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Objective:To evaluate the effect of hydrogen on the expression of hippocampal cold-inducible RNA-binding protein (CIRP) after cardiac arrest-resuscitation in rats.Methods:Ninety clean-grade healthy male Sprague-Dawley rats, weighing 280-320 g, were randomly divided into 3 groups: sham group (group Sham, n=20), cardiac arrest-cardiopulmonary resuscitation group (group CPR, n=35), and hydrogen-rich saline group (group H 2, n=35). Cardiac arrest was induced by transoesophageal cardiac pacing followed by CPR in group CPR.Only femoral arteriovenous puncture and tracheal intubation were performed in group Sham.Hydrogen-rich saline 5 ml/kg was intraperitoneally injected immediately after recovery of spontaneous circulation (ROSC) and at 6 and 12 h after ROSC in group H 2 , while the equal volume of normal saline was given instead in the other two groups.Neuro-functional deficit was assessed using neurologic deficit scores (NDS) at 1 and 3 days after ROSC.The animals were sacrificed immediately after intubation in group Sham and at 6 h and 1, 2 and 3 days after ROSC in CPR and H 2 groups, and the hippocampal tissues were obtained to detect the expression of nuclear and cytoplasmic CIRP by Western blot. Results:Compared with group Sham, NDS was significantly decreased at each time point after ROSC in group CPR and group H 2, the expression of nuclear CIRP was significantly down-regulated at 1, 2 and 3 days after ROSC, and the expression of cytoplasmic CIRP was up-regulated at 1 and 2 days after ROSC in group CPR, and the expression of nuclear CIRP was significantly down-regulated at each time point after ROSC, and the expression of cytoplasmic CIRP was down-regulated at 2 and 3 days after ROSC in group H 2 ( P<0.05). Compared with group CPR, NDS was significantly increased at each time point after ROSC, the expression of nuclear CIRP was down-regulated at 6 h after ROSC, and the expression of cytoplasmic CIRP was down-regulated at 1 and 2 days after ROSC in group H 2 ( P<0.05). Conclusion:The nechanism by which hydrogen reduces brain injury after cardiac arrest-resuscitation may be related to down-regulating hippocampal CIRP expression in rats.
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Objective To evaluate the effect of mild hypothermia combined with hydrogen-rich saline on cerebral injury after cardiac arrest and resuscitation in rats.Methods Healthy male Sprague-Dawley rats,aged 7-8 weeks,weighing 280-320 g,were divided into 5 groups (n=33 each) using a random number table method:sham operation group (group S),cardiac arrest and resuscitation group (group CAR),hydrogen-rich saline group (group H2),mild hypothermia group (group MH),and mild hypothermia plus hydrogen-rich saline group (group MH+H2).Cardiac arrest was induced with transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the cerebral injury model.Hydrogen-rich saline 5 ml/kg was intraperitoneally injected immediately after return of spontaneous circulation (ROSC) in H2 and MH+H2 groups,while the equal volume of normal saline was given instead in the other groups.The body temperature of rats was cooled down to 32-34℃ within 15 min starting from the time point immediately after ROSC and maintained for 4 h in MH and MH+H2 groups.Fifteen rats were selected at 24 h after ROSC to assess the neurological function score (NDS).Eighteen rats in each group were sacrificed at 24 h after ROSC,and brains were removed for microscopic examination of the pathological changes in hippocampal CA1 region after hematoxylin and eosin staining and for determination of pyramidal cell count and expression of glucose-regulated protein 78 (GRP78),C/EBP-homologous protein (CHOP),caspase-12,caspase-3,Bcl-2 and Bax in hippocampal CA1 region (by Western blot).Results Compared with group S,the NDS was significantly decreased,the pyramidal cell count was reduced,the expression of GRP78,CHOP,caspase-12,caspase-3 and Bax was up-regulated,and the expression of Bcl-2 was down-regulated in the other four groups (P＜0.05).Compared with group CA-R,the NDS and pyramidal cell count were significantly increased,the expression of GRP78 and Bcl-2 was up-regulated,and the expression of CHOP,caspase-12,caspase-3 and Bax was down-regulated in H2,MH and MH+H2 groups (P＜0.05).Compared with group H2 or group MH,the NDS and pyramidal cell count were significantly increased,the expression of caspase-3 and Bax was down-regulated,the expression of Bcl-2 was up-regulated (P＜0.05),and no significant change was found in the expression of GRP78,CHOP and caspase-12 in group MH+H2 (P＞ 0.05).Conclusion Combination of mild hypothermia and hydrogen-rich saline offers enhanced efficacy in reducing cerebral injury after cardiac arrest and resuscitation over mild hypothermia or hydrogen-rich saline alone in rats.
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Objective To evaluate the changes in expression of cold-inducible RNA-binding protein (CIRP) in hippocampus during brain injury in a rat model of cardiac arrest-cardiopulmonary resuscitation.Methods Seventv-two clean-grade healthy male Sprague-Dawley rats,weighing 280-350 g,aged 8-10 weeks,were divided into 2 groups using a random number table:sham operation group (S group,n=18) and ischemia-reperfusion group (I/R group,n=54).Tracheal intubation was performed and artery and veins were punctured in group S.Ventricular fibrillation was induced by transoesophageal cardiac pacing to establish the model of cardiac arrest in group I/R.Rats were sacrificed at 12,24 and 48 h after resuscitation and the hippocampus was harvested for determination of CIRP,tumor necrosis factor-alpha (TNF-α) and interleukin-lbeta (IL-1β) protein and mRNA expression (by quantitative polymerase chain reaction or Western blot) and for determination of pathological changes of hippocampi (with a light microscope).Results Compared with group S,the expression of CIRP mRNA in hippocampus was up-regulated at 24 and 48 h after resuscitation,the expression of TNF-α mRNA was up-regulated at 12,24 and 48 h after resuscitation,the expression of IL-1β mRNA was up-regulated at 12 and 24 h after resuscitation,and the expression of CIRP,TNF-α and IL-1β was up-regulated at 12,24 and 48 h after resuscitation in group I/R (P＜0.05).Pathological changes in hippocampal CA1 region were found in group I/R.Conclusion The expression of CIRP in hippocampus is up-regulated,which promotes central inflammatory responses during brain injury in a rat model of cardiac arrest-cardiopulmonary resuscitation.
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Objective The purpose of this study was to assess the safety of carbon dioxide pneumoperitoneum on patients during robotic rectectomy.Methods 50 patients [American Society of Anesthesiologists (ASA) physical status Ⅱ,18 and 65 years of age] underwent rectal cancer surgery were selected in our study.According to whether or not robotic assisted surgery was performed,they were divided into a robotic surgery group (group RS) and a laparoscopic surgery group (group LS) by surgical approach,25 patients in each group.All participants were given the same anesthesia protocol.Arterial blood samples 1 ml was obtained from the left radial artery for blood gas analysis to measure the partial pressure of arterial carbon dioxide (PaCO2) and and calculate the arterial-to-end-tidal carbon dioxide pressure difference (Pa-ETCO2) just 10 min after endotracheal intubation (T0),at 30 min(T1),1 h(T2),2 h(T3) after pneumoperitoneum and 30 minutes after release (T4).Meanwhile,the airway peak pressure was monitored.Blood samples (4 ml) extracted at T0,T3 and T4 were centrifuged and measured the serum levels of interleukin (IL)-6 and IL-10 by enzyme linked immunosorbent assay (ELISA).The time to resuscitation,extubation time,intraoperative medication and perioperative adverse events were all recorded.Results Compared with group LS,PaCO2 in the RS group was increased significantly at T1,T2 and T3 after pneumoperitonum and the IL-6 was lower at T4 (P ＜ 0.05).There were no statistically significant differences in Pa-ETCO2,airway peak pressure,IL-10,time to resuscitation,extubation time and the incidence of adverse events between the two groups (P ＞ 0.05).Conclusions It is safe for normal adult patients performed by intravenous anesthesia during robotic-assisted rectal surgery and the inflammatory response is small,which is beneficial to the patient's postoperative recovery.
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Objective To observe different behavior of proliferation,migration and invasion of SGC-7901 cells when exposured to dexrnedetomidine of different concentrations.Methods Human gastric cancer cells SGC-7901 were inoculated on culture plate for 24 h,then were randomly divided into 5 groups:control group (group C),dexmedetomidine 312.5μg/ml group (group D1),dexme detomidine 625μg/ml group (group D2),dexmedetomidine 1 250 μg/ml group (group D3),dexmedetomidine 2 500 μg/ml group (group D4).Each group was medicated and incubated for 48 h,then the cell proliferation,migration and invasion immediately were detected by CCK-8 and Transwell.Results SGC-7901 cell viability of groups D1,D2,D3 和 D4 had no significant difference compared with that of group C.The invasion ability and migration ability of SGC-7901 cells in groups D1,D2,D3 and D4 were significantly higher than those in group C (P ＜ 0.05 or P ＜ 0.01).Conclusion Dexmedetomidine can promote migration and invasion of SGC-7901 cells.
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Objective To investigate the effect of mild hypothermia combined with mitochondrial divison inhibitor 1 in mitochondrial after cerebral ischemia-reperfusion (IR).Methods Fourty male healthy Sprague-Dawley (SD) rats, weighing 280-320 g, were randomly divided into 5 groups (n=8 each): group Sham, group IR, hypothermia group (group H), Mdivi-1 group (group M) and hypothermia+Mdivi-1 group (group HM).Animal models of global cerebral IR were established by transoesophageal cardiac pacing inducing cardiac arrest followed by cardiopulmonary resuscitation (ischemia 4 min and reperfusion 6 h).The group Sham was similarly treated to group IR except the cardiac arrest and cardiopulmonary resuscitation.In groups H and HM, the core temperature was cooled down to 32-34℃ within 15 min starting from the beginning of reperfusion, and maintained for 6 h.In the other groups, the core temperature was maintained at the normal temperature.In groups M and HM, the animals were given Mdivi-1 (1.2 mg/kg) intravenously at the beginning of the reperfusion and the other groups were given the same Volume of dimethylsnlfone (DMSO).After 6 h of reperfusion, the rats were sacrificed, and bilateral hippocampi were immediately removed for determination the protein level of dynamin-related proten 1 (Drp1) and cytochrome C (Cyt-C) expression by Western blot and obsevation of the mitochondrial structure of pyramidal cell in hippocampal CA1 under electronic microscope.Results Compared with group Sham, the expression of Drp1 and Cyt-C was up-regulated in groups IR, H, M and HM (P＜0.05).Compared with group IR, the expression of Drp1 and Cyt-C was down-regulated in groups H, M and HM (P＜0.05).Compared with groups H and M, the expression of Drp1 and Cyt-C was down-regulated in group HM (P＜0.05).There was no significant difference in the expression of Drp1 and Cyt-C between groups H and M.The mitochondria were rod-shaped with clear and sound structure in group Sham, while mitochondria showed various degree of fission, swollen structures, matrix deposit, vacuoles formation and cristae collapse in other groups.The changes of group HM were relatively slight.Conclusion Mild hypothermia combined with mitochondrial divison inhibitor 1 alleviate mitochondrial damage after global cerebral IR of rats.The combined effect is better than that of any individual application.
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Objective To observe the effect of continuous incision infusion different concentra-tion of ropivacaine for postoperative analgesia after radical mastectomy.Methods One hundred pa-tients under radical mastectomy,aged 40-70 years,ASA Ⅰ or Ⅱ,were randomly divided into four groups (n =25 each):0.2% (group R1),0.3% (group R2),0.4% (group R3)ropivacaine incision continued infiltration group and patient-controlled intravenous analgesia (group PCIA)as control group.VAS pain scores,sedation Ramsay score and side effects were recorded at each time point in rest and turning over 90°,2 h (T1 ),4 h (T2 ),8 h (T3 ),12 h (T4 ),24 h (T5 ),48 h (T6 )after the operation.Results VAS scores in group R1 at T1-T6 in rest and turn over 90°were significantly high-er than that of group PCIA (P <0.05).There were no significant differences among the group PCIA, group R2 and group R3.Sedation score in PCIA group was significantly higher than that in the other three groups (P <0.05),and the adverse reactions,such as nausea and vomiting,in group PCIA (2 cases)were more serious than that in the other groups (0 cases ).There were no significant differences among the other groups.Conclusion Ropivacaine plays an effective role in infiltration an-algesia when its concentration reaches 0.3% subcutaneous after radical mastectomy.
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Objective To evaluate the effect of hydrogen sulfide on hippocampal endoplasmic reticulum stress during global cerebral ischemia-reperfusion (I/R) in rats.Methods Seventy-two pathogen-free healthy male Sprague-Dawley rats,weighing 280-320 g,aged 8-10 weeks,were divided into 3 groups (n=24 each) using a random number table:sham operation group (group Sham),global cerebral I/R group (group I/R) and global cerebral I/R plus sodium hydrosulfide group (group I/R+NaHS).Cardiac arrest was induced with transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the global cerebral I/R model.Immediately after recovery of spontaneous circulation,sodium hydrosulfide 2.5 mg/kg was intraperitoneally injected in group I/R+NaHS,and normal saline 5 ml/kg was given in group I/R.The hippocampi were immediately removed at 24 h of reperfusion for determination of the expression of glucose-regulated protein 78 (GRP78),C/EBP-homologous protein (CHOP) and caspase-12 in hippocampal tissues (by Western blot).At 1,3 and 7 days of reperfusion,the hippocampal tissues were obtained and stained with haematoxylin and eosin for examination of the pathological changes in hippocampal CA1 region (under a light microscope) and for determination of apoptosis in hippocampal cells (using TUNEL staining),and the apoptosis rate was calculated.Results Compared with group Sham,the apoptosis rate of hippocampal tissues at 1,3 and 7 days of reperfusion in group I/R and at 3 and 7 days of reperfusion in group I/R+NaHS were significantly increased,and the expression of GRP78,CHOP and caspase-12 in hippocampal tissues was significantly up-regulated in I/R and I/R+NaHS groups (P＜0.05).Compared with group I/R,the apoptosis rate of hippocampal tissues was significantly decreased,and the expression of GRP78,CHOP and caspase-12 was down-regulated at 1,3 and 7 days of reperfusion (P＜0.05),and the pathological changes were significantly attenuated in group I/R+NaHS.Conclusion The mechanism by which hydrogen sulfide reduces apoptosis in hippocampal cells is related to inhibition of endoplasmic reticulum stress during global cerebral I/R in rats.
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Objective To evaluate the effect of hypothermia on the expression of dynamin?related protein 1 ( Drp1) in brain tissues during global cerebral ischemia?reperfusion ( I∕R) in rats. Methods Thirty?six healthy male Sprague?Dawley rats, weighing 280-320 g, were divided into 3 groups ( n=12 each) using a random number table: sham operation group ( group Sham ) , global cerebral I∕R group ( group I∕R) and hypothermia group ( group H) . Cardiac arrest was induced by transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the global cerebral I∕R model in anesthetized rats in I∕R and H groups. In group H, the body temperature ( rectal temperature) was cooled down to 32-34 ℃ within 15 min starting from the beginning of reperfusion, and maintained at this level for 6 h. At 72 h of reperfusion, neurological deficit was scored, and the rats were sacrificed, and the whole brain was removed for examination of the pathological changes in hippocampal CA1 region and for determination of nor?mal pyramidal cell count and neuronal apoptosis in hippocampal CA1 region and expression of Drp1 and cy?tochrome c (Cyt c) in hippocampal tissues (by Western blot). The apoptosis rate was calculated. Re?sults Compared with group S, the neurological deficit score and apoptosis rate were significantly in?creased, and the number of normal pyramidal cells was decreased in I∕R and H groups, the expression of Drp1 and Cyt c in hippocampal tissues was significantly up?regulated in group I∕R ( P0.05) . Compared with group I∕R, the neurological deficit score and apoptosis rate were significantly de?creased, the number of normal pyramidal cells was increased, and the expression of Drp1 and Cyt c in hip?pocampal tissues was down?regulated in group H ( P<0.05) . Conclusion The mechanism by which hypo?thermia inhibits cell apoptosis during global cerebral I∕R may be related to down?regulation of Drp1 expres?sion in rats.
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Immune response after blood transfusion is closely related to prognosis of the patients receiving blood productions. Thus, the safety and effectiveness are paid increasing attention.This article reviews immunological consequence and clinical manifesta-tions and response strategies after transfusion, which aims to provide reference for clinical transfusion decisions.
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Objective To investigate the efficacy and safety of dexmedetomidine on prevention of emergence agitation in adult patients during recovery period after abdomen surgery.Methods 1 20 ASA I -II patients scheduled for elective abdominal surgery under general anesthesia were randomly divided into three groups:dexmedetomidine group (group A),midazolam group (group B)and the saline control group (group C),40 cases in each group.40min before the end of surgery,dexmedetomidine 0.6μg/kg was continued intravenous infusion 1 0min in group A,midazo-lam 30μg/kg and 1 mL physiological saline were respectively intravenously injected in group B and group C.The post-operative recovery room (PACU)of restlessness,sedation,blood pressure,SpO2 and extubation time were observed. Results In of midazolam group,the time of anesthesia recovery[(1 8.2 ±1 .9)min],extubation[(32.1 ±3.9)min] and PACU staying[(48.7 ±3.1 )min]were significantly longer compared with the dexmedetomidine group[(1 3.1 ± 2.4)min,(26.5 ±2.2)min and (39.8 ±3.4)min,P =0.023,0.040 and 0.003]and the saline group[(1 2.6 ± 2.3)min,(24.8 ±2.9)min and (38.6 ±4.3)min,P =0.01 7,P =0.023 and P =0.001〗.The postoperative seda-tion scores of dexmedetomidine [(2.3 ±0.2 )points,P =0.025 ]and midazolam group [(2.4 ±0.1 )points,P =0.020]were significantly higher than the saline control group[(1 .1 ±0.5)points].The postoperative agitation score of dexmedetomidine (1 .3 ±0.5)points was lower than midazolam group [(2.5 ±0.5)points,P =0.01 1 ]and the saline control group[(2.4 ±0.6)points,P =0.020].HR and MAP of three groups at 2 min before extubation were observed,in the immediate extubation and at 5 min after extubation,the HR of dexmedetomidine group[(62.7 ± 4.1 )times/min,(67.3 ±3.4)times/min and (63.2 ±4.3)times/min]was significantly delayer than midazolam group [(72.3 ±3.4)times/min,(84.9 ±5.3)times/min and (82.1 ±3.1 )times/min],(P =0.002,P =0.001 and P =0.001 )and the saline control group [(73.6 ±2.9 )times/min,(85.3 ±4.7 )times/min and (83.3 ± 4.5)times/min],(P =0.001 ,P =0.023 and P =0.038)at the three time.In the immediate extubation,the MAP of patients in dexmedetomidine group[(87.3 ±4.2)mmHg)]was lower than midazolam group[(93.1 ±4.3)mmHg, P =0.001 ]and the saline control group[(95.6 ±5.8)mmHg,P =0.001 ].At 5 min after extubation,the MAP of patients in both of dexmedetomidine[(84.5 ±3.1 )mmHg)]and midazolam[(85.1 ±2.9)mmHg]group were lower than that in the saline control group[(92.3 ±4.6)mmHg,P =0.023 and P =0.038〗.Conclusion Dexmedetomi-dine could be one of the ideal drug to relieve emergence agitation in adult patients during recovery period after abdo-men surgery and the curative effect is better than midazolam.
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Objective To evaluate the effects of different concentrations of hydroxyethyl starch (HES) 130/0.4 applied for different time periods on injury to human renal tubular epithelial cells.Methods Human renal kidney epithelial cells HK-2 at the logarithmic growth phase were seeded in 96-well plates at a density of 1 × 105 cells/ml (0.1 ml/well),in culture flasks (5 ml/flask) or in cluture dishes (5 ml/dish).HK-2 cells were randomly divided into 4 groups (n=49 each) using a random number table:control group (group C) and 0.3％,1.5％ and 3.0％ HES 130/0.4 groups (H1,H2 and H3 groups).In H1,H2 and H3 groups,HK-2 cells were incubated with 0.3％,1.5％ and 3.0％ HES 130/0.4,respectively.The equal volume of PBS was added to the culture medium in group C.At day 1,3,5 and 7 of incubation,the cell viability was measured.At day 3,5 and 7 of incubation,cell apoptosis was detected,and apoptosis rate was calculated.On day 7 of incubation,the cells were stained with toluidine blue for examination of intracellular HES deposition (under light microscope) and pathological changes (with transmission electron microscope).Results Compared with group C,the cell viability was significantly decreased on day 5 and 7 of incubation,and apoptosis rate was increased on day 3,5 and 7 of incubation in group H3,and no significant difference was detected in the parameters mentioned above in H1 and H2 groups.Microscopic examination showed that intracellular HES deposition was observed in H2 and H3 groups,and pathological changes were obvious,and apoptotic cells were also found in H3 group.Conclusion Application of high-concentration HES 130/0.4 for a long period can lead to injury to human renal tubular epithelial cells,however,application of high-or low-concentration HES 130/0.4 for a short period produces no influence on the cells.
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BACKGROUND:Although the mechanism why neuronal cels wil die after transient cerebral ischemia has not been completely elucidated, many researches nowadays have investigated the pathological mechanism in the level of celular organs, such as mitochondria. OBJECTIVE:To summarize and discuss the functions of neuronal mitochondria and apoptosis signaling pathways in transient cerebral ischemia. METHODS: A computer-based online retrieval was performed to search papers in CNKI and PubMed databases using the key words of “cerebral ischemia, mitochondrion, apoptosis, reactive oxygen species, reperfusion, superoxide dismutase, nitric oxide synthase, Bcl-2 protein family, review” in Chinese and English, respectively. Papers published recently or in the prestigious journals were selected in the same field. After excluding objective-independent papers and repeated studies, 50 papers were included for further analysis. RESULTS AND CONCLUSION:Recently mitochondria are found to play an important role after transient cerebral ischemia by producing a lot of reactive oxygen species to activate many kinds of signaling pathways and regulate mitochondria-mediated apoptosis. Reactive oxygen cannot only induce biomacromolecule injury but also induce apoptosis signal transduction. Deeply investigation is needed on the pathological mechanism after transient cerebral ischemia.
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Objective To evaluate the role of autophagy in apoptosis in cortical neurons of rats in the early phase of oxygen-glucose deprivation (OGD).Methods Female Sprague-Dawley rats at 16-18 days of gestation,weighing 350-400 g,were sacrificed after being anesthetized with pentobarbital sodium.The fetal rats were obtained and the primary cortical neurons were isolated and seeded in culture plates.The neurons were then divided into 4 groups (n =7 each) using a random number table:control group (group C),OGD 30 min group,OGD 1 h group,OGD 2 h group,and OGD 3 h group,OGD + autophagy inducer rapamycin group (OGD + R group),and OGD + autophagy inhibitor 3-methyladenine (3-MA) group (OGD + 3-MA group).The neurons were incubated in sugar-free DMEM medium containing 5％ CO2 and 95％ N2 for 30 min,1,2 and 3 h in OGD 30 min,1 h,2 h,and 3 h groups,respectively.Rapamycin (final concentration of 100 nmol/L) and 3-MA (final concentration of 10 mmol/L) were added to sugar-free DMEM medium in OGD + R and OGD + 3-MA groups,respectively,and the neurons were then incubated for 1 h.The CCK-8 assay was used to detect the neuronal viability after the end of OGD.The expression of caspase-3 and LC3 Ⅱ was measured by Western blot.Results Compared with C group,the survival rates of cortical neurons were significantly decreased in the other groups,the expression of LC3 Ⅱ was up-regulated in OGD 30 min,1 h,2 h and 3 h groups,no significant change was found in caspase-3 expression in OGD + R group,and the expression of caspase-3 was up-regulated in the other groups.Compared with OGD 1 h group,the survival rates of cortical neurons were significantly decreased in OGD2 h,OGD3 h and OGD + 3-MA groups,the survival rates of cortical neurons were increased,and the expression of caspase-3 was down-regulated in OGD + R group,the expression of LC3 Ⅱ was up-regulated in OGD + 3-MA group,and the expression of LC3 Ⅱ was down-regulated in OGD2 h and 3 h groups.Conclusion Autophagy initiated in the early phase of OGD can inhibit apoptosis in cortical neurons of fetal rats.
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Objective Research has indicated that hydrogen sulfide(H2S) can regulate the function of N-methyl-D-aspartate re-ceptors(NMDARs) in the brain, but its effect on brain resuscitation requires further investigation.The study was to speculate the effect of H2 S on brain resuscitation as well as the underlying mechanism of neuroresuscitation by investigating the effects of hydrogen sulfide and hypo-thermia on the expression of NR2A, NR2B and phospho-cAMP response element binding protein (p-CREB) of NMDARs in the hippocampus after global cerebral ischemia following by reperfusion. Methods 100 male SD rats were randomly divided into five groups(n=20):sham operation group, model group, mild hypothermia group, NaHS group, NaHS combined mild hypothermia group.Pulsinelli-Brierley four-ves-sel occlusion method was induced to build the injury rat model by reperfusion after global cerebral ischemia .After 15 minutes'ischemia, im-mediate injection of 14μmol/kg NaHS was performed intraperitoneally on NaHS group and NaHS combined mild hypothermia group , while skin cooling(rectal temperature=32-33℃) was done on mild hypothermia group and NaHS combined mild hypothermia group .6 hours late,r hip-pocampus were extracted from rat heads.Respectively, spectrophotometer was applied to measure the content of H2S, Western blot for the expres-sions of NR2 A,NR2 B and pC-REB, and RTP-CR for mRNA level of brain derived neurotrophic (BDNF). HE staining was also performed on brain tissues 72hours after reperfusion on 4 rats from each group to evaluate the pathological changes of pyramidal neurons in CA1 region. R esul ts The content of H 2 S increased in each of the four groups after ischemia-reperfusion compared with sham operation group ( 15.2 ±2.0 nmol/g) (P0.05).The gray values of NR2A and NR2B in each group increased compared with sham operation group(P1 in NaHS group and NaHS combined mild hy-pothermia group.Compared with the expression of p-CREB(0.55 ±0.06) in model group, there were significant increases in mild hypother-mia group(0.99 ±0.15), NaHS group(1.05 ±0.12), NaHS combined mild hypothermia group(1.02 ±0.15)(P<0.05).Compared with the expression of BNDF mRNA(0.83 ±0.12) in model group, there were significant increases in mild hypothermia group (1.11 ±0.13), NaHS group(1.27 ±0.16), NaHS combined mild hypothermia group(1.35 ±0.16)(P<0.05).In comparison to model group, there were signifi-cant alleviation in the injury of pyramidal neurons in hippocampal CA1 region in mild hypothermia group, NaHS group, NaHS combined mild hypothermia group, with the best effect in NaHS combined mild hypothermia group . Conclusion Hydrogen sulfide combined mild hypo-thermia can selectively activate synaptic NMDA receptors and trigger the prosurvival CREB signaling pathway to exert brain resuscitation .
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Objective To investigate the effect of dezocine combined with sufentanil on postop-erative analgesia and side effects in the upper-abdominal surgery and hip replacement surgery,and ex-plore the potential mechanisms.Methods One hundred patients scheduled for selective upper-abdomi-nal operation and hip replacement surgery were randomly divided into group dezocine (group D), dezocine 0.3 mg/kg combined with sufentanil 1 μg/kg group(group DS1),dezocine 0.3 mg/kg com-bined with sufentanil 1.5 μg/kg group(group DS2)and dezocine 0.3 mg/kg combined with sufentanil 2 μg/kg group(group DS3).Analgesia was maintained by remifentanil 6-8 μg·kg-1·h-1 under total intravenous anesthesia.Patients were administered 5 μg sufentanil during sewing the skin.Visual Analogue Score (VAS)of both silence and 90°turn over situation,Ramsay score,and adverse effects at 1 h (T1 ),4 h (T2 ),8 h (T3 ),12 h (T4 ),24 h (T5 ),36 h (T6 ),48 h (T7 )after the operation were recorded respectively.Results The total amount of sufentanil and dezocine of group DS1 group showed a significant higher than the other three groups (P <0.05).The VAS in silence of group DS1 were higher than group DS3 at T1-T3 (P <0.05).There was no significant difference in VAS under 90°turn over situation.The side effect of group DS3 were higher than the other three groups (P <0.05).Conclusion Dezocine combined with sufentanil for postoperative patient-controlled intravenous analgesia(PCIA)is effective and safe in patients undergoing upper-abdominal surgery and hip replace-ment surgery,and while dezocine 0.3 mg/kg combined with sufentanil 1.5 μg/kg,it has the best effect of postoperative analgesia and least side effects.
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Objective To evaluate the effect of hydrogen-rich saline on the regulatory T cells (Tregs ) in the peripheral blood during global cerebral ischemia-reperfusion (I/R ) in rats .Methods Seventy-seven male Sprague-Dawley rats ,aged 2-3 months ,weighing 260-300 g ,were randomly divided into 3 groups using a random number table:sham operation group (group S , n=11) ,group I/R (n=33) ,and hydrogen-rich saline group (group H , n=33 ) .Global cerebral I/R was produced by 4-vessel occlusion method .The bilateral carotid arteries were blocked for 15 min followed by reperfusion in I/R and H groups .In group H ,0.6 mmol/L hydrogen-rich saline 5 ml/kg was injected intraperitoneally at 0 and 6 h of reperfusion ,while the equal volume of normal saline was injected instead in the other two groups .Before ischemia (T0 ) in group S and at 6 ,24 and 72 h of reperfusion (T1-3 ) in I/R and H groups ,7 rats were chosen ,the blood samples from the peripheral vein were collected for determination of the number of Tregs . Then the animals were sacrificed and the spleen was removed for measurement of transforming growth factor-β1 (TGF-β1) content .The left 4 rats of each group were sacrificed at T0 and T1-3 and the brains were obtained for examination of the pyramidal cell morphology in the hippocampal CA 1 region and for determination of the number of pyramidal cells in brain tissues .Results Compared with group S , the number of pyramidal cells in the hippocampal CA1 region ,the number of Tregs in the peripheral blood and content of TGF-β1 in the spleen were significantly decreased at T1-3 in group I/R ( P<0.05) .Compared with group I/R ,the number of pyramidal cells in the hippocampal CA 1 region and the number of Tregs in the peripheral blood at T2-3 ,and the content of TGF-β1 in the spleen at T1-3 were significantly increased ( P<0.05) ,and the pathological changes of pyramidal cells were attenuated in group H .Conclusion The mechanism by which hydrogen-rich saline attenuates global cerebral I/R injury may be related to the increased number of Tregs in peripheral blood and promoted secretion of TGF-β1 in rats .
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Objective To evaluate the effects of hydrogen-rich saline on the expression of miR-210 and miR-21 in hippocampus during global cerebral ischemia-reperfusion (I/R) in rats.Methods Seventy-two healthy male Sprague-Dawley rats,aged 9-10 weeks,weighing 250-300 g,were randomly divided into 3 groups (n =24 each):sham operation group (group S),group I/R,and hydrogen-rich saline group (group H).Global cerebral I/R was produced by 4-vessel occlusion method.In group H,0.6 mmol/L hydrogen-rich saline 5 ml/kg was injected intraperitoneally at 0 and 6 h of reperfusion,while the equal volume of normal saline was injected instead of hydrogen-rich saline in the other two groups.Rats were sacrificed at 24 and 72 h of reperfusion,and then the bilateral hippocampi were removed for detection of the expression of miR-210 and miR-21 using RT-PCR.The global brain tissues were also obtained and stained with HE for examination of the changes in pyramidal cells in the CA1 region of hippocampus.Results Compared with group S,the expression of miR-210 and miR-21 was significantly up-regulated,and the number of pyramidal cells was decreased in group I/R (P ＜ 0.05).Compared with group I/R,the expression of miR-210 and miR-21 was significantly down-regulated,and the number of pyramidal cells was increased in group H (P ＜ 0.05).The pathological changes were significantly ameliorated in group H.Conciusion The mechanism by which hydrogen-rich saline attenuates global cerebral I/R injury is related to downregulation of the expression of miR-210 and miR-21 in rat hippocampus.
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ObjectiveTo explore the effects of different doses of PcTx1,a specific blocker of acid-sensing ion channel 1a,on global cerebral ischemia/repedfusion (I/R) injury in rats,MethodsSixty adult male Sprague Dawley rats (weighing 250-300 g) were randomly divided into 6 grups ( n =10 each):sham operation group (group S),I/R group,different doses of PcTx1 ( 10 ng/ml,group P1 ; 25 ng/ml,group P2 ; 50 ng/ml,group P3 ;and 500 ng/ml,group P4 ) groups.Global cerebral ischemia was induced by the modified procedure of Pulsinelli 4-vessel occlusion.In groups P1,P2,P3 and P4,different doses of PcTx1 ( 10,25,50 and 500 ng/ml),6 μl each,were respectively injected into the lateral cerebral ventricle at the initiation of reperfusion,while equal volume of double distilled water was injected instead in group I/R.Six rats in each group were sacrificed at 24 h of reperfusion,and the brains were immediately removed,Thereafter,the contents of malondialdehyde (MDA),reduced glutathione (GSH) and ritric oxide (NO),the activities of constitutive NO synthase (eNOS) snd inducible NO synthase (iNOS) were detected in hippocampus.Four rats in each group were sacrificed at 72 h of reperfusion,and hematoxylin and eosin staining was used to observe the pathomorphological changes of the hippocampal neurons.ResultsCompared with group S,the other groups showed decreases in the contents of GSH,while increases in the contents of MDA and NO and the activities of cNOS and iNOS ( P ＜ 0.05 or 0.01 ).The contents of GSH increased,while the contents of MDA and NO and the activities of cNOS and iNOS decreased in groups P2,P3 and P4 compared with group I/R ( P ＜ 0.05 or 0.01).Compared with group P1,the contents of GSH increased,the contents of MDA and the activities of cNOS decreased in groups P2,P3 and P4,and the contents of NO and the activities of iNOS decreased in groups P3 and P4 ( P ＜ 0.05 or 0.01 ).Compared with group P2,the activities of iNOS decreased in groups P3 and P4(P ＜ 0.05 or 0.01).The damage to neurons in hippocampal CAI was severe in groups I/R and P1,but it was attenuated in groups P3 and P4.ConclusionPcTx1 25,50 and 500 ng/ml (6 μl)injected into lateral cerebral ventricle can attenuate global cerebral I/R injury in rats,and the dose 50 ng/ml (6 μl) is more suitable.
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Objective To investigate the role of acid-sensing ion channel 1a(ASIC1a) in global cerebral ischemia-reperfusion injury in rats.Methods Forty male SD rats weighing 250-300 g were randomly divided into 4 groups (n =10 each): sham operation group (group S),cerebral ischemia-reperfusion group (group I/R),solvent control group (group SC) and group PcTX1 (a ASIC1 a blocker,group P).Global cerebral ischemia-reperfusion was induced by four-vessel occlusion.PcTX1(500 ng/ml)6 μl or solvent 6 μl was injected into the crerbral ventricular at the begining of reperfusion in groups P and SC respectively.The rats were sacrificed at 24 h of reperfusion,and then the hippocampi were removed for determination of Caspase-3,Bcl-2 and Bax protein expression and microscopic examination.Results Compared with group S,the expression of Caspase-3,Bcl-2 and Bax protein was up-regulated in groups I/R,SC and P (P ＜ 0.05).Compared with group I/R,the expression of Caspase-3 and Bax was down-regulated,and the expression of Bcl-2 was up-regulated in group P ( P ＜ 0.05).There was no significant difference in Caspase-3,Bcl-2 and Bax protein expression between groups I/R and SC (P ＞ 0.05).The histopathologic damage was ameliorated in group P as compared with group I/R.Conclusion ASIC1a can induce global cerebral ischemia-reperfusion injury in rats by up-regulating Caspase-3 and Bax expression,and down-regulating Bcl-2 expression and inducing apoptosis.