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Objective To observe the effects of three pretreatments of electroacupuncture with different waveforms for septic brain injury in rats, and to explore the optimal waveform. Methods Eighty male Sprague-Dawley rats were divided randomly into five groups (n = 16):sham group,cecal ligation and puncture group (group CLP),continuous wave group (group CW),dilata-tional wave group (group DW)and intermittent wave group (group IW).A rat sepsis model was pre-pared by cecal ligation and puncture.Brain water content was detected.Tumor necrosis factor (TNF)-α,interleukin(IL)-6,malondialdehyde (MDA)and superoxide dismutase (SOD)in serum and frontal cortex were detected 48 h after sham or CLP operation.Pathological changes of frontal cortex,ex-pression of Toll-like receptor-4 (TLR4),and apoptosis of nerve cells were observed by hematoxylin and eosin staining (H&E),immunohistochemistry and TUNEL assay,respectively.Results Com-pared with the sham group,encephaledema,as well as brain injury and neuron apoptosis increased in group CLP (P <0.05).Concentrations of tumor necrosis factor-α,interleukin-6,and malondialdehyde in serum and frontal cortex significantly increased,and the activities of superoxide dismutase significantly de-creased (P < 0.05 ).The expression of TLR4 significantly increased (P < 0.05 ).Compared with group CLP,the aforementioned indicators in the continuous,dilatational,and intermittent wave groups significantly improved (P < 0.05 ).Compared among the electroacupunctured groups,the effect of dilatational wave was the most significant,followed by intermittent wave,and continuous wave was the least one (P <0.05).Conclusion EA pretreatment with different waveforms at Baihui and Tsusanli acupoints could reduce the septic brain injury,and DW might be the best one.The mechanism might be related with the inhibition of inflammation and oxidative stress response and the decrease in nerve cell apoptosis.
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Objective To evaluate the the protectice effect of dexmedetomidine combined limb remote ischemic postcondition on alleviating focal cerebral ischemic reperfusion injury in rats .Methods 48 healthy adult male SD rats were randomly divided into 4 groups(n= 12) :control group(C) ,limb remote ischemic postcondition group(R) and dexmedetomidine postconditioning group(D) and combination group(R/D) .The rat model of focal cerebral ischemic reperfusion injury was induced by middle cerebral artery oc‐clusion(MCAO) .The group C only received MCAO ,the left femoral artery was isolated without blocking ;the group R received 120 min brain ischemia ,the left femoral artery was occluded by 3 cycles of 10 min occlusion/10 min reperfusion before brain reperfu‐sion ;the group D received dexmedetomidine 3 μg/kg by intraperitoneal injection before brain reperfusion .The group R/D combined the above two kinds of processing method .The neurologic function was evaluated at 24 h of reperfusion and then the rats were sac‐rificed at 48 h of reperfusion .The brain was removed for determining the cerebral infarct volume .Results The neurologic function scores after 24 h reperfusion in the group D ,R and R/D were superior to those in the group C (P< 0 .01) .The rat cerebral infarct volume percentages after 48 h reperfusion in the group D ,R and R/D were significantly lower than those in the group C ( P <0 .01) .The infarct area volume percentage in the group R/D was significantly lower than that in the group R ,the difference showed statitistical significance(P< 0 .01) .The infarct volume percentage in group R/D was significantly decreased compared with the group D(P< 0 .05) .Conclusion Both dexmedetomidine and limb remote ischemic postcondition can attenuate the focal cerebral is‐chemic reperfusion injury in rats .Their combination can significantly reduce the cerebral infarction volume and has synergic protec‐tion effect .
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Objective To investigate the role of large-conductance Ga2+-activated K+ (BKCa) channels and protein kinase G (PKG) in ketamine-induced isolated tracheal smooth muscle relaxation in rats with asthma.Methods Healthy Sprague-Dawley rats,weighing 250-300 g,were used in this study.Asthma was induced with egg albumin.Thirty-six tracheal rings of 15 rats in which asthma model was successfully established were randomly divided into 3 groups (n =12 each):ketamine treatment group (group AK),IBTX (BKCa channel blocker) +ketamine treatment group (group AKI),and KT-58232 (PKG inhibitor) + ketamine treatment group (group AKK).Tracheal rings were suspended in an organ bath filled with oxygenated Kreb's solution at 36.5-37.5 ℃.In group AK,the tracheal rings were precontracted with acetyleholine 0.1 mmol/L,and the rings were then exposed to ketamine 0.4 g/L for 15 min.In group AKI,before acetyleholine and ketamine were added to the solution,the rings were pretreated with IBTX 3μmol/L for 30 min.In group AKK,before acetyleholine and ketamine were added to the solution,the rings were pretreated with KT-5823 2μmol/L for 30 min.The tension of rings was measured by using a force-displacement transducer.Results The amplitude of relaxation of isolated tracheal smooth muscle was significantly decreased in groups AKI and AKK as compared with group AK (P ＜ 0.05).Conclusion Ketamine induces isolated tracheal smooth muscle relaxation through activating BKCa channels and PKG signaling pathway in rats with asthma.
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Objective To evaluate the effects of different concentrations of dexmedetomidine on large-con-ductance Ca2+-activated K+ (BKca) channels in the rat mesenteric arterial smooth muscle (MASM) cells.Methods Sprague-Dawley rats of both sexes,weighing 180-220 g,were used in this study.Single MASM cell was freshly isolated from mesenteric arteries in two steps.Ten cells were chosen and studied.When holding potential was 40 mV and the concentration of free calcium ions was 10-7 mol/L,inside-out patch-clamp technique was used to record the single BKCa channel current before and after application of different concentrations of dexmedetomidine (0,10-9,10-8,10-7,10-6,10-5 mol/L).Total open probability (NPo),amplitude (Am),mean open time (To) and mean close time (To) of single BKca channel were observed and recorded.Results Compared with the baseline value,dexmedetomidine 10-7,10-6 and 10-5 mol/L increased NPo in a concentration-dependent man-ner,and dexmedetomidine 10-9,10-8,10-7,10-6,10-5mol/L shortened Tc (P ＜0.05 or 0.01).Compared with the value obtained when the concentration of dexmedetomidine was 10-9 mol/L,Tc was significantly shortened when the concentration of dexmedetomidine was 10-8 mol/L (P ＜ 0.05),and no significant change was found in Am and To obtained when different concentrations of dexmedetomidine were applied (P ＞ 0.05).Conclusion Dexmedetomidine 10-7,10-6 and 10-5 mol/L activate BKca channels in rat MASM cells in a concentration-depen-dent manner,which is one of the mechanisms of decrease in blood pressure by dexmedetomidine.
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Objective To investigate the effects of hydrogen inhalation on the brain injury after intestinal ischemia/reperfusion (I/R) in rats.Methods Fifty-four healthy male Sprague-Dawley rats aged 6-8 months,weighing 285-350 g,were randomly allocated to one of 3 groups (n =18 each):sham operation group (group S),intestinal I/R group (group I/R) and hydrogen inhalation group (group H2).Intestinal I/R was produced by occlusion of the superior mesenteric artery for 90 min followed by reperfusion.2％ hydrogen was inhaled for 3 h starting from the end of ischemia.The cognitive function was detected at 1,2 and 5 days of reperfusion using Morris water maze test.The animals were sacrificed after the test and brains were isolated for detection of the cerebral edema and morphology in brain tissues.The cerebral water content ((wet weight-dry weight)/ wet weight × 100％) was measured.The pathological changes in the prefrontal cortex was observed under light microscope.The neuronal apoptosis was detected by TUNEL.Results Compared with the S group,the number of normal neurons in the prefrontal cortex was significantly decreased,the latency and swimming distance were both prolonged,the frequency of crossing the original platform was decreased,and the cerebral water content and the number of apoptotic neurons were increased in groups I/R and H2 (P ＜ 0.05).Compared with I/R group,the number of normal neurons in the prefrontal cortex was significantly increased,the latency and swimming distance were both shortened,the frequency of crossing the original platform was increased,the cerebral water content and the nunber of apoptotic neurons were decreased in group H2 (P ＜ 0.05).The pathological changes were obvious in I/R group,however,they were significantly attenuated in H2 group.Conclusion H2 inhalation can reduce the brain damage and improve the cognitive dysfunction after intestinal I/R in rats.
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Objective To investigate the effects of intestinal ischemia-reperfusion(I/R)on cerebral microglial activation in rats.Methods One hundred and twenty-eight healthy male SD rats weighing 250-300 g were randomly allocated to one of two groups(n =64 each):group sham operation(group S)and intestinal I/R group.Intestinal I/R was produced by occlusion of superior mesenteric stery for 90 main followed by reperfusion.Sixteen animals were sacrificed at each of the 4 time points:2,6,24 and 48 h of reperfusion in each group.Their intestines were obtained for microscopic examination.Their brains were harvested for detection of microglial activation (by immuno-histochemistry).The reactive oxygen species(ROS),MDA and NO contents and SOD,nitric oxide synthase(NOS)and inducible nitric oxide synthase(iNOS)activities in the brain were measured.Results The microglia were in quiescent condition.Ibal staining was negative or light in group S.Intestinal I/R significantly increased intestinal Chiu score,cerebral microglial activation at 6,24 and 48 h of repeffusion which peaked at 24 h of reperfusion in group I/R as compared with group S.Cerebral ROS,MDA,NO levels and NOS,iNOS activities were significantly higher while SOD activity was significantly lower in group I/R than in group S.Concluslon Intestinal I/R can activate microglia and induce the release of nitrogen and oxygen free radicals resulting in cerebral injury.
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ObjectiveTo investigate the effects of sevoflurane postconditioning on myocardial neutrophil infiltration in patients undergoing cardiac valve replacement under cardiopulmonary bypass (CPB).Methods Twenty-four ASA Ⅱ or Ⅲ patients (NYHA Ⅱ or Ⅲ ) of both sexes aged 20-50 yr with BMI of 19-25 kg/m2 undergoing cardiac valve replacement under CPB were randomly divided into 2 groups ( n =12 each):group control (group C) and group sevoflurane postconditioning (group S).Anesthesia was induced with midazolam,fentanyl,etomidate and rocuronium and maintained with iv infusion of fentanyl,midazolam and vecuronium.The patients were intubated and mechanically ventilated (VT 8-10 ml/kg,RR 10-14 bpm,I∶E 1∶2,FiO2 100％ ).PETCO2 was maintained at 35-40 mm Hg.In group S sevoflurane was inhaled immediately after aorta and vena cava were unclamped.The end-tidal sevoflurane concentration was maintained at 1.7％ for 5 min.Arterial blood samples were collected before surgery and at 1,2 and 4 h after aortic unclamping for determination of plasma cardiac troponin T concentration.Myocardial specimens were obtained from right auricular appendage after opening of pericardium and at 1 h after aortic unclamping for microscopic examination and determination of myocardial myeloperoxidase expression.ResultsSevoflurane postconditioning significantly decreased plasma cardiac troponin T concentration and myocardial myeloperoxidase expression and ameliorated histo-pathological damage in group S as compared with group C.ConclusionMyocardial neutrophil infiltration is involved in the protective effect of sevoflurane postconditioning against myocardial injury in patients undergoing cardiac valve replacement under CPB.