OBJECTIVETo observe the myocardial protective effect of electroacupuncture (EA) at Neiguan (PC 6) in the patients with valve replacement via extracorporeal circulation.

METHODSFifty patients of rheumatic cardiac disease planned for valve replacement were graded as II or III level according to America Society of Anesthesiologists (ASA) and were randomized into an observation group and a control group, 25 cases in each one. The same anesthesia and valve replacement via extracorporeal circulation were adopted in the patients of the two groups. In the observation group, 30 min before operation, EA was used to stimulate bilateral Neiguan (PC 6) till the end of operation. The venous blood was collected at 5 time points separately, named before aorta blockage (T1), 15 min after aorta open (T2), 30 min after aorta open (T3), 6 h after opening (T4) and 24 h after opening (T5). The concentrations of malondial dehyde (MDA), superoxide dismutase (SOD) and cardiac troponin 1 (cTnI) were determined in serum. The heart re-beating and the total dosage of vasoactive drugs after operation were recorded.

RESULTSCompared with those before aorta blockage, MDA and cTnI at each time point of aorta open were all apparently increased in the patients of the two groups (all P<0. 05), and SOD was reduced apparently (P<0. 05). Compared with the control group, at the time points from T3 to T5 , MDA and cTnL were lower apparently in the observation group as compared with those in the control group (all P<0. 05) and SOD was higher than that in the control group (P<0. 05). The dosage of vasoactive drugs was reduced apparently (P<. 05).

CONCLUSIONEA at Neiguan (PC 6) alleviates oxidative stress injury and has the protective effect on ischemic reperfusion myocardium.

Acupuncture Points ; Adult ; Cardiac Surgical Procedures ; Electroacupuncture ; Female ; Heart Valves ; surgery ; Humans ; Male ; Malondialdehyde ; blood ; Middle Aged ; Oxidative Stress ; Rheumatic Heart Disease ; blood ; metabolism ; surgery ; therapy ; Superoxide Dismutase ; Troponin I ; blood

Objective To study the effect of transcutaneous electrical acupoint stimulation(TEAS) on endtidal concentration of sevoflurane in upper abdominal operation.Methods The use of prospective,randomized,blinded principles.A total of 50 patients underwent selective epigastric operations with ASA Ⅰ - Ⅱ were randomly divided into group A(25 cases) and B(25 cases).In group A,TEAS was performed and sevoflurane was inhaled during operation.In group B,only sevoflurane was inhaled and TEAS was not performed during operation.Electrical stimulation on Nei-guan,He-gu and Zu-sanli was performed for 30min before induction of anesthesia in group A and meanwhile patients in group B were waiting for 30min in operating room.After intubation,in group A,TEAS was performed persistently and sevoflurane was inhaled,meanwhile remifentanil was infused persistently during operation.In group B,only sevoflurane was inhaled and remifentanil was infused persistently during operation.At time points:before TEAS( T0 ),skin incision( T1 ),exploratory laparotomy( T2 ),30min after exploratory laparotomy ( T3 ),60min after exploratory laparotomy( T4 ),blood glucose and angiotensin Ⅱ were measured,recorded 10min after the start of surgery,once for each end-tidal sevoflurane concentration.Results End-tidal concentration of sevoflurane of group A ( 1.4 ± 0.2 ) ％,was significantly lower than group B( 1.9 ± 0.4 ) ％ ( t =3.147,P ＜ 0.01 ).Cortisol and angiotensin Ⅱ were increased at T1 and T2 compared with T0 in both groups(F =2.256,2.432,2.132,2.334,all P＜0.05).Cortisol and angiotensin Ⅱwere decreased in group A compared with in group B at T1 ～T4(t =2.159,2.232,2.453,2.602,al1 P ＜0.05).Conclusion TEAS can decrease end-tidal concentration of sevoflurane and stress response.TEAS combined with sevoflurane has synergistic effect on general anesthesia.

Objective To evaluate the effect of electro-acupuncture pretreatment on endoplasmic reticulum stress during global cerebral ischemia-reperfusion (I/R ) in rats .Methods One hundred and forty-four adult male Sprague-Dawley rats ,weighing 400-500 g ,were randomly divided into 3 groups ( n=48 each) using a random number table:sham operation group (group S ) , I/R group and electro-acupuncture pretreatment group (group EA) .Global cerebral I/R was induced by 4-vessel occlusion method .Bilateral vertebral arteries were permanently occluded by cauterization and bilateral carotid arteries were occluded for 5 min , followed by reperfusion .Electro-acupuncture of Dazhui and Baihui acupoints lasting for 30 min was performed once a day for 5 consecutive days starting from 5 days before ischemia in group EA .At 6 ,12 ,24 and 48 h of reperfusion ,12 rats were sacrificed in each group and hippocampi were removed for microscopic examination and for determination of apoptosis rate (by TUNEL ) and expression of growth arrest-and DNA damage-inducible gene 153 (GADD153 ) protein (by Western blot ) .Results Compared with group S ,the apoptosis rate was significantly increased and the expression of GADD153 protein was up-regulated at 6 ,12 ,24 and 48 h of reperfusion in I/R and EA groups ( P<0.05) .Compared with group I/R ,the apoptosis rate was significantly decreased and the expression of GADD 153 protein was down-regulated at 6 ,12 ,24 and 48 h of reperfusion in group EA ( P< 0.05) .The pathological changes were significantly attenuated in group EA as compared with group I/R .Conclusion Electro-acupuncture pretreatment can down-regulate the expression of GADD 153 protein , reduce endoplasmic reticulum stress , and decrease cell apoptosis ,thus attenuating global cerebral I/R injury in rats .

Objective To evaluate the effect of electroacupuncture (EA) preconditioning on activity of AMP-activated protein kinase (AMPK) in hippocampal neurons during cerebral ischemiareperfusion (I/R) in mice.Methods A total of 60 male C57BL6 mice,aged 7 weeks,weighing 20-22 g,were randomly divided into 5 groups (n=12 each) using a random number table:control group (C group),sham operation group (S group),I/R group,acupuncture at acupoint Baihui preconditioning group (EA + I/R group),and acupuncture at non-acupoint preconditioning group (NEA + I/R group).Baihui acupoints were stimulated with electric stimulator (frequency 2 Hz/15 Hz,intensity 1 mA) for 30 min once a day for 5 consecutive days.At 24 h after the last stimulation,the model of cerebral I/R injury was established.Bilateral common carotid arteries were occluded by clipping for 15 min followed by reperfusion.Neurological deficit score (NDS) was assessed at 3 days after operation.Then the mice were sacrificed and the brains were immediately harvested for microscopic examination and for determination of apoptosis in hippocampal neurons (using TUNEL) and expression of phosphor-AMPKα (pAMPKα) and caspase-3 (by Western blot).Results Compared with group C,NDS and the number of apoptotic neurons in hippocampal CA1 region were significantly increased,and the expression of pAMPKα and caspase-3 was up-regulated in I/R and EA+I/R groups,and no significant change was found in the parameters mentioned above in group S.Compared with group I/R,NDS and the number of apoptotic neurons in hippocampal CA1 region were significantly increased,the expression of pAMPKα was up-regulated,and the expression of caspase-3 was down-regulated in group EA +I/R,and no significant change was found in the parameters mentioned above in group NEA+I/R.The pathological changes in hippocampal CA1 region were significantly attenuated in group EA + I/R as compared with group I/R.Conclusion The mechanism by which EA preconditioning mitigates apoptosis in hippocampal neurons during cerebral I/R is related to promotion of AMPK activation in mice.

Objective To investigate the effect of mild hypothermia on the expression of small ubiquitin-like modifier-specific proteases 3 (SENP3) in the brain tissues during cerebral ischemia-reperfusion (I/R) in mice.Methods Ninety-six male C57/BL6 mice,aged 10-12 weeks,weighing 22-30 g,were randomly divided into 3 groups (n =32 each) using a random number table:sham operation group (group S),group I/R,and mild hypothermia group (group H).Cerebral I/R was produced by occlusion of bilateral common carotid arteries for 15 min followed by reperfusion.The surface cooling was started immediately after reperfusion,and the rectal temperature was maintained at 32-34 ℃ for 3 h.At 6,12,24 and 72 h of reperfusion,8 mice were selected from each group and sacrificed.The hippocampi were removed for examination of the pathological changes (with light microscope) and for determination of cell apoptosis (using TUNEL) and expression of SENP3 (by Western blot).The apoptosis rate was calculated.Results Compared with group S,the apoptosis rate in hippocampal CA1 region was significantly increased,and the expression of SENP3 was significantly up-regulated at each time point of reperfusion in group I/R (P＜0.05).Compared with group I/R,the apoptosis rate in hippocampal CA1 region was significantly decreased,and the expression of SENP3 was significantly down-regulated at each time point of reperfusion (P＜0.05),and the pathological changes were significantly reduced in group H.Conclusion The mechanism by which mild hypothermia reduces cerebral I/R injury is associated with inhibition of SENP3 expression in the brain tissues of mice.

Objective To evaluate the effect of mild hypothermia on the activity of hippocampal pro tein kinase R-like endoplasmic reticulum kinase (PERK) in a mouse model of cerebral ischemia-reperfusion (I/R).Methods One hundred and twenty male C56BL6 mice,weighing 20-30 g,aged 7 weeks,were randomly divided into 3 groups (n=40 each) using a random number table:sham operation group (group S),I/R group,and mild hypothermia group (group H).Cerebral I/R was induced by occlusion of bilateral common carotid arteries for 15 min followed by reperfusion in anesthetized mice.In group H,surface cooling was performed immediately after reperfusion,and the rectal temperature was maintained at 32-34 ℃ for 3 h.In I/R and S groups,the rectal temperature was maintained at 36.8-37.2 ℃.At 6,12,24 and 72 h of reperfusion,10 mice were sacrificed in each group,and the hippocampi were removed for determination of the number of apoptotic neurons in hippocampal CA1 region (by TUNEL),and phosphorylated PERK (p-PERK) expression (by Western blot).Results Compared with group S,the number of apoptotic neurons was significantly increased,and the expression of p-PERK was up-regulated at each time point in I/R and H groups (P＜0.05).Compared with group I/R,the number of apoptotic neurons was significantly decreased,and the expression of p-PERK was downregulated at each time point in group H (P＜0.05).Conclusion Mild hypothermia can reduce endoplasmic reticulum stress through inhibiting hippocampal PERK activity,thus attenuating cerebral injury in a mouse model of cerebral I/R.

Objective To investigate the effect of mild hypothermia on glucose regulated protein 78 (GRP78) expression in hippocampus following transient cerebral ischemia-reperfusion (I/R) in aged rats.Methods One hundred and forty-four male aged Sprague-Dawley rats,weighing 450-550 g,were randomly divided into 3 groups (n=48 each): sham operation group (group S),I/R group and mild hypothermia group (group H).Global cerebral I/R was induced by 4-vessel occlusion method.Bilateral vertebral arteries were permanently occluded by cauterization,and bilateral carotid arteries were occluded for 5 min.The surface cooling was started immediately after reperfusion and maintained for 3 h.During surface cooling,the body temperature was maintained at 32-34 ℃(rectal).At 6,12,24 and 48 h of reperfusion,the expression of GRP78 was determined using immuno-histochemisty and Western blot,and the viable neurons in CA1 area were counted.Results The number of viable neurons was significantly smaller at each time point,and the expression of GRP78 was significantly higher at 6,12 and 24 h of reperfusion,while lower at 48 h of reperfusion in I/R group,and the number of viable neurons was significantly smaller,and the expression of GRP78 was significantly higher at each time point in group H than in group S (P＜ 0.05).The number of viable neurons was significantly larger at 12,24 and 48 h of reperfusion,and the expression of GRP78 was significantly higher at each time point in group H than in group I/R (P ＜ 0.05).Conclusion Mild hypothermia can further up-regulate GRP78 expression in hippocampus following transient cerebral I/R in aged rats,thus reducing endoplasmic reticulum stress and cerebral I/R injury.

Objective To evaluate the changes in 5'-adenosine monophosphate-activated protein kinase (AMPK) signal transduction pathway in hippocampal neurons of aged rats during transient global cerebral ischemia/reperfusion (I/R).Methods Ninety-six aged male Sprague-Dawley rats aged 18-22 months,weighing 450-600 g,were randomly allocated to one of two groups (n=48 each):sham operation group (group OS) and transient global cerebral I/R group (group OTIR).Ninety-six yong male Sprague-Dawley rats aged 3 months,weighing 200-250 g,were randomly divided into 2 groups (n=48 each):sham operation group (group AS) and transient global cerebral I/R group (group ATIR).The global cerebral I/R was produced by 3 min four-vessel occlusion followed by reperfusion according to Pulsinelli.On 3,5 and 7 days of reperfusion,12 rats in each group were chosen and sacrificed.Their brains were removed and hippocampal CA1 region was dissected for detection of neuronal apoptosis (by TUNEL) and expression of phosphorylated AMPKα (p-AMPKα) (by Western blot).The apoptotic rate (AR) was calculated.Results Compared with OS group,the AR was significantly increased and the expression of p-AMPKα was up-regulated at each time point in OTIR group,and the AR was significantly decreased and the expression of p-AMPKα was down-regulated at each time point in AS group (P ＜ 0.05).Compared with AS groupthe AR was significantly increased at each time point and the expression of p-AMPKα was up-regulated on day 3 and 5 of reperfusion in ATIR group (P ＜ 0.05).The AR was significantly lower at each time point and the expression of p-AMPKα was down-regulated on day 5 and 7 of reperfusion in ATIR group than in OTIR group (P ＜ 0.05).Conclusion Transient global cerebral I/R can activate AMPK signal transduction pathway in hippocampus of aged rats.The activation of AMPK signal transduction pathway is stronger and the cerebral I/R injury is more severe in aged rats than in young rats.

Objective To evaluate the changes in cholinergic anti-inflammatory pathway in hippocampi global in aged rats with cerebral ischemia/reperfusion (I/R ) injury .Methods One hundred and twenty male Sprague-Dawley rats , aged 18-22 months ,weighing 450-600 g ,were randomly divided into 2 groups ( n= 60 each):sham operation group (group S) and global cerebral I/R group (group I/R) .The animals were anesthetized with intraperitoneal 10% chloral hydrate 0.4 ml/100 g .Global cerebral I/R was induced by 4-vessel occlusion method described by Pulsinelli .Fifteen rats were sacrificed at 1 ,3 ,5 and 7 days of reperfusion ,and brains were removed for determination of neuronal apoptosis and expression of α7 nicotinic acetylcholine receptor (α7nAChR ) , choline acetyltransferase (ChAT ) ,tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in the hippocampal CA1 region .The apoptosis rate was calculated .Results Compared with group S ,the apoptosis rate was increased and the expression of α7nAChR ,ChAT ,TNF-αand IL-1βwas up-regulated in group I/R ( P<0.05 or 0.01 ) . The expression of α7nAChR and ChAT was up-regulated gradually during reperfusion and peaked at 5 day of reperfusion ( P< 0.05 ) .Conclusion Global cerebral I/R injury can activate cholinergic anti-inflammatory pathway in aged rat hippocampi ,and the activation of this pathway is the endogenous mechanism of inhibition of excessive inflammatory responses in brain tissues .

Objective To evaluate the role of AMP?activated protein kinase ( AMPK) in neuronal apoptosis in the hippocampus of aged mice during cerebral ischemia?reperfusion ( I∕R ) . Methods Seventy?two male C57∕BL6 mice, aged 18-20 months, weighing 34-36 g, were randomly divided into 3 groups ( n=24 each ) using a random number table: sham operation group ( S group ) , I∕R group and AMPK inhibitor compound C group ( CC group) . The cerebral ischemia was produced by 15 min transient occlusion of bilateral common carotid arteries followed by reperfusion. In group CC, compound C 20 mg∕kg was injected intraperitoneally immediately after occlusion, while the equal volume of normal saline was given in I∕R group. At 48 h of reperfusion, the mice were sacrificed, and the brains were immediately harvested for examination of pathologic changes in hippocampal CA1 region and for determination of neuronal apoptosis ( using TUNEL) and expression of phosphor?AMPKα ( p?AMPKα) and caspase?3 ( by Western blot) . Results In I∕R and CC groups, the examination showed the pathologic changes in hippocampal CA1 region, the disordered arrangement of pyramidal cells and the nucleus condensation. Compared with S group, the neuronal apoptotic rate was significantly increased, and the expression of p?AMPK and caspase?3 was up?regulated at 48 h of reperfusion in I∕R and CC groups. Compared with I∕R group, the expression of p?AMPK was significantly down?regulated, and no significant change was found in the neuronal apoptotic rate and caspase?3 expression in CC group. Conclusion AMPK is not involved in neuronal apoptosis in the hippocampus of aged mice during cerebral I∕R.