Analgesic effect and safety evaluation of PECS block under ultrasound guidance in multimodal analgesia after modified radical mastectomy / 临床麻醉学杂志

Objective To evaluate the efficacy and safety of PECS block under ultrasound guidance in multimodal analgesia after modified radical mastectomy.Methods Sixty female patients aged 18-65 years, ASA grade Ⅰ or Ⅱ, undergoing elective unilateral modified radical mastectomy were enrolled.Patients were randomly divided into PECS group (group P, n=30) or control group (group C, n=30).Two groups of patients were given flurbiprofen axetil 1 mg/kg via intravenous injection before operation.After general anesthesia induction, patients in group P received ultrasound guided pectoral nerves block with 30 ml of 0.375% ropivacaine.Patients in group C didn`t receive nerve block.Anesthesia maintenance was performed by combined intravenous-inhalation Anesthesia.Postoperative VAS pain scores (at 0, 3, 6, 12, and 24 postoperative hours), does of intraoperative remifentanil, rescue analgesic requirements in the first 24 h after surgery, adverse reactions were recorded.Results VAS score in group P was lower than that in group C at 0, 3, 6 and 12 h after surgery (P<0.05), there was no difference at 24 h.The dose of remifentanil and the rescue analgesic requirements in group P were lower than those in group C (P<0.05).There was no significant difference in postoperative adverse reactions between the two groups.Conclusion As a supplementary mode of multimodal analgesia, PECS block is a safe and reliable technique that provide better analgesia effect for modified radical mastectomy.

Effects of dexmedetomidine on expressions ofmesenteric artery proteins in rats / 西安交通大学学报(医学版)

Objective To observe the effects of dexmedetomidine (DEX) on the expressions of TNF-α, IL-1β and apoptosis-related proteins in rat mesenteric artery.Methods Male SD rats of SPF grade were sacrificed and the mesenteric artery was separated under the stereo-microscope.We established an experimental model of vascular injury induced by lipopolysaccharide (LPS) and randomly divided the injured vessels into dexmedetomidine treatment group and control group.DEX treatment group was divided into 10-8, 10-7, and 10-6 mol/L subgroups according to the different concentrations of DEX.RNA and total protein was extracted in each group.The mRNA expressions of TNF-α, IL-1β and CaSR were detected by RT-PCR and the protein expression of TNF-α, Caspase-3 and AMPK were tested by Western blot.Results DEX (10-8, 10-7, and 10-6mol/L) obviously reduced vascular inflammatory reaction induced by lipopolysaccharide, reduced the mRNA and protein expressions of TNF-α as well as mRNA expression of IL-1β.Caspase 3 protein expression significantly lowered in blood vessels in DEX group compared with LPS group.DEX had no obvious effect on lipopolysaccharide-induced vascular AMPK and CaSR mRNA or protein expressions.Conclusion DEX obviously deceased the expressions of inflammation-related proteins, suggesting that DEX has anti-inflammatory effects.

Effects of Sufentanil in inhibiting Hep3B cell viability and promoting cell apoptosis in liver cancer / 西安交通大学学报(医学版)

Objective To investigate the effects and mechanism of Sufentanil on Hep3B cell viability in liver cancer.Methods Sufentanil of different concentrations (0.01,0.1,1,5,10,1 5 μmol/L)was used to treat Hep3B cells.The changes of cell cycle,apoptosis and protein expression were detected to explore the potential mechanisms by MTT method,flow cytometry and Western blot,respectively.Results Reduced viability of Hep3B cells,arrested cell cycle in the G0/G1 phase,decreased expression of survivin protein,and increased expression of caspase-3 protein were observed with the increase of Sufentanil concentration. Conclusion Sufentanil inhibited the viability of Hep3B cells through affecting cell cycle,promoting cell apoptosis and changing protein expressions of survivin and caspase-3.

Effects of ropivacaine infiltration combined with dezocine on agitation during recovery from general anesthesia in patients undergoing cerebral surgery / 中华麻醉学杂志

Objective To investigate the effects of ropivacaine infiltration combined with dezocine on the agitation during recovery from general anesthesia in the patients undergoing cerebral surgery.Methods Sixty patients of both sexes,aged 18-64 yr,of ASA physical status Ⅰ or Ⅱ,undergoing elective neurosurgery under general anesthesia,were randomly divided into 4 groups (n =15 each) using a random number table:control group (group C),ropivacaine group (group R),dezocine group (group D),and ropivacaine + dezocine group (group RD).Group C received local infiltration with normal saline 20 ml at 10 min before skin incision,and normal saline 2 ml was injected intravenously at 30 min before the end of operation.The patients received local infiltration with 0.5％ ropivacaine 20 ml at 10 min before skin incision,and normal saline 2 ml was injected intravenously at 30 min before the end of operation in group R.Group D received local infiltration with normal saline 20 ml at 10 min before skin incision,and dezocine 10 mg was injected intravenously at 30 min before the end of operation.The patients received local infiltration with 0.5％ ropivacaine 20 ml at 10 min before skin incision,and dezocine 10 mg was injected intravenously at 30 min before the end of operation in group RD.The time for recovery from anesthesia,extubation time,and development of agitation after extubation in PACU were recorded.Agitation was assessed and scored.Ramsay sedation score and VAS score were recorded immediately after extubation.The development of cardiovascular events and respiratory depression was recorded within 10 min after extubation.Before induction of anesthesia (T0),at the end of surgery (T1) and immediately after extubation (T2),blood samples were collected from the dorsal artery of foot for deter mination of the levels of blood glucose,plasma cortisone,epinephrine and norepinephrine.Results Compared with group C,the agitation score,incidence of agitation,VAS score,and incidence of postoperative hypertension were significantly decreased in R,D and RD groups,especially in R and D groups.The time for recovery from anesthesia and time for extubation were significantly shorter in R and RD groups than in group C.Ramsay sedation scores were significantly higher at the onset of extubation in R,D and RD groups than in group C.Ramsay sedation scores were significantly higher in D and RD groups than in group R.Compared with group C,the levels of blood glucose,plasma cortisone,epinephrine and norepinephrine were significantly decreased in R,D and RD groups,especially in group RD.Conclusion Ropivacaine infiltration combined with dezocine can reduce the agitation during recovery from general anesthesia in the patients undergoing cerebral surgery.

Effect of sufentanil preconditioning on myocardial P-Akt expression in rats during myocardial ischemia-reperfusion / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the protective effect of sufentanil preconditioning against myocardial ischemia-reperfusion (I/R) injury and the role of PI3K/Akt signaling pathway.</p><p><b>METHODS</b>Sixty male SD rats weighing 250-350 g were randomly divided into 5 equal groups, namely the sham-operated group, I/R group, sufentanil preconditioning group (Spc group), sufentanil preconditioning +PI3K inhibitor group (Spc+W group), and PI3K inhibitor group (W group). Myocardial I/R model was established by ligation of the anterior descending branch of the left coronary artery for 30 min followed by reperfusion for 120 min. Sufentanil was administered in 3 doses via the femoral vein before the occlusion, each at 1 µg/kg infused within 5 min at a 5-min interval. In Spc+W and W groups, PI3K inhibitor wortmannin (15 µg/kg) was given intravenously 5 min before sufentanil preconditioning and 35 min before ischemia, respectively. Heart rate and mean arterial pressure (MAP) were continuously monitored during I/R. At the end of reperfusion, blood samples were obtained to determine plasma activation of CK-MB and LDH. Acute infarct size was measured by triphenyltetrazolium chloride staining, and the myocardial tissues were obtained to detect the expression of phosphorylated Akt using Western blotting.</p><p><b>RESULTS</b>Phosphorylated Akt expression was significantly up-regulated in I/R and Spc groups as compared with the sham group, and was significantly higher in Spc group than in I/R group. After reperfusion, sufentanil preconditioning significantly decreased myocardial infarct size (P<0.01) and lowered the levels of CK-MB (P<0.01) and LDH (P<0.01) compared with those in the I/R group. The I/R , Spc+W and W groups showed no significant differences in myocardial infarct size or the levels of CK-MB and LDH.</p><p><b>CONCLUSION</b>The protective effect of sufentanil preconditioning against myocardium against I/R injury in rats may involve PI3K/Akt signaling pathway activation.</p>

Effect of propofol on noise-induced hearing loss in guinea pigs / 中华麻醉学杂志

Objective To evaluate the effect of propofol on noise-induced hearing loss in guinea pigs.Methods Forty-eight healthy adult male guinea pigs,aged 3 months,weighing 400-500 g,were randomly divided into 4 groups (n =12 each) using a random number table:control grotup (C group),propofol group (P group),noise-induced hearing loss group (N group),and propofol + noise-induced hearing loss group (P + N group).A loading dose of propofol 5 mg/kg was infused intravenously over 5 min,followed by infusion at 20 mg· kg-1 · h-1 for 115 min in P and P + N groups,while the equal volume of normal saline was given in N group.N and P+ N groups were exposed to the noise of 4 kHz center frequency and 118-122 dB sound pressure level for 120 min.Distortion product otoacoustic emission (DPOAE) was measured before noise exposure (T1) and at 1 h after the end of noise exposure (T2) and the amplitudes were recorded at the frequencies of 2,4,6 and 8 kHz.After the second measurement of DPOAE,all the animals were sacrificed and organs of Corti were harvested for determination of cochlear 8-isoprostaglandin F(2alpha) (8-iso-PGF2α) content (by ELISA assay) and out hair cell (OHC) count.The rate of OHC lesions was calculated.Results The DPOAE amplitude was significantly lower at frequencies of 4,6 and 8 kHz at T2 than at T1 in N and P + N groups (P ＜ 0.05).Compared with C group,the DPOAE amplitude was significantly decreased at frequencies of 4,6 and 8 kHz at T2,while the cochlear 8-isoPGF2α content and rate of OHC lesions were increased in N and P + N groups (P ＜ 0.05).Compared with N group,the DPOAE amplitude was significantly increased at frequencies of 4,6 and 8 kHz at T2,while the cochlear 8-iso-PGF2α content and rate of OHC lesion were decreased in P + N group (P ＜ 0.05).Conclusion Propofol can reduce noise-induced hearing loss in guinea pigs possibility through decreasing oxidative stress response-induced damage to cochlear OHCs.

Effects of dexmedetomidine on isolated rat mesenteric arterial rings / 西安交通大学学报(医学版)

Objective To investigate the dilating effect of dexmedetomidine (DEX)on isolated vascular smooth muscles and to explore the mechanism.Methods Tension of isolated mesenteric arterial rings of male Sprague-Dawley rats was recorded.The effects of DEX on the rings and the effects of DEX on vascular reaction induced by various drugs were recorded. Results DEX completely relaxed the contraction induced by phenylephrine (PE)and KCl in a concentration-dependent manner in endothelium intact mesenteric arterial rings in rats.The vasodilating effect of DEX was increased by sodium nitroprusside.In phenylephrine (10-5 mol/L)based on pre-vasoconstriction,adding acetylcholine could not suppress DEX’s vasodilating effect.Vasodilation was not related to the endothelial cells.In physiological saline solution without calcium,DEX significantly inhibited the contraction induced by addition of CaCl2 .Conclusion DEX can induce vasodilation in a concentration-dependent manner,which is not dependent on the endothelial cells.

Effects of ulinastatin postconditioning and combination of ulinastatin preconditioning and postconditioning on myocardial apoptosis in patients undergoing cardiac valve replacement with cardiopulmonary bypass / 中华麻醉学杂志

Objective To evaluate the effects of ulinastatin postconditioning and combination of ulinastatin preconditioning and postconditioning on myocardial apoptosis in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Eighty New York Heart Association (NYHA) class Ⅱ or Ⅲ patients of both sexes,aged 21-59 years,scheduled for cardiac valve replacement with CPB,were randomly divided into four groups (n =20 each):normal saline control group (group C),ulinastatin preconditioning group (group U1),ulinastatin postconditioning group (group U2) and ulinastatin preconditioning plus postconditioning group (group U3).In group U1,uinastatin 20000 U/kg was infused via the central vein at 500-1000 U·kg-1 · min-1 after endotracheal intubation until 10 minutes before blocking the ascending aorta.In group U2,ulinastatin 10000 U/kg was infused via the aortic root at 4000-5000 U· kg-1 · min-1 at 5-7 minutes before opening the aorta.In group U3,ulinastatin preconditioning and postconditioning were performed as described in groups U1 and U2.In group C,the same volume of normal saline was infused instead of ulinastatin.Blood samples were taken from the radial artery at 10 minutes before blocking the ascending aorta,40 minutes after blocking the ascending aorta,45 minutes after opening the aorta and at the end of operation for determination of plasma concentrations of tumor necrosis factor-alpha (TNF-α) and soluble tumor necrosis factor receptor 1 (sTNF-R1).Myocardial tissues were obtained from the right atrial appendage at 45 minutes after opening the aorta for determination of the expression of TNF-α,bcl-2,bax,caspase-3,and apoptosis.The bcl-2/bax ratio and apoptotic index were calculated.Results Plasma concentrations of TNF-α and sTNF-R1 and the expression of TNF-α,bax,caspase-3 and apoptotic index were lower and the expression of bcl-2 and bcl-2/bax ratio were higher in groups U1,U2 and U3 than in group C and they were lower in group U3 than in groups U1 and U2 (P ＜ 0.05).Conclusion Ulinastatin postconditioning can inhibit myocardial apoptosis in patients undergoing cardiac valve replacement with CPB,and the efficacy of combination of ulinastatin preconditioning and postconditioning is stronger than that of ulinastatin postconditioning.The mechanism is involved in balancing the expression of bax and bcl-2 and down-regulating the expression of TNF-α and its receptor.

Effect of isoflurane anesthesia on noise-induced hearing loss in guinea pigs / 中华麻醉学杂志

Objective To evaluate the effect of isoflurane anesthesia on noise-induced hearing loss in guinea pigs.Methods Forty-eight healthy adult male guinea pigs,aged 3 months,weighing 400-500 g,were randomly divided into 4 groups (n =12 each) using a random number table:control group (C group),isoflurane group (I group),noise-induced hearing loss group (N group),and isoflurane + noise-induced hearing loss group (I + N group).Isoflurane was inhaled for 140 min at a concentration of 1％ in I and I + N groups.N and I + N groups were exposed to the noise of 4 kHz center frequency and 118-122 dB sound pressure level for 120 min starting from 20 min after administration.Mean arterial pressure (MAP) was recorded at 10,40,70,100 and 120 min of exposure to noise and cochlear blood flow (CoBF) was recorded before administration and at 10,40,70,100 and 120 min of exposure to noise.Auditory brainstem response (ABR) threshold was recorded before administration and at 1 h,72 h,and 10 days after the end of exposure to noise.Arterial blood samples were obtained and the plasma noradrenaline (NE) concentration was detected by HPLC before exposure to noise and immediately after the end of exposure to noise.Results Compared with group C,MAP and the change rate of CoBF were significantly decreased,and the plasma NE concentration was increased immediately after the end of exposure to noise in I group,and MAP was increased,the change rate of CoBF was decreased,and the plasma NE concentration immediately after the end of exposure,and ABR threshold after the end of exposure were increased in N and I + N groups.Compared with N group,MAP was significantly decreased,the change rate of CoBF was increased,the plasma NE concentration immediately after the end of exposure,and ABR threshold at 1 and 72 h after the end of exposure were increased,and no significant was found in ABR threshold at 10 days after the end of exposure in I + N group.Conclusion Isoflurane anesthesia exerts temporary but not permanent protective effects against noise-induced hearing loss in guinea pigs and partial inhibition of activation of sympathetic nerve and increased CoBF may be involved in the mechanism.

Correlation between postoperative cognitive dysfunction and serum level of S100β and NSE in on-pump heart valve replacement / 临床麻醉学杂志

Objective To explore the correlation between postoperative cognitive dysfunction (POCD)and serum level of S100βand NSE in patients undergoing on-pump heart valve replacement. Methods Ninety-eight patients underwent elective heart valve replacement were enrolled and divided into two groups:POCD group (group P)and none POCD group(group NP)by the result of neurocog-nitive testing with MMSE performed preoperatively and on the first postoperative day.Serum S-100βprotein and NSE were measured before operation(T0 ),at the end of operation(T1 ),24 h(T2 )and 48 h(T3 ) postoperatively.Results The incidence of POCD on the first postoperative day was 45 (45.9%).Compared with T0 ,the S100βincreased at T1 in both groups (P <0.05),NSE increased at T1 and T2 in both groups,and NSE increased in group NP at T3 (P <0.05).There was no signifi-cant difference of NSE between groups P and NP.The prolonged recovery time(OR = 1.222,P =0.004)and increased concentration of S100βat the end of operation(OR=1.85,P =0.009)were pre-dictors of POCD on the first postoperative day.Conclusion There was a higher incidence of POCD af-ter on-pump heart valve replacement surgery.The prolonged recovery time and increased concentra-tion of S100βat the end of operation might be predictors of POCD.

Effects of propofol on the changes in myocardial Toll-like receptor 4 and TNF-αand NF-κb protein expressions and ultrastructure in ischemia-reperfusion inj ury in rats / 西安交通大学学报(医学版)

Objective To investigate the effects of propofol on the changes in myocardial Toll-like receptor 4 (TLR-4)and TNF-αand NF-κb protein expressions in ischemia-reperfusion injury (I/R).Methods Thirty healthy male SD rats weighing 250-320 g were randomly divided into 3 groups (n=10 for each):Group A,sham operation;Group B,I/R;and Group C,propofol + I/R.In Groups B and C myocardial I/R was induced by occlusion of the left anterior descending artery (LAD)for 30 min,followed by 120 min reperfusion.In Group C propofol was given intravenously 1 0 min before myocardial ischemia,followed by continuous infusion of propofol at 5 mg/(kg·h)until the end of 120 min reperfusion.In Groups A and B normal saline instead of propofol was given. The myocardial tissues were taken at the end of 120 min;ultrastructural changes of myocardial cells were observed under X-ray electron microscope and the expressions of TLR-4 mRNA as well as TNF-αand NF-κb protein were determined.Results Ultrastructural observation under electron microscope showed significantly worsened damage in myocardial tissue structure and mitochondria in Groups B and C compared with Group A.The myocardial expressions of TLR-4 and TNF-αand NF-κb protein were significantly higher in Groups B and C than in control Group A.The myocardial expressions of TLR-4 and TNF-αand NF-κb protein were down-regulated in Group C compared with Group B.Conclusion Intravenous injection of propofol can protect against myocardial damage.Propofol can suppress the increase in myocardial TLR-4 and TNF-αand NF-κb protein expressions induced by I/R.

Effect of dexmedetomidine on noise-induced hearing loss in guinea pigs / 中华麻醉学杂志

Objective To evaluate the effect of dexmedetomidine on noise-induced hearing loss in guinea pigs.Methods Twenty-four adult male guinea pigs,aged 3 months,weighing 400-500 g,were randomly divided into 3 groups (n =8 each) using a random number table:dexmedetomdine group (group D),noise-induced hearing loss group (group N) and dexmedetomidine + noise-induced hearing loss group (group DN).A loading dose of dexmedetomidine 5 μg/kg was infused over 5 min,followed by 135 min of infusion at a rate of 10 μg· kg-1 · h-1.The equal volume of normal saline was infused in group N.Groups N and DN were exposed to noise of 4 kHz center frequency and 118-122 dB SPL for 120 min starting from 20 min of administration.Mean arterial pressure (MAP) and cochlear blood flow (COBF) were recorded before administration and every 5 min during drug administration.The changing rate of COBF was calculated.Arterial blood samples were collected for determination of plasma concentration of noradrenaline (NE) by high performance liquid chromatography at 20 and 140 min of administration.Auditory brainstem response (ABR) threshold was recorded before administration and at 1 and 72 h and 10 days after the end of administration.Results Compared with group N,MAP was significantly decreased,the changing rate of COBF was increased at 5-10 min and 30-140 min of administration,ABR threshold was decreased at 1 and 72 h and 10 days after the end of administration,and the plasma concentration of NE was decreased at 140 min of administration in D + N group (P ＜ 0.05).Conclusion Dexmedetomidine can attenuate noise-induced hearing loss in guinea pigs possibly through inhibiting activation of sympathetic nerves and increasing COBF.

Effect of propofol on liver injury in mice with acute liver failure / 中华麻醉学杂志

Objective To evaluate the effect of propofol on liver injury in mice with acute liver failure (ALF).Methods Eighty adult male ICR mice,aged 1 months,weighing 20-25 g,were randomly divided into 3 groups (n =20 each) using a random number table:control group (group Ⅰ),ALF group (group Ⅱ),and ALF + propofol group (group Ⅲ).ALF model was established with intra-peritoneal D-galactosamine (D-GaIN) and lipopolysaccharide (LPS).Propofol 5 mg/kg was injected via the tail vein every 1 h within 6 h after injection of DGaIN and LPS in group Ⅲ,while the equal volume of normal saline was given instead in the other groups.Venous blood samples were taken from the tail vein at 1,3 and 6 h after injection of D-GaIN and LPS (T1-3) to detect the activities of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and serum tumor necrosis factor-alpha (TNF-α),interleukin-1β (IL-1β) and IL-10 concentrations (by ILISA).The survival within 12 h after injection of D-GaIN and LPS was observed and the survival rates were calculated.The mice were sacrificed and livers were removed for microscopic examination of pathologic changes.Results Compared with group Ⅰ,the activities of AST and ALT were significantly increased at each time point in Ⅱ and Ⅲ groups and the serum TNF-α concentrations at T1,2 and IL-1β and IL-10 concentrations at each time point were significantly increased in group Ⅱ,and the serum TNF-α concentrations at T1,and IL-1β and IL-10 concentrations at T2,3 were significantly increased in group Ⅲ (P ＜ 0.05).Compared with group Ⅱ,the activities of AST and ALT at each time point,serum TNF-α concentrations at T1,2 and IL-1β and IL-10 concentrations at T2,3 were significantly decreased and the survival rate within 12 h after injection of D-GaIN and LPS was increased in group Ⅲll (P ＜ 0.05).The pathologic changes of liver tissues were gradually attenuated in Ⅱ and Ⅲ groups.Conclusion Propofol can reduce the liver injury in mice with ALF through inhibiting inflammatory responses.

Effect of sufentanil preconditioning on expression of Toll-like receptor 4 in myocardium during myocardial ischemia-reperfusion in rats / 中华麻醉学杂志

Objective To investigate the effect of sufentanil preconditioning on the expression of Toll-like receptor 4 (TLR4) in myocardium during myocardial ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each):sham operation group (group S),I/R group and sufentanil preconditioning group (group SPC).Myocardial ischemia was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 2 h of reperfusion.In group SPC,the rats were subjected to 3 consecutive cycles of 5 min sufentanil infusion at 0.2 μg· kg-1 ·min-1 via the femoral vein at 5 min interval before ischemia.In groups S and I/R,the rats were subjected to the equal volume of normal saline instead.HR and mean arterial pressure (MAP) were recorded at 30 min before ischemia (T0),immediately before ischemia (T1),at 30 min of ischemia (T2),and at 30 and 120 min of reperfusion (T3-4).At the end of reperfusion,blood samples were obtained to determine the serum concentration of TNF-α.The rats were then sacrificed and hearts were removed for measurement of myocardial infarct size and expression of TLR4 and NF-κB p65 in myocardium (using Western blot).Results There was no significant difference in HR among the three groups (P ＞ 0.05).Compared with group S,MAP was significantly decreased at T2-4,the serum concentration of TNF-α was increased,and the expression of TLR4 and NF-kB p65 protein in myocardium was upregulated in groups I/R and SPC (P ＜ 0.01).Compared with group I/R,no significant difference was found in MAP at all time points (P ＞ 0.05),and myocardial infarct size was significantly decreased,serum concentrations of TNF-α were decreased,and the expression of TLR4 and NF-κB p65 protein in myocardium was down-regulated in group SPC (P ＜ 0.01).Conclusion The mechanism by which sufentanil preconditioning alleviates myocardial I/R injury may be related to down-regulation of TLR4 expression in rat myocardium.

Effect of ischemic postconditioning on phosphatidylinositol-3-OH kinase and extracellular signal-regulated protein kinase in rats with hepatic ischemia-reperfusion injury / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the effect of ischemic postconditioning on phosphatidylinositol-3-OH kinase (PI3K) and extracellular signal-regulated protein kinase 1/2(ERK1/2) in rats after hepatic ischemia reperfusion in rats and investigate the mechanism of ischemic postcoditioning of the liver.</p><p><b>METHODS</b>Three cycles of 1 min-off-1 min-on ischemic postconditioning regime were used in a rat model of 70% hepatic ischemia-reperfusion injury. The changes in the liver function, hepatocyte apoptosis, phosphorylation of Akt and ERK1/2 were assessed in rats treated with sham operation, LY294002+sham operation (LY+S), PD98059+sham operation (PD+S), ischemia reperfusion (IR), ischemic postconditioning (IPO), LY294002+ ischemic postconditioning (LY+IPO), or PD98059+ischemic postconditioning (PD+IPO).</p><p><b>RESULTS</b>Ischemic postconditioning significantly alleviated hepatic ischemia-reperfusion-induced liver function injury and hepatocyte apoptosis and increased phosphorylation of Akt and ERK1/2. LY294002 and PD98059 antagonized the effects of ischemic postconditioning in the liver.</p><p><b>CONCLUSION</b>Activation of PI3K and ERK1/2 may mediate the protective effect of ischemic postconditioning against hepatic ischemia- reperfusion injury in rats.</p>

Effects of phosphocreatine on apoptosis following myocardial ischemia-reperfusion in diabetic melllitus rats / 中华麻醉学杂志

Objective To investigate the effects of phosphocreatine on apoptosis following myocardial ischemia-reperfusion (I/R) in diabetic rats. Methods Male SD rats weighing 150-170 g were used in this study.Diabetes mellitus was induced by high fat diet and intraperitoneal streptozotocin. Twenty-seven rats in which diabetes mellitus was successfully induced were randomly divided into 3 groups ( n = 9 each): sham operation group (group S);myocardial I/R group(group I/R )and phosphocreatine group (group PP). Myocardial I/R was induced by 30 min occlusion of left anterior descending branch of coronary artery followed by 2 h reperfusion in I/R and PP groups. In group PP phosphocreatine 1 g/kg was given intraperitoneally 30 min before myocardial I/R. Blood samples were collected at the end of 2 h reperfusion for determination of plasma concentration of calcium troponin T (cTnT). The animals were then sacrificed and iscbemic myocardial specimens were isolated. The expression of Bcl-2, Bax and Caspase-3 in isehemic myocarcdium was determined and Bcl-2/Bax ratio was calculated. Myocardial apoptosis was detected by TUNEL and apoptotic index was calculated. The ultrastructure of cardiomyocytes was examined with electron microscope. Results Myocardial I/R significantly increased plasma cTnT concentration and Bcl-2, Bax and Caspase-3 expression in myocardium and apoptosis index and decreased Bcl-2/Bax ratio. Phosphocreatine significantly attenuated I/R-induced above-mentioned changes and myocardial damage. Conclusion Phosphocreatine can reduce myocardial I/R injury in diabetic mellitus rats by reducing myocardial apoptosis through up-regulation of Bcl-2 expression and down-regulation of Bax and Caspase-3 expression.

Effects of ulinastatin postconditioning and combination of ulinastatin preconditioning and postconditioning on myocardial apoptosis in patients undergoing cardiac valve replacement with cardiopulmonary bypass / 中华麻醉学杂志

Objective To evaluate the effects of ulinastatin postconditioning and combination of ulinastatin preconditioning and postconditioning on myocardial apoptosis in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Eighty NYHA class Ⅱ or Ⅲ patients of both sexes,aged 21-59,scheduled for cardiac valve replacement with CPB,were randomly divided into 4 groups ( n =20 each):normal saline control group ( group C ),ulinastatin preconditioning group ( group U1 ),ulinastatin postconditioning group (group U2 ) and ulinastatin preconditioning plus postconditioning group(group U3 ).In group U1,uinastatin 20 000U/kg was infused via central vein at 500-1000 U·kg-1 ·min-1 from after tracheal intubation until 10 min before ascending aortic cross-clamping.In group U2,ulinastatin 10 000 U/kg was perfused via aortic root at 4000-5000 U· kg-1 · min-1 at 5-7 min before aortic unclamping.In group U3,ulinastatin preconditioning and postconditioning were performed as described in groups U1 and U2.In group C same volume normal saline was infused instead of ulinastatin.Blood samples were taken from radial artery at 10 min before ascending aortic cross-clamping,40 min after ascending aortic cross-clamping,45 min after aortic unclamping and the end of operation for determination of plasma concentrations of TNF-α and soluble tumor necrosis factor receptor 1 (sTNF-R1).Myocardial tissues were obtained from right atrial appendage at 45 min after aortic unclamping for determination the expression of TNF-d,Bcl-2,Bax and caspase-3 and apoptosis.The Bcl-2/Bax ratio and apoptotic index were calculated.Results Plasma concentrations of TNF-α and sTNF-R1 and the expression of TNF-α,Bax,caspase-3 and apoptotic index were lower,the expression of Bcl-2 and Bcl-2/Bax ratio were higher in groups U1,U2 and U3 thah group C and in group U3 than groups U1,U2 ( P ＜ 0.05 ).Conclusion Ulinastatin postconditioning can inhibit myocardial apoptosis in patients undergoing cardiac valve replacement with CPB,and efficacy of combination of ulinastatin preconditioning and postconditioning is stronger than that of ulinastatin postconditioning.The mechanism is involved in balancing the expression of Bax and Bcl-2 and down-regulating the expression of TNF-α and its receptor.

Effect of sevoflurane preconditioning on the expression of Toll-like receptor 4 during myocardial ischemia reperfusion in rats / 中华麻醉学杂志

Objective To investigate the effect of sevoflurane preconditioning on the expression of Toll-like receptor 4(TLR4) during myocardial ischemia reperfusion(IR) in rats.Methods Thirty male SD rats weighing 250-300 g were randomly divided into 3 groups (n=10 each):sham operation group (S group) , IR group and sevoflurane preconditioning group(SP group).Myocardial ischemia was produced by temporary ligation of anterior descending branch of left coronary artery for 30 min followed by 2 h reperfusion. In SP group, the animals inhaled 2.5% sevoflurane for 30 min followed by 15 min washout before ischemia. The rats were sacrificed at 2 h of reperfusion, hearts removed and myocardial tissues obtained for microscopic examination.The expression of TLR4, NF-κB and TNF-α was detected using Western blot. Results The expression of TLR4, NF-κB and TNF-α was significantly up-regulated in IR and SP groups compared with group S (P＜0.05).The expression of TLR4, NF-κB and TNF-α was significantly down-regulated in group SP compared with group IR (P＜0.05).The myocardial injury was attenuated in group SP.Conclusion Sevoflurane preconditioning can attenuate myocardial IR injury by inhibiting the up-regulation of TLR4 expression and reducing the inflammatory response.

Effects of ischemic postconditioning on mitochondrial permeability transition and mitochondrial transmembrane potential following hepatic ischemia-reperfusion in rats / 中华麻醉学杂志

Objective To investigate the effects of ischemic postconditioning on mitochondrial permeability transition and mitochondrial transmembrane potential(△Ψm)following hepatic ischemia-reperfusion(I/R)in rats.Methods Forty male SD rats weighing 220-260 g were randomly divided into 5 groups with 8 animals in each group:sham operation group(group S);atractyloside+sham operation group(group A+S);I/R group;ischemic postconditioning group(group IPO)and atractyloside+ischemic postconditioning group(group A+IPO).The animals were anesthetized with intramuscular injection of atropine 0.05 mg/kg.Hepatic I/R was produced by occlusion of hepatic blood flow for 60 min followed by 6 h reperfusion.In group A+S,atractyloside 5 mg/kg was injected intravenously before abdomen Was closed.In group IPO,the animals were subjected to 3 cycles of 1 min reperfusion interspersed with 1 min hepatic isehemia at the end of 60 min hepatic ischemia.In group A+IPO,atractyloside 5 mg/kg was injected intravenously before reperfusion. Venous blood samples were collected for determination of serum ALT and AST activities immediately before ischemia and at 6 h of reperfusion. The animals were then sacrificed.Their livers were removed for microscopic examination, detection of apoptosis and determination of cytochrome c (Cyt c) expression, △Ψm and mitochonerial permeability transition pore (MPTP)activity. Apoptosis index (AI) was calculated. Results There was no significant difference in serum ALT and AST activities, AI, Cyt c expression, △Ψm and MPTP activity between S and A + S groups (P＞0.05). Compared with group S, serum ALT and AST activities and AI were significantly increased, Cyt c expression was up-regulated, △Ψm was decreased and MPTP activity was increased in groups I/R, IPO and A+IPO(P＜0.05).Compared with group I/R, serum ALT and AST activities and AI were significantly decreased,Cyt c expression was down-regulated, △Ψm was increased and MPTP activity was decreased in group IPO(P＜0.05), while no significant change was found in group A+IPO(P＞0.05).Compared with group IPO,serum ALT and AST activities and AI were significantly increased, Cyt c expression was up-regulated, △Ψm was decreased and MPTP activity was increased in group A + IPO(P＜ 0.05).Microscopic examination showed that hepatic injury was reduced in group IPO compared with group I/R, while aggravated in group A+ IPO compared with group IPO. Conclusion Ischemic postconditioning can protect liver from I/R injury by attenuating the I/R-induced increase in MPTP opening and decrease in △Ψm in rats.

Protective effects of midazolam on noised-induced hearing loss in guinea pigs / 西安交通大学学报(医学版)

Objective To investigate the protective effects of midazolam on noise-induced hearing loss in guinea pigs by testing reactive oxygen species (ROS) level in the cochlea and plasma SOD and MDA. Methods Totally forty male pigmented guinea pigs were randomly divided into four groups: control (C) , midazolam (M), normal saline (S) and noise-induced deafened (D) groups, with ten guinea pigs in each. Groups M, S and D were exposed to a continuous noise (4kHz , octave band, 100dB SPL) 3h every day for 3 consecutive days. Group M was treated with midazolam, which was administered intramuscularly (0.1mg/kg) 24h before noise exposure, and immediately upon and during noise exposure. Group S was exposed to noise and treated with the same volume of normal saline intramuscularly, the time of injection was the same as that of Group M. Group C was not exposed to noise, but was treated with midazolam intramuscularly, the time of injection and the dosage were the same as those of Group M. Group S was exposed to noise and treated with normal saline intramuscularly ,the time of injection was same with that of Group M.Group D was exposed to noise only. All animals received auditory brainstem response (ABR) threshold recording before and immediately after noise exposure. Blood was collected when the guinea pigs were killed after the last ABR threshold recording, and serum SOD activity and MDA content were detected. Both the cochleae were removed and prepared for ROS assay. Results After noise exposure, ABR threshold shift (1.6±1.5) and ROS content [(291.10±2.30)u/mL] in Group M were significantly lower than those in Groups S and D [41.7±3.3, 44.3±3.9; (348.52±3.60)u/mL, (315.56±6.70)u/mL, P<0.05]. Serum SOD activity and MDA content were significantly increased in Group M, but the amplitude was less than that in Groups S and D.Conclusion Midazolam can prevent noise-induced hearing loss by reducing the increased ROS level in the cochlea after noise exposure.