 83.16±11.10,respectively. Compared with that of the first age group, with the increased age, the density of positive cells of heat shock protein 70 was significantly increased (P ＜ 0.01); it was 83.16±11.10 and 85.83±9.33 in the hippocampus of rats aged 61-90 days and 91-120 days, re spectively (P ＞ 0.05).CONCLUSION: Ketamine can induce the expression of heat shock protein 70 in the hippocampus of rats, indicating that neurons of the hippocampus may be damaged; with the increase of dose, its damaging effect is enhanced.The damage of ketamine is greater in adult rats than in young rats.
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Objecitve:To study the effects of ketamine on the large conductance Ca~(2+)-activated potassium (BK)channels in cultured newborn rat hippocampal neurons. Method:All experiments were carried out on 3-7 days old neurons. Single channel current signals were recorded in symmetrical high K~+ solution(140mM) under cell-attached patch and inside-out patch. Result:(1)In inside-out patch, with the unitary conductance being 176.5?16.5pS,the BK channel activity was markedly activated by internal Ca~(2+) but was blocked by potassium channel blocker (TEA). (2) In cellattached patch,when the concentration of ketamine was 0.01,0.05,0.20mmol/L and membrane potential kept at?60mV,the open probability (Po) decreased from 0.042?0.011 at baseline to 0.027?0.008,0.030?0.015,0.032?0.021 respectively(P0.05). Conclusion:Ketamine has dual effects on the BK channels,the inhibition may be related to its side effects,and the activation to the mechanism in anesthesia.
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Objective To evaluate the myocardial protection afforded by ketamine midazolam in its septic shock and its possible mechanism by studying the impact of ketamine midazolam on myocardial HSP 70 expression in LPS induced septic shock in rats Methods 112 healthy adults SD rats of both sexes, weighing 180 205g were randomly assigned to one of following groups:(Ⅰ)control group received normal saline ip (group NS); (Ⅱ) endotoxin group received LPS 20mg?kg -1 ip(group E); (Ⅲ) endotoxin midazolam group received midazolam 0 5mg?kg -1 20 min before LPS (group EM); (Ⅳ) endotoxin ketamine group received ketmine 80mg?kg -1 20 min before LPS (group EK); endotoxin ketamine midazolam group received ketmine 80mg?kg 1 and midazolam 0 5mg?kg -1 20 min before LPS (group EKM) One hour later half of the initial dose of ketamine and/or midazolam was given to reinforce their effect Heart was harvested 2h after LPS or when the rats died of LPS induced septic shock(pupil did not respond to light) for determination of HSP 70 expression using monoclone antibody immunocytochemistry The survival time of every rat was recorded Results The expression HSP 70 was higher in group E than that in group NS and was lower than that in group EK and EKM The survival rate of group EK and EKM was higher than that of group E and EM (P0 05) Conclusions Ketamine can enhance myocardial HSP 70 expression in septic shock This may be one of the mechanisms of its myocardial protection Joint use of ketamine midazolam dose not affect the myocardial protective effect of ketamine
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Objective To observe the influences of combined general and epidural anesthesia on hemodynamics.Methods Twenty one patients were randomly divided into two groups, general anesthesia (GA group, n=11) and combined general and epidural anesthesia (GA+EA group, n=10). With Swan Ganz technique, hemodynamic parameters were measured 5min following 0.6 and 1.0 MAC enflurane inhalation in GA group, and 5min following 0.6 MAC enflurane inhalation and 10min after combined epidural lidocaine in GA+EA group.Results Compared with the baselines, in both groups with 0.6 MAC enflurane inhalation, MAP decreased significantly (P0.05); in GA group with 1.0 MAC enflurane inhalation, MAP, HR, SVR, SI and CI decreased significantly (P0.05). As compared with those following 0.6 MAC enflurane inhalation, only in GA+EA group MAP and SVR decreased, and SI rose obviously (P
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To observe the hemodynamics changes of patients undergoing laparoscopic cholecystectomy under epidural or general anesthesia. Method: 25 patients were divided into two groups: general(GA, n=11)and epidural (EA, n=14) anesthesia groups. Hemodynamic parameters (HR, MAP, CVP, PCWP, PAP, CO, CI, SVR, PVR) were measured with Swan-Ganz technique after the patients being placed to rT position,CO2 being insufflated into peritoneal cavity, and at the end of operation. Result: 1. In the EA group, CVP reduced significantly after rT position placed, SV, CO, MAP and HR reduced significanty after peritoneal insufflation,but still within normal range. 2. In the GA group, CVP, SV, CO were significant ly reduced after rT position placed; After peritoneal insufflation, all parametere were significantly increased except SV had no significant change. Conclusion:Epidural anesthesia can be safely applied to the ASA Ⅰ-Ⅱ grade patients undergoing laparoscopic cbolecystectomy.
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Objective This experiment was designed to determine the effect of haloperidol on HSP70 induced by ketamine, and to explore the possibility of using haloperidol to prevent or treat the brain injury caused by ketamine.Methods 48 rats were divided into 8 groups, In group 1-3 different doses of haloperidol (1.0,5.0,10.0 mg/kg)were given 1h before the administration of ketamine. There were two control groups. In control group 1 normal saline was given twice with 1h interval between the two injections. In control group 2 ketamine 80.0 mg/kg was given 1h after the administration of normal saline.The volume of each injection was 3ml and intraabdominal injection was used as the route of administration.HSP70 mono-clone antibody immunocytochemistry was used to detect HSP70 expression in rat hippocampus, and MIAS-2000 photography analytic software to analyze HSP70 expression in hippocampus of the rat brain.Results Ketamine induced HSP70 expression in the rat brain. Pretreatment with haloperidol inhibited HSP70 expression induced by ketamine, and the inhibition was dose-dependent, but haloperidol given after the administration of ketamine could not decrease HSP70 expression.Conclusions Ketamine injures neurons of rat hippocampus and induces the expression of HSP70 and haloperidol pretreatment can prevent neuronal injury caused by ketamine, but haloperidol can not antagonize the injury caused by ketamine.
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0.05). TNF-? in group EK and EKM was lower than that in group E (P0.05). Conclusions Ketamine can inhibit the release of TNF-? caused by LPS and increase myocardial cAMP level, protecting myocardium from sepsis. This may be one of the anti-septic shock mechanisms of ketamine. Combination of midazolam with ketamine does not affect the anti-septic shock property of ketamine.
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005); (3)When sevoflurane concentrations were in the range from 1556?mol/L to 5875?mol/L ,the KD of experimental groups was significantly lower than that of the control (P
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Objective To investigate the stress response during cardiopulmonary bypass and the effects of propofol on it Methods Thirty one patients scheduled for valve replacement ,were divided randomly into propofol group (group A,n=16) and control group (group B, n=15) Anesthesia was induced with valium fentanyl vencuronium, was maintained with fentanyl enflurane vencuronium In group A propofol 6 8mg?kg -1 ?h -1 was infused intravenously during CPB MAP,venous plasma concentrations of epinephrine(E) ,norepinephrine(NE) and blood glucose were measured before CPB(T1),cooling to 33℃(T2) and 30℃(T3), stable hypothemia(T4), rewarming to 30℃(T5) and 33℃(T6),and 15 min after CPB(T7) respectively Results In rewarming period, NE and E levels in group B increased significantly (P0 05) The dose of sodium nitroprussid was lower in group A than that in group B, and the dose of dopamine was not different between both groups Conclusions The stress response increases in rewarming stage during CPB ,which can be suppressed by the continuous infusion at anesthetic dose of propofol
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ve To evaluate the protective effect of low-dose aprotinin on lungs from acute injury induced by cardiopulmonary bypass(CPB).Methods Twenty-eight ASA II-III patients (13 male, 15 female) aged (40.39?8.51) years, weighing (56.79?7.61) kg scheduled for elective valve replacement, were divided into two groups of 14 each: control group and aprotinin group. Patients who had infectious disease or received glucocorticoid before operation were excluded. The mean duration of CPB was (127.93?52.96) min and the mean aortic cross-clamping time was (68.54?30.71) min.The patients were premedicated with intramuscular phenobarbital 0.1 and scopolamine 0.3 mg. Anesthesia was induced with midazolam 0. 1-0.2mg?kg, fentanyl 10-20?g,kg-1 and intubation was facilitated with vecuronium 0.1-0.12 mg?kg-1. Radial artery and right internal jugular vein were cannulated for direct BP and CVP monitoring. Anesthesia was maintained with intermittent boluses of fentanyl and vecuronium supplemented with enflurane inhalation. The patients were mechanically ventilated. Tidal volume was maintained at 10-12 ml?kg , respiratory rate 12 bpm and I:E ratio 1:2.In aprotinin group 1 ? 10~6KIU of aprotinin was added to the priming solution, 1 ? 10~6 KIU aprotinin was infused after induction of anesthesia until thoracotomy and 2.5 ? 105KIU.h-1 was infused from thoracotomy until the end of surgery. In control group aprotinin was replaced by same volume of lactated Ringer solution. Peripheral blood samples were taken before induction of anesthesia, before CPB and 1,24 h after termination of CPB, for determination of IL-10 and TNF-?. Respiratory index [P( A-a)DO2/PaO2] was calculated before CPB, 10 min and 60 min after CPB. Results There was no significant difference in age, weight, duration of operation CPB time and aortic cross-clamping time between the two groups. The TNF-? concentration was not significantly different before induction of anesthesia and CPB between the two groups. But at 1 and 24 h after CPB TNF-? level was significantly higher than the baseline value before anesthesia in control group and that in aprotinin group. The IL-10 concentration greatly increased at 1 h after CPB in both groups as compared with that before anesthesia, but was much higher in the aprotinin group than that in the control group. Respiratory index at 10 min and 60 min after CPB was higher than the baseline value in control group andthat in the aprotinin group (P
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Objective To investigate the anesthetic action of intraperitoneal (i.p.) emulsified isoflurane and determine ED50 and LD50 in rats. Methods One hundred and thirty SD rats aged 6-8 weeks veighing 120-150 g were randomly divided into three groups: (A) control group ( n = 10) ; (B) ED50 group ( n = 60) ; (C) LDSO group (n = 60) . Group B and C were further divided into 6 subgroups with 10 animals (5 male, 5 female) in each subgroup. In control group a single bolus of 30% emulsified fat 2ml/100g body weight was administered i. p. In ED50 group a single bolus of 2.30% -6.0% vol/vol emulaified isoflurane 1.5 ml/100 g was administered i. p. and righting reflex was recorded. In LD50 group a single bolus of 4.09% - 10.64% vol/vol emulsified isoflurane 2 ml?100 g-1 was given i.p. and toxic response and lethal dose were recorded. The concentration ratio of the two neighbouring subgroups was 1:0.825. Results The ED50 of emulsified isoflurane was (0.57?0.07) ml.kg-1 and 95% confidence limit (CL) was (0.51-0.64)ml?kg-1 . The average onset time of action was (2.64 ?0.99) min and the average duration of action was (28 ? 11) min. The LD50 of emulsified isoflurane was (1. 26 ?0.10) ml?kg-1 and 95% confidence limit was 1.10-1.45 ml?kg-1 . The therapeutic index (LD50/ED50)was 2. 24. Conclusion Intraperitoneal emulsified isoflurane can provide effective general anesthesia and can be used for animal experiments which need anesthesia of short duration.
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Objective To determine the difference between sevoflurane- and anoxic preconditioning in protecting newborn rat heart muscle cells from anoxia-reoxygenation injury. Methods The second generation of primary cultured cardiac myocytes from 2-3d newborn SD rats were randomly divided into 4 groups: control group (C), anoxia/reoxygenation group (A/R) in which cultured cardiac myocytes were exposed to 2h anoxia followed by 48h reoxygenation; anoxic preconditioning group (IP) in which before A/ R the cardiac myocytes were pretreated with 20 min anoxia; sevoflurane preconditioning group (S) in which cardiac myocytes were pretreated with 20 min 2.5% sevoflurane (1.5 MAC) before A/R. Ultrastructure of heart muscles cells was observed 1 h after reoxygenation, Cell survival was determined by MTT rapid colorimetric assay and apoptosis was measured by flow cytometry at 0, 1, 12, 24, 36 and 48 h after reoxygenation. Results (1) In S and IP group there was no significant change in ultrastructure and no apoptosis cell was found, whereas in A/R group the change in ultrastructure was significant , and apoptosis cells were found. (2) The cell survival in group S and group IP was significantly lower than that in group C but significantly higher than that in group A/R. (P 0.05) . The survival of cardiac myocytes increased with prolongation of reoxygenation time in group S and group IP. (3) The apoptosis percentage of cells in group S and group IP was significantly higher than that in group C and lower than that in group A/R(F