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.

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 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 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 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 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 explore the clinical value of hs-CTnT among acute myocardial infarction patients.Methods 60 acute myocardial infarction patients were treated from July 2014 to October 2016 in our hospital, set as the observation group where venous blood samples were collected on admission, 4 hours after admission, 12 hours after admission and the control group (60 health human where the venous blood samples were collected in the morning), respectively.The hs-CTnT, myohemoglobin, creatine kinase isoenzyme and tropnin T were recorded for analysis.Results On arrival of hospital, the positive rate of CK-MBmass, Myo, hs-cTnT, cTnT was 75.0%、71.7%, 90.8%, 80.0%, respectively.Hs-cTnT positive rate raised to 100.0% and CK-MBmass (83.3%), Myo (75.0%), cTnT (88.3%) after 4 hours.Besides, after hospitalization, the hs-cTnT positive rates raised up.The rates apparently increased at different times (P<0.05).The positive predictive value was 90.0% and sensibility 91.0%, which was significantly higher than other indicators (P<0.05).Conclusion The high sensitivity and specify of hs-cTnT indicator level could be one of the early diagnosis index for acute myocardial infarction.

Objective To investigate the effects of hydrogen-rich saline on hippocampal mammalian target of rapamycin (mTOR)/tau pathway after operation in aged rats.Methods One hundred fifty healthy male Sprague Dawley rats, aged 18 months, weighing 400-540 g, were randomly divided into 5 groups (n=30 each) using a random number table: control group (group C);sham operation group (group S);operation group (group O);hydrogen-rich saline treatment group (group HS);normal saline group (group NS).Splenectomy was performed in group O.Hydrogen-rich saline 1 ml/100 g was injected intraperitoneally at 5 min before splenectomy in group HS.Normal saline 1 ml/100g was injected intraperitoneally at 5 min before splenectomy in group NS.Morris water maze test was performed at 1, 3 and 7 days after surgery, and the escape latency and swimming distance were recorded.After the end of the test, the rats were sacrificed, and the brains were removed for examination of the pathological changes in the hippocampal CA3 region (under light microscope), and for determination of the expression of mTOR mRNA and tau mRNA (using reverse transcriptase polymerase chain reaction) and mTOR and pS396 tau (by Western blot).Results Compared with C and S groups, the escape latency and swimming distance were significantly prolonged, and the expression of mTOR protein and mRNA, tau mRNA and pS396 tau was up-regulated in O, HS and NS groups (P＜0.05).Compared with O and NS groups, the escape latency and swimming distance were significantly shortened, and the expression of mTOR protein and mRNA, tau mRNA and pS396 tau was down-regulated in group HS (P＜0.05).The pathological changes of the hippocampal tissues were mitigated in group HS when compared with group O.Conclusion The mechanism by which hydrogen-rich saline mitigates postoperative cognitive dysfunction may be associated with inhibited activation of hippocampal mTOR/tau pathway in aged rats.

Objective To evaluate the role of hippocampal adenosine monophosphate-activated protein kinase (AMPK) signaling pathway in reduction of postoperative cognitive dysfunction by electroacupuncture (EA) preconditioning in aged rats.Methods A total of 150 healthy male Sprague-Dawley rats,aged 18-20 months,weighing 400-500 g,were randomly divided into 5 groups (n=30 each) using a random number table:control group (group C);splenectomy group (group O);preconditioning with EA at non-acupoint group (group NEA);preconditioning with EA at Baihui acupoint group (group EA);preconditioning with EA at Baihui acupoint + AMPK inhibitor group (group EAC).EA and EAC groups received EA at Baihui acupoints with a sparse-dense wave at an intensity of 1 mA and a frequency of 2 Hz/15 Hz for 30 nin,once a day,for 5 consecutive days,and splenectomy was performed at 24 h after the end of the last stimulation.Group NEA received EA at the points 2 mm lateral to the acupoints of Baihui,and the other treatments were similar to those previously described in group EA.Compound C 20 mg/kg was injected intraperitoneally at 5 min before operation in group EAC.Morris water maze test was performed at 1,3 and 5 days after operation,and the escape latency and swimming distance were recorded.The rats were then sacrificed,and brains were removed for examination of the pathological changes in the hippocampal CA3 region and for determination of the expression of AMPK,phosphorylated AMPK (p-AMPK),nuclear factor kappa B (NF-κB),interleukin-1beta (IL-1β),and tumor necrosis factor-alpha (TNF-α) by Western blot.Results Compared with group C,the escape latency and swimming distance were significantly prolonged,and the expression of AMPK,p-AMPK,NF-κB,IL-13,and TNF-α was significantly up-regulated in O,NEA,EA and EAC groups (P＜0.05).Compared with group O,the escape latency and swimming distance were significantly shortened,and the expression of AMPK,p-AMPK,NF-κB,IL-1β and TNF-α was significantly down-regulated in EA and EAC groups (P＜0.05),and no significant change was found in the parameters mentioned above in group NEA (P＞0.05).Compared with group EA,the escape latency and swimming distance were significantly prolonged,the expression of AMPK and p-AMPK was significantly down-regulated,and the expression of NF-κB,IL-1β and TNF-α was significantly up-regulated in group EAC (P＜0.05).Conclusion Activation of hippocampal AMPK signaling pathway is involved in EA preconditioning-induced improvement in postoperative cognitive dysfunction in aged 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 .