0 05) The incidences of atherogenesis and intimal thickening and the ratio of the atherosclerotic area to total area (intimal area plus intraluminal area) and the ratio of intimal area to total area , were remarkably lower inTEA group than those in hypercholesterol group(P

Objective To evaluate the feasibility of application of preoperative acute hypervolemic hemodilution (AHH) to the patient with carcinoma during major surgery Methods Forty ASA Ⅰ Ⅱ patients scheduled for resection of esophagus or cardia cardinoma were randomized to two groups: in AHH group with the routine infusion of lactated Ringer's solution, Gelofusine solution 15ml/kg was infused intravenously at a rate of 80 ml/min immediately before incision under isoflurane inhalation anesthesia, and in control group only lactated Ringer's solution was administered routinly under isoflurane inhalation anesthesia In both groups, MAP, HR, CVP,SpO 2 and P ET CO 2 were monitored during the whole anesthetic procedures; Hb, Hct, Pt and Aptt were measured before and after the hemodilution, at the end of operation, 24h and 1 week after operation; The volume of infusion, blood loss and blood transfusion were recorded during the operation Results Following hemodilution in AHH group , CVP increased markedly (P0 05); the required volume of lactated Ringer's solution and blood loss remained unchanged significantly,but transfusion volume reduced significantly in AHH groups (P

Objective To evaluate the hemorrheological changes after tourniquet deflation.Methods Twenty rabbits were subjected to lower extremity tourniquet inflation for 3 h. Venous blood samples were taken before tourniquet inflation and 2min after tourniquet deflation for measurement of hemorrheological parameters: low-shear viscosity and high-shear viscosity of whole blood; plasma high-shear viscosity , hematocrit; fibrinogen; aggreability,deformability and stiffness of erythrocyte; and blood sedimentation K value. The levels of parameters before tourniquet inflation served as baseline values. The gastrocnemius muscle samples were taken before tourniquet inflation and 5 min after torrniquet deflaion for observation of ultrastructure of small blood vessel.Results Compared with the baseline values, the levels of low- and high- shear viscosities of whole blood, plasma viscosity, fibrinogen, blood sedimentation K value, and aggreability and stiffness of erythrocyte increased significantly (P

Objective To investigate the effects of different target plasma concentrations of propofol given by TCI on end-tidal isoflurane concentration when the depth of anesthesia was maintained at BIS 50 and evaluate the reliability of electromyography (EMG) as an anesthesia depth monitor. Methods Sixty ASA Ⅰ-Ⅱ patients aged 40-65 yrs weighing 40-85 kg undergoing elective abdominal surgery under general anesthesia were randomly allocated to one of three groups with 20 patients in each group : group Ⅰ isoflurane; group Ⅱ isoflurane + TCI propofol (1 ?g?ml-1) and group Ⅲ isoflurane + TCI propofol (2 ?g?ml-1). The patients were premedicated with intramuscular phenobarbital 0.1 g and scopolamine 0.3 mg. Anesthesia was induced with midazolam 0.05 mg?kg , fentanyl 3 ?g?kg-1 and propofol 0.5-1.0 ?g?kg-1. Tracheal intubation was facilitated with vecuronium 0.12 mg?kg-1. After intubation anesthesia was maintained with isoflurane inhalation alone (group Ⅰ) or isoflurane combined with TCI propofol at a target plasma concentration of 1 ?g?ml-1 ( group Ⅱ) or 2 ?g?ml-1 ( group Ⅲ). MAP, HR, SpO2, PETCO2, BIS, EMG and end-tidal isoflurane concentration were continuously monitored during anesthesia. BIS was maintained at 45-55 after tracheal intubation during maintenance of anesthesia.Results The three groups were comparable with respect to age, sex, body weight, duration of anesthesia and the total amount of fentanyl used during anesthesia. There were no significant differences in MAP, HR and SpO2 among the 3 groups. When BIS was maintained at 50, the end-tidal isoflurane concentration was 0.76?0.03% (group Ⅰ), 0.43? 0.08% (group Ⅱ) and 0.21?0.07% (group Ⅲ) respectively. EMG was maintained at 26-29 during operation. During emergence from anesthesia EMG value increased with BIS value. When the patients opened their eyes at command EMG value was about 40. The correlation between BIS and EMG was poor. Conclusion At the samedepth of anesthesia (BIS = 50) the end-tidal isoflurane concentration was greatly reduced when combined with TCI propofol. EMG value decreases with increasing depth of anesthesia but as an anesthesia depth monitor it still needs improving.

Objective To establish a neuropathic pain model by transection of L4 spinal nerve in rats.Methods Twenty-eight male SD rats weighing 270-310 g were randomly divided into 3 groups: A experimental group (n = 12) received transection of right L4 spinal nerve; B sham operation group ( n = 8) in which right L4 spinal nerve was exposed but not transected and C control group ( n = 8) received no surgery. The paw withdrawal threshold (PWT) to mechanical stimulation was measured by using modified von Frey test. The response to cold stimulation evoked by applying acetone to the plantar region of hindpaw was measured and scored. The threshold to both noxious mechanical and thermal stimuli was measured once a week for 8 weeks. Results In experimental group the pain threshold to mechanical stimuli (von Frey hair stimulation) and cold stimuli (acetone test) on the operated side were significantly decreased after L4 spinal nerve transection as compared to the baseline values before operation and significantly lower than in sham operation and control groups. There was no significant change in the withdrawal response of the hindpaw to mechanical and cold stimuli after surgery on the unoperated side. Conclusion Hyperalgesia to mechanical and cold stimuli develops after L4 spinal nerve transection on the operated side and lasts more than 8 weeks

Objective To investigate the effect of nicorandil pretreatment on myocardial mitochondria in a rabbit model of myocardial ischemia-reperfusion (I/R). Methods Tirty-two healthy male New Zealand white rabbits weighing 2.0-2.5 kg aged 4 months were randomly allocated into 4 groups ( n = 8 each): Ⅰ group sham operation (group S); Ⅱ group I/R; Ⅲ group nicorandil pretreatment (group N) and Ⅳ group nicorandil + 5 hydroxydecanoic acid (group N + 5-HD). Myocardial I/R was induced by 30 min occlusion of left circumflex coronary artery followed by 120 min reperfusion. In group N and N + 5-HD a bolus of nicorandil 100 μg/kg was given iv at 10 min before myocardial ischemia followed by continuous infusion at 10 μg· kg-1 · min-1 until the beginning of myocardial ischemia. In group Ⅳ a bolus of 5-HD 5 mg/kg was injected iv at 20 min before myocardial ischemia.The animals were sacrificed at the end of 120 min reperfusion. The mitochondrial membrane potential was measured by flow cytometry using JC-1 fluorescence probe as indicator. Bcl-2, Bax and cytochrome c protein expression was determined by immuno-histochemistry. Myocardial ultrastructure was examined with transmission electron microscope. Results Red fluovescence intensity indicating normal live cells was significantly higher, the green fluorescence intensity indicating apoptotic cells was lower and red/green fluorescence intensity ratio was higher; the Bcl-2/Bax ratio was significantly higher and cytochrome c protein expression lower in group N than in group I/R.5-HD administration negated the protective effect of nicorandil pretreatment against myocardial I/R injury. Conclusion Nicorandil stabilizes mitochondrial membrane potential, decreases cytochrome c protein releasing, and suppresses mitochondrial apoptotic signal transduction by opening the mito-KATP channels.

Objective Role of melanocortin receptor 4 (MCAR) in excitatory amino acid release from rat astrocytes in spinal cord. Methods Astrocytes were isolated from the spinal cord of newborn pathogen-free Wistar rats ( 1-3 days after birth) and cultured in serum-free Neurobasal/B27 liquid culture medium. After 4 passages the primary cultured astrocytes were randomly divided into 3 groups (6 wells each): group Ⅰ control (group C); group Ⅱ the astrocytes were exposed to TNF-α 10 μg/L (group T) and group Ⅲ the astrocytes were exposed to TNF-α 10 μg/L and HS014 (selective MC4R antagonist) 1 μmol/L (group TH). The astrocytes were incubated at 37 ℃ for 3 h. The supernatant was collected for determination of glutamic acid (Glu) and aspartic acid (Asp)concentrations by HPLC-MS/MS. Results TNF-α significantly increased Glu and Asp release from astrocytes in group T as compared with group C. The Glu and Asp concentrations were significantly lower in group TH than in group T. Conclusion MG4R is involved in the excitatory amino acid release from astrocytes in the spinal cord.

Objective To evaluate the role of c?Jun N?terminal kinase ( JNK) and p38 mitogen?ac?tivated protein kinase ( p38MAPK) signaling pathways in attenuation of myocardial ischemia?reperfusion ( I∕R) injury by morphine postconditioning. Methods Healthy adult male Sprague?Dawley rats, weighing 180-240 g, were used in the study. Their hearts were excised and retrogradely perfused in a Langendorff apparatus with Krebs?Ringer ( K?R) buffer saturated with 95% O2?5% O2 at 37℃. After 15 min of equili?bration, 52 isolated hearts were divided into 4 groups ( n=13 each) using a random number table: control group (group C), I∕R group, morphine postconditioning group (group MP), and morphine postcondition?ing plus anisomycin group ( group MP+A) . The hearts were continuously perfused with K?R buffer for 105 min in group C. In group I∕R, the hearts were subjected to 45 min of global ischemia by stopping perfusion with K?R buffer, followed by 60 min of reperfusion by restoration of perfusion with K?R buffer. In group MP, the hearts were subjected to 45 min of global ischemia, followed by 10 min of reperfusion with K?R buffer containing 3?0 μmol∕L morphine and then by 50 min of reperfusion with K?R buffer. In group MP+A, the hearts were subjected to 45 min of global ischemia, followed by 10 min of reperfusion with K?R buffer containing 3?0 μmol∕L morphine and 1?0 μmol∕L anisomycin ( an activator of JNK and p38MAPK) and then by 50 min of reperfusion with K?R buffer. At 60 min of reperfusion, 8 hearts in each group were selected for measurement of the myocardial infarction and amount of creatine kinase?MB ( CK?MB) released from the myocardium, and the myocardial infarct size was calculated. At 20 min of reperfusion, 5 hearts in each group were selected to detect the expression of phosphorylated JNK ( p?JNK ) , phosphorylated p38MAPK ( p?p38MAPK) and cytochrome c ( Cyt c) in myocardial tissues ( by Western blot) and content of nicotinamide adenine dinucleotide ( NAD+) in myocardial tissues ( by spectrophotometry ) . Results Compared to group C, the myocardial infarct size and amount of CK?MB released from the myocardium were significantly increased, the expression of p?JNK, p?p38MAPK and Cyt c was significantly up?regulated, and the content of NAD+ was significantly decreased in I∕R, MP and MP+A groups ( P<0?05) . Compared to group I∕R, the myocardial infarct size and amount of CK?MB released from the myocardium were signifi?cantly decreased in MP and MP+A groups, and the expression of p?JNK, p?p38MAPK and Cyt c was sig?nificantly down?regulated, and the content of NAD+ was significantly increased in group MP (P<0?05). Compared to group MP , the myocardial infarct size and amount of CK?MB released from the myocardium were significantly increased, the expression of p?JNK, p?p38MAPK and Cyt c was significantly up?regula?ted, and the content of NAD+ was significantly decreased in group MP+A (P<0?05). Conclusion The mechanism by which morphine postconditioning attenuates myocardial I∕R injury is related to inhibition of activation of JNK and p38MAPK signaling pathways in rats.

Objective To evaluate the effect of dexmedetomidine on acute kidney injury after cardiac valve replacement with cardiopulmonary bypass (CPB).Methods One hundred patients of both sexes with rheumatic heart disease,aged 32-64 yr,weighing 46-75 kg,of American Society of Anesthesiologists physical status Ⅱ or Ⅲ (New York Heart Association class Ⅱ or Ⅲ),scheduled for elective cardiac valve replacement with CPB,were divided into 2 groups (n =50 each) using a random number table:control group (group C) and dexmedetomidine group (group D).Dexmedetomidine was intravenously infused in a loading dose of 1 μg/kg over 10 min before induction of anesthesia followed by an infusion of 0.4 μg · kg-1 · h-1 until 24 h after operation in group D,while the equal volume of normal saline was given in group C.The urine output per hour during the postoperative 48 h period was recorded.At 6,12,24,36 and 48 h after operation,blood samples were collected from the median cubital vein for determination of serum creatinine levels.The development and severity of acute kidney injury were determined according to the urine output and serum creatinine level.Results Compared with group C,the incidence and severity of acute kidney injury were significantly decreased in the postoperative 48 h period in group D (P＜0.05).Conclusion Dexmedetomidine infused in a loading dose of 1 μg/kg over 10 min before induction of anesthesia followed by an infusion of 0.4 μg · kg-1 · h-1 until 24 h after operation can reduce the development and severity of acute kidney injury after cardiac valve replacement with CPB in patients.

Objective To evaluate the effect of tripterine on hydrochloric acid-induced acute lung injury(ALI)in mice.Methods Eighteen pathogen-free healthy adult male ICR mice,aged 7-9 weeks,weighing 25-30 g,were divided into 3 groups(n=6 each)using a random number table:control group(group C),hydrochloric acid-induced ALI group(group ALI)and tripterine group(group T).ALI was induced by a single intratracheal instillation of hydrochloric acid 2 ml/kg(pH 1.5)via a 24-gauge angiocatheter inserted into the trachea in pentobarbital sodium-anesthetized mice.Tripterine 3 mg/kg was injected intraperitoneally once a day for 3 consecutive days,and then the model was established in group T.The mice were sacrificed at 6 h after instillation,and lung specimens were obtained for microscopic examination and for determination of the levels of tumor necrosis factor-alpha(TNF-α),interleukin-6(IL-6),macrophage migration inhibitory factor(MIF)and myeloperoxidase(MPO)in lung tissues.Results Compared with group C,the levels of TNF-α,IL-6,MIF and MPO were significantly increased at 6 h after instillation in ALI and T groups(P<0.01).Compared with group ALI,the levels of TNF-α,IL-6,MIF and MPO were significantly decreased at 6 h after instillation in group T(P<0.01).The pathological changes of lung tissues were significantly attenuated in group T compared with group ALI.Conclusion Tripterine can attenuate hydrochloric acid-induced ALI in mice.