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PURPOSE: The aim of this study was to investigate whether propofol could attenuate hypoxia/reoxygenation-induced apoptosis and autophagy in human renal proximal tubular cells (HK-2) by inhibiting JNK activation. MATERIALS AND METHODS: HK-2 cells were treated with or without propofol or JNK inhibitor SP600125 for 1 hour and then subjected to 15 hours of hypoxia and 2 hours of reoxygenation (H/R). Cell viability and LDH release were measured with commercial kits. Cell apoptosis was evaluated by flow cytometry. The expressions of p-JNK, cleaved-caspase-3, Bcl-2, and autophagy markers LC3 and p62 were measured by Western blot or immunofluorescence. RESULTS: HK-2 cells exposed to H/R insult showed higher cell injury (detected by increased LDH release and decreased cell viability), increased cell apoptosis index and expression of cleaved-caspase-3, a decrease in the expression of Bcl-2 accompanied by increased expression of p-JNK and LC3II, and a decrease in expression of p62. All of these alterations were attenuated by propofol treatment. Similar effects were provoked upon treatment with the JNK inhibitor SP600125. Moreover, the protective effects were more obvious with the combination of propofol and SP600125. CONCLUSION: These results suggest that propofol could attenuate hypoxia/reoxygenation induced apoptosis and autophagy in HK-2 cells, probably through inhibiting JNK activation.
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Humans , Hypoxia , Apoptosis , Autophagy , Blotting, Western , Cell Survival , Flow Cytometry , Fluorescent Antibody Technique , PropofolABSTRACT
Objective To observe the influence of IL-12,IL-15 on CIK cell in the normal culture;to observe the anti-tumor effect in the circumstance of different combination of cytokines,and to provide a new insight for preparing high effective and qualified CIK cell in vitro.Methods The optimal concentrations of IL-2,IL-12 and IL-15 were determined,respectively.After the peripheral blood from healthy blood donors was collected,monocytes were selected and co-cultured with different cytokines into different groups,as group A(IL-2 normal culture group),group B(IL-2 and IL-12 group),group C(IL-2 and IL-15 group),group D(IL-2,IL-12 and IL-15 group),and group E(cytokine control group).The monocytes in different groups were calculated by globulimeter,the activity of cells was detected by Trypan blue staining,positive ratio of CD3,CD8,CD56 on the celluar membrane was detected by flow cytometry,and the anti-tumor effect of CIK to SMMC-7721 was detected by MTSmethod,inthedayof0,5,10,15,20 after the culture.Results Statistical analysis indicated that,the proliferation multiplication of CIK cells was significantly higher in group B,group C and group D after 10,15 and 20 days of culture than those in group A(P＜0.05);and group D had higher proliferation multi-plication than that of group C(P＜0.05).The percentage of CD3 + CD8 +,CD3 + CD56+ in CIK cell membrane in group B,C,D was significantly higher than that in group A after 15 and 20 days of culture (P＜0.05).The percentage of CD3+ CD8+,CD3+ CD56+ in CIK cell membrane in group D was significantly higher than that in group B after 15 and 20 days of culture (P＜0.05).The killing rate of CIK cells for liver cancer in each group at 10,15,20 days of culture was significantly higher than that of group A when the target target ratio was 5 ∶ 1 (P＜0.05).The killing rate of CIK cells for liver cancer in group D,C at 10,15,20 days of culture was significantly higher than that of group B(P＜0.05).Conclusion IL-12and IL-15 could improve the proliferation of CIK cells,and IL-15 also has the effect of enhancing CIK cells the tumor-killing to SMMC-7721 activity.
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Objective To evaluate the role of caveolin-1 (Cav-1) in penehyclidine hydrochioride (PHC)-induced inhibition of lipopolysaccharide(LPS)-induced activation of Toll-like receptor 4 (TLR4) /p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway in macrophages of mice.Methods Macrophages of mice were seeded in 6 em diameter dishes (5 ml per dish) and divided into 5 groups (n=20 each) using a random number table:Scr-siRNA group (S group),Scr-siRNA + LPS group (LPS group),Ser-siRNA+LPS +PHC group (LPS+P group),Cav-1-siRNA+LPS group (C+LPS group) and Cav-1-siRNA+LPS+PHC group (C+LPS+P group).Macrophages were transfected with Scr-siRNA for 24 h in S,LPS and LPS+P groups and with Smart pool Cav-1 siRNAs for 24 h in C+LPS and C+LPS+P groups.LPS at the final concentration of 1 μg/ml was added after the end of transfection,and macrophages were then incubated for 2 h in LPS,LPS+P,C+LPS and C+LPS+P groups.In LPS+P and C+LPS+P groups,PHC at the final concentration of 2 μg/ml was added at 2 h of incubation with LPS,and macrophages were then incubated for 2 h.The expression of Cav-1 and TLR4 was detected by Western blot.The expression of p38 MAPK was determined by immunofluorescence.The level of tumor necrosis factor-alpha (TNF-α) in the culture medium was determined by enzyme-linked immunosorbent assay.The activity of myeloperoxidase (MPO) in macrophages was measured by colorimetry.Results Compared with group S,the expression of TLR4 and p38 MAPK was significantly up-regulated,and the concentration of TNF-α in the culture medium and activity of MPO were increased in the other four groups,the expression of Cav-1 was significantly downregulated in LPS and C+LPS groups (P ＜0.05),and no significant change was found in the expression of Cav-1 in group LPS+P (P＞0.05).Compared with group LPS,the expression of Cav-1 was significantly up-regulated,the expression of TLR4 and p38 MAPK was down-regulated,and the concentration of TNF-α in the culture medium and activity of MPO were decreased in group LPS+P,and the expression of Cay-1 was significantly down-regulated,the expression of TLR4 and p38 MAPK was up-regulated,and the concentration of TNF-α in the culture medium and activity of MPO were increased in group C+LPS (P＜0.05).Compared with group LPS+P,the expression of Cav-1 was significantly down-regulated,the expression of TLR4 and p38 MAPK was up-regulated,and the concentration of TNF-α in the culture medium and activity of MPO were increased in group C+LPS+P (P＜0.05).Compared with group C+LPS,the expression of Cav-1 was significantly up-regulated,the expression of TLR4 and p38 MAPK was down-regulated,and the concentration of TNF-α in the culture medium and activity of MPO were decreased in group C+LPS+P (P＜0.05).Conclusion The mechanism by which PHC inhibits LPS-induced activation of TLR4/p38 MAPK signaling pathway in macrophages is related to up-regulating Cav-1 expression in mice.
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Objective To observe intravenous lidocaine in patients undergoing hysteroscopy surgery under Narcotrend monitoring. Methods 80 patients undergoing elective hysteroscopy surgery were randomly divided into normal saline group(group S)and lidocaine group(group L). Before anesthesia induction ,group L was given lido-caine injection of 1.5 mg/kg,then with 2 mg/(kg·h)for infusion to the end of surgery. Group S received normal sa-line instead of lidocaine as the control. All patients received Narcotrend(NT)monitoring anesthesia depth of seda-tion and received intravenous anesthesia with propofol and remifentanil. Operation time (T1),dosage of propofol and remifentanil,total waking time(T2),postoperative pain of 0.5 h(T3),4 h(T4),24 h(T5)by postoperative visual analogue scale(VAS),incidence of sore throat,lidocaine adverse reactions were recorded. Results Age, weight,T1,T2 and dosage of propofol between two groups had no statistical significance (P > 0.05). Dosage of remifentanil of group L was obviously less than that in group S (P < 0.05). VAS score T3 ,T4 of group L was obviously less than those in group S(P < 0.05). No significant difference was found on T5. Sore throat incidence of group L was lower than that in group S(P < 0.05). Lidocaine adverse reactions were not found in L group. Conclusions Intravenous lidocaine in hysteroscopy surgery is safe and effective under Narcotrend monitoring.
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Objective To observe intravenous lidocaine in patients undergoing hysteroscopy surgery under Narcotrend monitoring. Methods 80 patients undergoing elective hysteroscopy surgery were randomly divided into normal saline group(group S)and lidocaine group(group L). Before anesthesia induction ,group L was given lido-caine injection of 1.5 mg/kg,then with 2 mg/(kg·h)for infusion to the end of surgery. Group S received normal sa-line instead of lidocaine as the control. All patients received Narcotrend(NT)monitoring anesthesia depth of seda-tion and received intravenous anesthesia with propofol and remifentanil. Operation time (T1),dosage of propofol and remifentanil,total waking time(T2),postoperative pain of 0.5 h(T3),4 h(T4),24 h(T5)by postoperative visual analogue scale(VAS),incidence of sore throat,lidocaine adverse reactions were recorded. Results Age, weight,T1,T2 and dosage of propofol between two groups had no statistical significance (P > 0.05). Dosage of remifentanil of group L was obviously less than that in group S (P < 0.05). VAS score T3 ,T4 of group L was obviously less than those in group S(P < 0.05). No significant difference was found on T5. Sore throat incidence of group L was lower than that in group S(P < 0.05). Lidocaine adverse reactions were not found in L group. Conclusions Intravenous lidocaine in hysteroscopy surgery is safe and effective under Narcotrend monitoring.
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Objective To investigate the effects of penehyclidine hydrochloride on activities of nuclear factor kappa B (NF-kB) and activator protein-1 (AP-1) during actue lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 3 equal groups (n =10 each) using a random number table:sham operation group (group S),blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloride group (group PHCD).The model of actue lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.In PHCD group,PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,blood samples were obtained for measurement of concentrations of tumor necrosis factor-alpha (TNF-α) in serum.The lungs were then removed for determination of lung water content,myeloperoxidase (MPO) activaty (by colorimetric assay),NF-κB and AP-1 activaties (using electrophoretic mobility shift assay) in lung tissues,and for microscopic examination of pathologic changes (under light microscope).The left lung was lavaged,and lung permeability index (LPI) was calculated.Results Compared with S group,lung water content,LPI,serum TNF-α level and activites of MPO,NF-κB and AP-1 were significantly increased in THSR and PHCD groups.Compared with THSR group,lung water content,LPI,serum TNF-α concentrations and activites of MPO,NF-κB and AP-1 were significantly decreased in PHCD group.The pathological damage to lung tissues was significantly reduced in PHCD group as compared with THSR group.Conclusion PHCD can inhibit activities of NF-κB and AP-1 in lung tissues,thus mitigating acute lung injury induced by blunt chest trauma-HSR in rats.
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Objective To investigate the effects of penehyclidine hydrochloride on Fas/FasL expression during acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male SPF Sprague-Dawley rats, aged 8 weeks, weighing 245-275 g, were randomly assigned into 3 equal groups using a random number table: sham operation group (group Sham) , blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloric group (group PHCD).The model of acute lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.Blood was withdrawn via the femoral artery 5 min later until mean arterial pressure was decreased to 35-45 mmHg within 15 min, and maintained at this level for 60 min, followed by resuscitation.In PHCD group, PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established, the rats were sacrificed, the lungs were then removed for microscopic examination of pathologic changes and for determination of Fas, FasL and caspase-8 expression, and interleukin-6 (IL-6) and IL-1β contents in lung tissues.Apoptotic index was calculated.Results Compared with group Sham, the expression of Fas, FasL and caspase-8 was significantly up-regulated, and AI and contents of IL-6 and IL-1β were increased in THSR and PHCD groups (P＜O.05).Compared with group THSR, the expression of Fas, FasL and caspase-8 was significantly down-regulated,and AI and contents of IL-6 and IL-1β were decreased in group PHCD (P＜0.05).The pathologic changes of lungs were significantly reduced in group PHCD compared with group THSR.Conclusion The mechanism by which penehyclidine hydrochloride inhibits lung cell apoptosis induced by blunt chest trauma-HSR is associated with inhibition of Fas/FasL expression in rats.
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Objective To investigate the effects of penehyclidine hydrochloride (PHC) on acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation in rats.Methods Forty male SpragueDawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 4 equal groups (n =10 each) using a random number table:sham operation group (S group),blunt chest trauma combined with hemorrhagic shock and resuscitation group (group THSR),PHC for prevention group (group P1)and PHC for treatment group (group P2).ALI was induced by dropping a 300 g weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs in anesthetized rats in THSR,P1 and P2 groups.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.In P1 group,PHC 2 mg/kg was injected intravenously at 30 min before blunt chest trauma.In P2 group,PHC 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,arterial blood samples were obtained for blood gas analysis and for measurement of concentrations of interleukin-6 (IL-6) and interleukin-1β (IL-1β) in serum by ELISA.Oxygenation index (OI) was calculated.The animals were sacrificed and bronchoalveolar lavage fluid (BALF) was collected for determination of white blood cell count and protein concentrations.Lungs were removed for examination of pathological changes and ultrastructure and for determination of Toll-like receptor (TLR4) and phosphor-p38 mitogen activated protein kinase (p-p38MAPK) expression (by Western blot).Results Compared with group S,PaO2 and OI were significantly decreased,PaCO2,protein concentrations in BALF,white blood cell count,and IL-6 and IL-1β concentrations in serum were increased,and TLR4 and p-p38MAPK expression was up-regulated in THSR,P1 and P2 groups.Compared with group THSR,PaO2 and OI were significantly increased,PaCO2,protein concentrations in BALF,white blood cell count,and IL-6 and IL-lβ concentrations in serum were decreased,TLR4 and p-p38MAPK expression was down-regulated in P1 and P2 groups.No significant differences were found in the parameters mentioned above between P1 and P2 groups.Conclusion PHC can mitigate acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation in rats,and inhibited activation of TLR4/ p38MAPK signaling pathway and attenuated inflammatory responses are involved in the mechanism.
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Objective To investigate the mechanism of myocardial ischemia and reperfusion-induced acute lung injury (ALl) and protective effect of ischemic postconditioning.Methods Forty SD rats were allocated to sham group,myocardial ischemia/reperfusion group (reperfusion group),ischemic postconditioning group (postconditioning group),and ischemic postconditioning + phosphatase and tensin homolog deleted on chromosome ten (PTEN) inhibiting group (inhibitor group) according to the random number table,with 10 rats per group.Myocardial ischemia/reperfusion was induced by left anterior descending coronary artery occlusion.Postconditioning was performed within 1 minute before reperfusion consisting of 3 10 s cycles of reperfusion followed by 10 s occlusion.Lung was immediately removed 120 minutes after reperfusion for HE stain,immunohistochemical detection of inflammatory factors and apoptosis factors,TUNEL assay of cell apoptosis,and Western blot of protein kinase B (Akt),phospho-Akt (p-Akt),glycogen synthase kinase-3β (GSK-3β),and phospho-GSK-3β (p-GSK-3β).Results Down-regulated B-cell lymphoma-2 (Bcl-2) and IL-10 and up-regulated Bcl-2 associated X protein (Bax),cysteinyl aspartate specific proteinase-3 (Caspase-3),IL-6 as well as IL-8 were observed in other 3 groups compared with sham group (P ＜0.01).Moreover,down-regulated Bax,Caspase-3,IL-6,IL-8 as well as TUNEL and up-regulated Bcl-2 as well as IL-10 were observed in reperfusion group compared to postconditioning group and tensor group (P ＜ 0.01).No statistical differences were found among the four groups in levels of Akt,p-Akt,and GSK-3β,but level of p-GSK-3β was significantly down-regulated in reperfusion group compared to other 3 groups(P ＜ 0.01).Conclusion Development of ALI may relate to down-regulation of p-GSK-3β evoked directly by the release of inflammation factors in early period of myocardial ischemia/reperfusion and ischemic postconditioning may attenuate the condition.
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Objective To investigate the role of gamma-aminobutyric acid (GABA) A receptor (GABAAR) in lung tissues in lipopolysaccharide (LPS)-induced acute lung injury in rats.Methods Thirty-two male Wistar rats,aged 8 weeks,weighing 200-230 g,were randomly divided into 4 groups (n =8 each) ∶ control group (group C),group LPS,GABA pretreatment + LPS group (group GABA) and GABAAR antagonist bicuculline pretreatment + LPS group (group BIC).Acute lung injury was induced by intravenous LPS 5 mg/kg in groups LPS,GABA and BIC,while the equal volume of normal saline was given in group C.GABA 50 mg/kg and bicuculline 10 μmol/kg were injected intraperitoneally 30 min before LPS injection in GABA and BIC groups,respectively.Arterial blood samples were collected at 6 h after LPS injection for measurement of arterial partial pressure of oxygen (PaO2).The animals were then sacrificed and lungs removed for determination of W/D lung weight ratio,GABAAR expression,contents of interleukin-6 (IL-6),tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) and superoxide dismutase (SOD) activity in lung tissues and for microscopic examination.Results Compared with group C,PaO2 was significantly decreased in the other three groups,and W/D lung weight ratio,TNF-α,IL-6 and MDA contents were significantly increased,GABAAR expression was up-regulated,and SOD activity was decreased in groups LPS and GABA (P ＜ 0.05).Compared with group LPS,W/D lung weight ratio,TNF-α,IL-6 and MDA contents were significantly increased,GABAAR expression was up-regulated,and SOD activity was decreased in group GABA (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group BIC and in PaO2 in groups GABA and BIC (P ＞ 0.05).Conclusion GABAA R in lung tissues is involved in the development of acute lung injury induced by LPS.
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Objective To assess effects of cerebral ischemic postconditioning(IPost)on neuronal apoptosis and phosphated glycogen synthase kinase-3β(GSK-3β)after cerebral ischemic/reperfusion.Methods The experiment was conducted at the center for animal experiment of Renmin Hospital,Wuhan University.Thirty male Wistar rats were randomly divided into three groups:sham operation(S),ischemic/reperfusion(I/R)and ischemic postconditioning(IPost).Each group contained ten rats.Global brain ischemia was produced with four-VO method.Animals were killed after two days.Apoptosis in neurons in the cortex region were detected by TUNEL assay; infarct areas were detected by TTC ; activity of p-GSK-3β was detected by spectrum assay; Statistical software SPSS13.0 was applicated to perform one-way ANOVA Student-Newman-Keul test; correlation was detected by linear regression.Results Compared with group S,TUNEL-positive cells and infarct areas increased(P ＜0.01),the activity of p-GSK-3β decreased in I/R and IPost groups(P ＜ 0.01).Compared with group I/R,TUNEL-positive cells and infarct areas significantly decreased(P ＜ 0.01),the activity of p-GSK-3β increased in group IPost(P ＜ 0.01).The activity of p-GSK-3β and TUNEL-positive cells had highly correlation,so as infarct areas(P ＜ 0.01).Conclusions IPost can lessen the ischemic/reperfusion injury of Cortex,through increas the activity of p-GSK-3[β and decreasing neuronal apoptosis.
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Objective To investigate the effect of penehyclidine hydrochloride on the cell apoptosis in lung tissues in a rat model of traumatic acute lung injury (ALI) .Methods Fifty-four SD rats weighing 225-275 kg were randomly divided into 3 groups ( n = 18 each) : control group (group C) , ALI group, penehyclidine hydrochloride group ( group P) . Traumatic ALI was induced by dropping a self-made impact device on the chest of anesthetized rats according to the technique described by Raghavendran et al. Intraperitoneal penehyclidine hydrochloride 2 mg/kg was injected immediately after blunt chest trauma and at 12 h after blunt chest trauma in group P. Six rats in each group were sacrificed at 3, 12 and 24 h after blunt chest trauma and the lung tissues collected for microscopic examination and determination of cell apoptosis (by TUNEL) and expression of Bax and Bcl-2 (by immuno-histochemical staining) . The apoptosis index was calculated. Results The apoptosis index and expression of Bax and Bcl-2 were significantly higher, while the ratio of Bcl-2/Bax was significantly lower at each time point in groups ALI and P than in group C ( P ＜ 0.05) . The apoptosis index and Bax expression were significantly lower,while the Bcl-2 expression and ratio of Bcl-2/ Bax higher at each time point in group P than in group ALI.The microscopic examination showed that penehyclidine hydrochloride injection significantly attenuated the pathologic changes. Conclusion Penehyclidine hydrochloride can reduce the traumatic ALI through inhibiting the cell apoptosis in rat lung tissues.
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Objective To investigate the effect of radix paeoniae rubra (RPR) on expressions of p38MAPK, NF-κB and iNOS in ltpopolysaccharide (LPS)-induced acute lung injury (ALI) and explore its protective mechanism. Methods Forty Wistar rats with ALI were divided randomly into five groups: saline control group (Group A) , LPS group (Group B), RPR for treatment group (Group C), RPR for prevention group (Group D) and SB203580 group (Group E). The effects of RPR on protein content and the ratio of neutrophiles in bronchoalveolar lavage fluid (BALF), contents of malondidehyde (MDA) and serum NO in lung tissue were observed. Arterial blood was collected for blood gas analysis. Expressions of p38MAPK, NF-κB and iNOS in rat lung tissues were detected. Results Compared with Group A, expressions of p38MAPK, NF-κB and iNOS were significantly increased (P <0.01 orP< 0.05) , the protein content and the ratio of neutrophiles in BALF, contents of MDA and serum NO were significantly higher (P<0.01 or P<0.05) in Groups B, C, D and E. There was a significant decrease in the level of arterial bicarbonate and partial pressure of oxygen in Groups B, C, D and E (P<0.01 or P<0.05). Compared with Group B, the expressions of p38MAPK, NF-κB and iNOS were significantly lower, and the protein content and the ratio of neutrophiles in BALF, contents of MDA and serum NO were significantly decreased, while the levels of arterial bicarbonate and partial pressure of oxygen were significantly higher in Groups C, D and E (P<0.05 or P<0.01). Compared with Group B, the lunginjury of Groups C, D and E was significantly alleviated, while there was no statistical difference among Groups C, D and E in the indices of lung injury. Conclusion Protective effect of RPR on LPS-induced ALI is closely related to the inhibited expressions of p38MAPK, NF-κB and iNOS.
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Objective To observe the effects of exogenous sodium phosphocreatine (PCr) on cerebral repeffusion injury of rats after ischemia in order to explore the potential mechanism. Method Thirty-six healthy adult male Wistar rats with body weight 200- 220 g were randomly (random number) divided into sham operation group, ischemic reperfusion (I/R) group and PCr treatment group. The I/R model was established by using electro-cauterizing bilateral vertebral arteries and occluding bilateral common carotid arteries with atraumatic carotid clasps for 10 min, and then the clasps were released for 48 hours reperfusion. In sham operation group, bilateral common carotid arteries were exposed without occlusion. In PCr treatnent group, PCr in dose of 150 mg/kg was administered intravenously 60 min before the occlusion of bilateral common carotid arteries. Normal saline was administered intravenously instead of PCr into rats of I/R group. After reporfusion for 48 hours, the rats were sacrificed and brains removed for detections of neuron apoptosis by using TUNEL, malondialdebyde (MDA) level by using chromtometry and calmodulin (CaM) activity by using ELISA. Results Compared with sham operation group, TUNEL-positive cells, MDA level and CaM activity increased in I/R group and PGr treatment group ( P ＜0.01). Compared with I/R group, TUNEL-positive cells, MDA level and CaM activity were lower significantly in PCr treatment group ( P ＜ 0.01). Conclusions PCr can lessen cerebral ischemic reperfusion injury and neuron apoptosis, the mechanism maybe relates to the attenuation of abnormalities in calcium balance and reduction of oxygen free radicals by PCr.
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Objective To study the effect of ephedrine on middle latency auditory-evoked potentials (MLAEP) during light general anesthesia , and evaluate the influence of ephedrine on anesthesia level. Methods 10 patients (ASAⅠ-Ⅱ) undergoing elective upper abdominal operations were concerned. Anesthesia: epidural anesthesia in combination with light general anesthesia with N 2O-O 2 . After success of epidural anesthesia and tracheal intubation , when anesthesia was smooth , before operation 0.1% ephedrine(0.15 mg/kg) was injected intravenously. These data HR, SBP, DBP, MBP were measured continuously before injection, 3 min after injection, 10 min after injection; the latentcies Nb and P1 of MLAEP were measured and rescorded. Results HR?SBP?DBP?MBP increased significantly 3 min after injection, 10 min after injection compared with these data before injection (P