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【Objective】 To explore the effects of intraoperative autologous blood(ABT) transfusion on thrombelastography(TEG) in patients underwent neurosurgical procedures. 【Methods】 96 patients (49 males and 47 females) aged 15~79 years who received neurosurgical procedures in our hospital from November 2018 to November 2020 were retrospectively analyzed and divided into autologous blood transfusion group(Group A, n=52)and allogeneic blood transfusion group(Group B, n=44)according to different blood transfusion strategy in operation. The red blood transfusion status, hemoglobin (Hb), hematocrit (Hct), platelet (Plt), fibrinogen(Fib), prothrombin time (PT), activated partial thromboplastin time(APTT), and TEG parameters [activated clotting time(ACT), coagulation time (K), angle rate of clot formation(Angle), maximum amplitude(MA)] before and 1 day after surgery were compared between the two groups. 【Results】 The amount of average blood transfusion didn′t differ significantly by groups (P>0.05). The incidence of extra allogeneic blood transfusion was 17.3%(9/52) in group A, and the amount of average allogeneic blood transfusion in group A was significantly lower than that in group B(333.3±81.7 vs 639.8±258.2, P<0.05). Before operation, the differences in Hb, Hct, Plt, Fib, PT, APTT, ACT, K, MA and Angle levels between the 2 groups were not statistically significant (P>0.05). One day after operation, the Hb(g/L) (109.4±15.8 vs 97.0±15.1), Hct (%) (32.0±4.3 vs 28.3±6.1), Plt(×109/L)(154.2±54.2 vs 120.7±41.6), Fib(g/L)(2.2±0.5 vs 1.6±0.6), MA(mm)(65.0±7.2 vs 60.7±8.7) and Angle levels(deg)(69.1±5.2 vs 62.6±9.8) in group A were significantly higher than those in group B(P<0.05), and the PT(s)(11.9±1.5 vs 12.8±0.9), APTT(s)(27.4±3.3 vs 30.4±5.4), ACT(s)(111.0±14.9 vs 119.1±12.3) and K levels(min)(87.2±25.7 vs 106.4±28.0) in group A were significantly lower than those in group B (P<0.05). 【Conclusion】 Intraoperative ABT in patients underwent neurosurgical procedures can reduce allogeneic blood transfusion, has less effect on coagulation function and TEG, and is safe and effective.
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ObjectiveTo assess the effects of intra-articular Hydromorphone with Ropivacaine for postoperative analgesia after arthroscopic knee surgery.Methods 90 patients undergoing arthroscopic knee surgery were randomly divided into 3 groups. Group R: 0.375% Ropivacaine 20ml; group H1: Hydromorphone 0.3 mg and 0.375 % Ropivacaine 20 ml; group H2: Hydromorphone 0.6 mg and 0.375 % Ropivacaine 20 ml. The visual analogue scale (VAS) at rest were recorded at 6, 12, 18 and 24 h after surgery, Duration of analgesia, number of patients and frequency requiring Parecoxib at 24 h after surgery were observed.Results Compared with group R, VAS of group H1 and group H2 were signiifcantly lower at 12 and 18h after the operation, duration of analgesia was much longer, number of patients and frequency requiring Parecoxib was lower in group H1 and H2 (P < 0.05); Compared with group H1, No signiifcant differences of VAS, duration of analgesia and number of patients and frequency requiring Parecoxib of group H2.Conclusions After knee arthroscopic surgery, intra-articular 0.3 mg Hydromorphone can signiifcantly improve the efifcacy of Ropivacaine for postoperative analgesia; the efifcacy of Hydromorphone can’t increased with the increase of dosage.
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Objective To investigate the effects of hydrogen gas inhalation on cerebral oxidative stress and inflammation after intestinal ischemia/reperfusion (I/R) in rats and to understand the mechanism of(I/R neuroprotection.Method Forty-eight healthy male SD rats weighing 285-350 g were randomly allocated to one of 3 groups (n =16 each group):sham operation group (Sham),intestinal I/R group (I/R) and intestinal IR plus hydrogen gas inhalation group (IR + H2).The I/R model was produced by occlusion of superior mesenteric artery (SMA) for 90 min followed by reperfusion.Inhalation of 2％ hydrogen gas was performed immediately after I/R for 3 h.All animals were sacrificed at 24 h after reperfusion in each group.Brain tissues of 8 animals in each group were harvested for detection of microglia by immunohistochemistry.The remaining 8 rats in each group were used for the following indicators analysis.The protein level of ionized calcium-binding adaptor molecular 1 (Iba-1,a marker of microglia) in the cortex was detected by Western blotting.The concentrations of ROS,MDA,IL-1β,IL-6,TNF-α,T-NOS,iNOS and NO in the cortex were measured.The MPO content and SOD activity were also measured.Result The Iba-1 staining was light in Sham group.However,the expression of Iba-1 was increased in I/R group,and H2 inhibited the expression of Iba-l.As compared with Sham group,the Iba-1 protein expression and the number of Iba-1 positive cells were increased significantly in I/R and I/R+ H2groups (P＜0.01 or 0.05).As compared with Sham group,ROS,MDA,IL-1β,IL-6,TNF-α,T-NOS,iNOS and NO levels,and MPO activity were also increased in I/R and I/R + H2groups (P＜0.01 or 0.05).As compared with I/R group,the above indicators in I/R + H2 group were markedly improved (P＜0.05 or 0.01).Conclusion The inhalation H2 could inhibit intestinal I/R-induced activation of microglia and reduce cerebral oxidative stress and inflarnmatory response in rats.
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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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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.
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Objective To investigate the effect of propofol on ketamine-induced cognitive dysfunction and neuronal apoptosis in hippocampus in aged rats. Methods Thirty-two male SD rats aged 18-24 months weighing 380-470 g were randomly divided into 4 groups ( n = 8 each) :control group (group C);propofol group (group P);ketamine group (group K) and propofol + ketamine group (group PK). Propofol 30 mg·kg-1·h-1 or/and ketamine 40 mg· kg-1·h-1 were infused for 2 h once a day for 7 consecutive days. After the last day of drug administration cognitive function was assessed using Morris water maze (escape latency and the number of animals' swimming across the platform). The animals were sncrificed after water naze test and their hippocampi were removed for determination of neuronal apoptosis (by TUNEL) and caspase-3 expression (by immuno-histochemistry) in hippocampal CA1 region. Results There was no significant difference in escape latency and the number of the animals,swimming across the platform, the neuronal apoptotic rate (the number of apoptotic neurons/the number of total neurons) and caspase-3 expression between group C and P. In group K and PK the escape latency was prolonged,the number of animals' swimming across the platform was decreased, neuronal apoptotic rate increased and the caspase-3 expression up-regulated as compared with group C. The ketamine-induced changes were significantly attenuated by coadministration of propofol in group PK. Conclusion Coadministration of propofol can ameliorate ketamine-induced cognitive dysfunction and hippocampal neuronal apoptosis.
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Essentialhypertension(EH)ischaracterizedbyanincreasedtotalperipheralresistance . Therearefourtypesofpotassiumchannelsinvascularsmoothmusclecells ,includingKca ,Kv ,Kir ,KATP , whichplayanimportantroleinregulatingthediameterofvascular .Thechangeofpotassiumchannelsmay havesomethingtodowiththepathogenesisofhypertension .Thisarticlereviewsthecharactersofpotassium channelsandtheirrolesinEH . [