The form and position of the ansa hypoglossi and the course of its com-ponents, the descending branch of the hypoglossal nerve and the communicatingbranches of the cervical nerves, were studied in 128 Chinese cadavers. It wasfound that only in half of the cases (55.7%) the ansa showed loop formationwhile in the other half the component nerves either joined each other at anacute angle or came together more gradually. The ansa may be found on thesurface of the carotid sheath or inside it. The point of union in percentageswas 48.2 half way between the mandible and the clavicle and 32.7 below thatlevel. In the majority of the cases (80.3%) the descending branch of thehypoglossal nerve ran down on the antero-lateral surface of the internal carotidartery, while in the rest it appeared in between the internal carotid artery andthe internal jugular vein.

Objective To evaluate the relationship between pharmacodynamics of sufentanil-induced respiratory depression and age factors. Methods Forty ASA Ⅰ or Ⅱ patients scheduled for elective abdominal surgery were randomly divided into 2 groups according to the age: young and middle-aged group (25-64 yr, group M) and elderly group (65-80 yr, group E). EC50 was determined by up-and-down sequential trail. The initial target effect-site concentration (Ce) of sufentanil was set at 0.40 and 0.35 μg/ml in group M and E respectively.Each time Ce decreased/increased by 10% in the next patient depending on whether or not the respiratory depression occurred. Respiratory depression was defined as VT ≤ 5 ml/kg, RR ≤ 8 bpm/min, SpO2 ≤ 94%,PET CO2 ≥ 55 mm Hg, and/or apnea ≥ 15 s. Results The EC50 and 95 % confidence interval of sufentanil causing respiratory depression were 0.61 (0.54-0.70) μg/ml and 0.41 (0.38-0.45) μg/ml in group M and E respectively with the significant difference. Conclusion The efficacy of sufentanil-induced respiratory depression is related to age factors and the elderly patients are more sensitive to sufentanil-induced respiratory depression.

Objective To evatluate the effect of dexmedetomidine on intraoperative wake-up test during cerebral functional area operation performed under combined iv propofol-remifentanil anesthesia.Methods Twenty-seven ASA Ⅰ or Ⅱ patients (both sexes) aged 17-43 yr with a body mass index of 20-24 kg/m2 undergoing op-eration on cerebral functional area during which intraoperative wake-up test was performed were randomly divided into control group (group C,n =13) and dexmedetomidine group (group D,n =14).Anesthesia was induced with midazolam,sufentanil,etomidate and rocuronium and maintained with TCl of propofol (Cp =3-5 μg/ml) and remifentanil (Ce =2-6 ng/ml).BIS value was maintained at 55-65.In group D after dura of brain was opened,a loading dose of dexmedetomidine 0.3 μg/kg was administered iv over 15 min followed by continuous iv infusion at 0.2 μg· kg-1 · h-1 while TCI of propofol and remifentanil were suspended.In group C after opening of dura,Cp of propofol TCI was reduced to 0.5 μg/ml and Ce of remifentanil to 0.5 ng/ml.The wake-up time and development of hypertension,tachycardia,headache,dysphoria,delirium and awareness were recorded.Results All patients were successfully awakened.There was no significant difference in wake-up time between the 2 groups (P ＞0.05).The incidences of hypertension,tachycardia,headache and awareness were significantly lower in group D than in group C (P ＜ 0.05).Conclusion Dexmedetomidine does not affect intraoperative wake-up time during operation on cerebral functional area performed under iv propofol-remifentanil anesthesia,but can significantly reduce the incidence of adverse effects.

Objective To explore the role of excitatory amino acid carrier 1 (EAAC1)in dorsal root ganglion (DRG) in the mechanism of developing morphine tolerance. Methods Thirty male SD rats were implanted intrathecal catheters and randomized into 6 groups with 5 rats each. The rats of 4 groups were made into the model of adjuvant-induced arthritis in the left hind limb and were administered intrathecally, morphine 10 μg(group M_(10)), morphine 20μg(group M_(20)), morphine 20 μg plus naloxone 10 μg(group MN) ,or saline(group C) respectively. The other 2 groups without were administered intrathecally saline (group C_0) or morphine 20 μg (group M0). The drugs were administered twice daily for 7 days. Mechanical withdrawl threshold(MWT) of the left hind limb was examined to evaluate the behavior. Immunohistochemistry was used to detect the expression of EAAC1 in the left L_(3-4) and L_(4-5) DRG. Results Morphine tolerance was formmed stably in the arthritis rats of group M_(10) and group M_(20) after administering morphine for 7 days. The expression of EAAC1 in DRG was downregulated. Conclusion DRG EAAC1 may be involved in the mechanism of developing morphine tolerance in rats with inflammatory pain.

Objective To investigate the changes in the expression of glutamate-aspartste transporter in spinal dorsal horn in rats with inflammatory pain and chronic morphine tolerance. Methods Thirty healthy male SD rats in which intrathecal (IT) catheters were successfully placed without complications were randomized into 3 groups ( n = 10 each): normal saline group ( group NS), arthritis group ( group A), and arthritis + morphine group (group AM). NS 50 μl was injected into the ankle joint of the left hindlimb in group NS, while complete Freund's adjuvant was injected in the other two groups instead. After 3 days, group NS and A received IT NS 10 μl twice a day for 7 consecutive days, group AM IT morphine 10 μg (10 μl) twice a day for 7 consecutive days. Mechanical pain threshold (MPT) was measured before IT administration and at day 2, 4, 6 and 8 after IT administration (T0-4). The animals were sacrificed after the last MPT measurement. The spinal cords were isolated for determination of GLAST expression in spinal dorsal horn. Results Compared with group NS, MPT was significantly decreased in the other groups and GLAST expression was down-regulated in group AM (P ＜ 0.05). Compared with group A, no significant change was found in MPT at T3,4 (P ＞ 0.05), while GLAST expression was down-regulated in group AM ( P ＜ 0.05). Conclusion The development of chronic morphine tolerance is related to the decrease in the function of GLAST in spinal dorsal horn in rats with inflammatory pain.

Objective To investigate the changes in the expression of calcitonin gene-related peptide (CGRP), substance P (SP) and brain-derived neurotrophic factor (BDNF) in dorsal root ganglion (DRG) and the effect of electroacupuncture (EA) on morphine tolerance in rats with chronic inflammatory pain (CIP) and morphine tolerance. Methods Twenty-five 8-month-old male SD rats weighing 230-250 g in which intrathecal (IT)catheters were successfully implanted without complications were randomly divided into 5 groups ( n = 5 each):groupA CIP + normal saline (NS) 10 μl IT twice a day for 7 consecutive days; group B CIP + morphine 10 μg/kg ( 10 μl) IT twice for the first day only; group C CIP + morphine 10 μg/kg ( 10 μl) IT twice a day for 7 consecutive days; group D CIP + EA (intensity 2 mA, frequency 2 Hz, wave length 0.6 ms) + morphine 10 μ g/kg (10 μl) IT twice a day for7 consecutive days; group E CIP + EA (intensity 2 mA, frequency 15 Hz,wave length 0.4 ms) + morphine 10μg/kg (10 μl) IT twice a day for7 consecutive days. CIP was induced by injecting complete Freund's adjuvant (CFA) into the ankle joint of the left hindlimb. IT morphine or NS was started on the 4th day after induction of CIP. EA of Yanglingquan and Zusanli lasting 30 min was performed once a day after first IT administration of morphine for 7 days. Paw withdrawal latency (PWL) to a thermal nociceptive stimulus was measured before induction of CIP, 1 day before (baseline) and at day 1-7 after administration (T0-8) . The animals were sacrificed after the last PWL measurement. The DRGs of the lumbar segment (L4-6) were removed for determination of CGRP, SP and BDNF mRNA expression using RT-PCR. Results PWL was significantly shorter at T1 than at T0 in all groups, and at T3-8 than at T2 in group B-E, while longer at T2 than at T1 in group B-E ( P ＜0.05). PWL was significantly longer in group B-E and CGRP, SP and BDNF mRNA expression higher in group C than in group A ( P ＜ 0.05). PWL was significantly longer in group C-E than in group B ( P ＜ 0.05). PWL was significantly longer and CGRP, SP and BDNF mRNA expression lower in group D and E than in group C ( P ＜0.05). PWL was significantly lower and CGRP, SP and BDNF mRNA expression higher in group E than in group D ( P ＜ 0.05). Conclusion Up-regulation of the expression of CGRP, SP and BDNF mRNA in DRG is involved in the devepopment of morphine tolerance. EA can inhibit the devepopment of morphine tolerance by inhibiting the expression of CGRP2 SP and BDNF mRNA.

ObjectiveTo evaluate the role of the spinal cord proteasome in chronic morphine tolerance in rats.MethodsTwenty-four healthy male SD rats in which intrathecal catheters were successfully placed without complications were randomized into 4 groups ( n =6 each):normal saline group ( group NS),chronic morphine tolerance group (group M),chronic morphine tolerance + proteasome inhibitor MG-132 group (group M + MG) and MG-132 group (group MG).Normal saline 10 μl,morphine 10 μg,morphine 10 μg+ MG-132 2.5 μg and MG-132 2.5 μg were injected intrathecally twice a day for 7 consecutive days in groups NS,M,M + MG and MG respectively.Tail flick latency was measured on day 1 before intrathecal injection and on day 1,3,5 and 7 of intrathecal injection to calculate the percentage of maximum possible antinociceptive effect (MPAE).After the last intrathecal injection,5 rats were sacrificed,and L3-5 spinal cord was removed for determination of the expression of glutamate-aspartate transporter (GLAST) and excitatory amino acids carrier 1 (EAAC1)by Western blot.Results MPAE was gradually decreased during the intrathecal injection in groups M and M + MG( P ＜ 0.05).Compared with group NS,MPAE was gradually incresed during the intrathecal injection in groups M and M + MG,and the expression of GLAST and EAAC1 in the spinal cord was significantly down-regulated in group M (P ＜ 0.05).There was no significant difference in the parameters mentioned above between group MG and group NS ( P ＞0.05 ).Compared with group M,MPAE was significantly increased and the expression of GLAST and EAAC1 in the spinal cord was significantlyup-regulatedingroupM+MG(P＜0.05or0.01).ConclusionSpinal cord proteasome is involved in the development of chronic morphine tolerance in rats.

From recent collection of 40 male adult cadavers from Chungking, the authors caIculated the coefficient of correlation between the average lengths of long bones of both sides and the stature measured from the cadavers. The figures range from 0.719～0.849, which denote a rather high degree of correlation. Hence, 10 regression formulae were computed. After a thorough analysis of the equations, it indicates that the relationship between stature and long bones of the lower limb reveals a higher coefficient of correlation and a lower standard error of estimation than that from the upper limb. Moreover, the reconstruction of stature from the sum of the lengths of femur and tibia (or fibula) appears still more reliable than that from the femur alone. The regression formulae obtained had been compared with the only data thus far found on the North China sample (Stevenson, 1929),it exhibits that all regression lines of both sources parallel with each other (Chungking lines being placed a little bit lower), with the exception of the two humerus lines which intersect. Therefore, whether regression formulae computed from this paper can be expected to give an approximation to reality in different districts of China or not demands further checking over with figures derived from the stature estimate made in different localities by the same method.

Objective:To evaluate the effect of hydrogen on mitochondrial dynamics in hippocampus of mice with sepsis-associated encephalopathy (SAE).Methods:A total of 224 clean-grade healthy male C57 mice, weighing 20-25g, aged 6-8 weeks, were divided into 4 groups ( n=56 each) using a random number table method: sham operation group (group Sham), sham operation + hydrogen group (group Sham+ H 2), SAE group and SAE + hydrogen group (group SAE+ H 2). Sepsis was produced by cecum ligation and puncture (CLP). Sham+ H 2and SAE+ H 2 groups inhaled 2% hydrogen for 1 h starting from 1 and 6 h after CLP, respectively.The postoperative 7-day survival rate was recorded.Brain tissues were obtained at 24 h after operation for examination of the pathological changes in hippocampal CA1 region (with a light microscope) and for determination of mitochondrial membrane potential (MMP) (by fluorescence spectrophotometry) and ATP content (by a bioluminescence assay) in hippocampal tissues.At 6, 12 and 24 h after operation, hippocampal mitochondria were isolated for determination of the expression of dynamin-related protein 1 (Drp1) and the mitochondrial fusion proteins mitofusin 2 (Mfn2) (by Western blot). Results:Compared with group Sham, the postoperative 7-day survival rate was significantly decreased, the contents of MMP and ATP were decreased, the expression of Drp1 was up-regulated, and the expression of Mfn2 was down-regulated( P<0.05), the pathological changes were aggravated in hippocampal CA1 region in SAE and SAE+ H 2 groups, and no significant change was found in the parameters mentioned above in group Sham+ H 2 ( P>0.05). Compared with group SAE, the postoperative 7-day survival rate was significantly increased, the contents of MMP and ATP were increased, the expression of Drp1 was down-regulated, and the expression of Mfn2 was up-regulated( P<0.05), the pathological changes were attenuated in hippocampal CA1 region in group SAE+ H 2. Conclusion:The mechanism by which hydrogen improves mitochondrial function is probably associated with promoting mitochondrial fusion and inhibiting mitochondrial fission in hippocampus of mice with SAE.

Objective To investigate the role of glycogen synthase kinase-3β (GSK-3β) in the trafficking of NR1-containing N-methyl-D-aspartate receptor (NMDAR) and NR2B-containing NMDAR in the spinal cord in rats with incisional pain (IP) and remifentanil-induced hyperalgesia.Methods Twenty-four male Sprague-Dawley rats,aged 2-3 months,weighing 240-260 g,were randomly divided into 3 groups ( n =8 each):control group (group C),remifentanil group (group R) and GSK-3β inhibitor TDZD-8 group (group TDZD-8).A 1-cm longitudinal incision was made in the plantar surface of the left hindpaw in anesthetized rats.In group C,dimethyl sulfoxide (DMSO) 2 ml/kg was injected and then the normal saline (equal to the volume of remifentanil) was infused for 60 min via the caudal vein.In group R,DMSO 2 ml/kg was injected before IP was made and then remifentanil was infused at a rate of 1.2 μg· kg- 1 ·min- 1 for 60 min.In group TDZD-8,TDZD-8 2 ml/kg was injected before IP was made and then remifentanil was infused at a rate of 1.2 μg·kg-1 ·min-1 for 60 min.Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were measured 24 h before infusion of normal saline or remifentanil and at 2,6,24 and 48 h after intravenous injection.The rats were sacrificed after the last measurement of the pain threshold and L4-6 segment of the spinal cord was removed to determine the expression of NMDAR NR1 and NR2B subunits in cell membrane (s) and cytoplasm (i) in the spinal cord by Western blot analysis.The ratios of sNR1/iNR1 and sNR2B/iNR2B were calculated.Results Compared with group C,PWT was significantly decreased and PWL was significantly shortened,the expression of sNR1 and sNR2B was up-regulated,the expression of iNR1 and iNR2B was down-regulated,and the ratios of sNR1/iNR1 and sNR2B/iNR2B were significantly increased in groups R and TDZD-8 (P ＜ 0.05).Compared with group R,PWT was significantly increased and PWL was significantly prolonged,the expression of sNR1 and sNR2B was down-regulated,the expression of iNR1 and iNR2B was up-regulated,and the ratios of sNR1/iNR1 and sNR2B/iNR2B were significantly decreased in group TDZD-8 ( P ＜ 0.05).Conclusion GSK-3β is involved in the regulation of trafficking of NR1-containing NMDAR and NR2B-containing NMDAR from cytoplasm to cell membrane in the spinal cord in rats with IP and hyperalgesia induced by remifentanil.