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Objective Low-dose naloxone has been shown to reduce side-effects of morphine while morphine analgesia is not antagonized and may even be enhanced. The purpose of this study was to evaluate the effects of low-dose naloxone infusion (50 ng? kg-1? h-1 ) on morphine analgesia and plasma levels of opioid peptides in patients after abdominal hysterectomy.Methods Forty-two ASA Ⅰ- Ⅱ patients aged 36-50 yrs, weighing 55-67 kg undergoing abdominal hysterectomy under combined spinal-epidural anesthesia were enrolled in this study. Spinal puncture was performed at L2-3 interspace. The patients received intrathecal 0.75% ropivacaine 2.0-2.6 ml. 2% lidocaine was used for epidural injection. The block height was maintained at T8-6 . For postoperative analgesia the patients were randomized to receive either intravenous morphine infusion at 10 ?g?kg-1 ?h-1 (group M, n = 21) or IV morphine infusion (10 ?g?kg-1?h-1)+ naloxone infusion at 50 ng?kg-1?h-1 (group MN, n = 21). Pain was assessed using VAS (0-10) with 0 representing no pain and 10 representing the worst possible pain. Blood samples were taken from peripheral vein before anesthesia (T0), at the end of surgery (T1) and at 6, 24, 48 h (T2,3,4) after operation for determination of plasma levels of ?-endorphin (?-EP), dynorphin A1-13 (Dyn) and leu-enkepholin (L-EK) .Results The patients were comparable with respect to, age, weight, occupation and duration of operation between the two groups. Two patients (1 patient in each group) were excluded from the study because of their refusal to have repeated blood samples taken. The analgesia was significantly better in group MN than that in group M in terms of VAS scores. Plasma level of ?-EP was significantly lower at 6 h after operation (T2 ) but significantly higher at 24 h postop. (T3 ) in group MN compared with that in group M ( P
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Objective To investigate the effects of transection of cervical sympathetic trunk (TCST) on the blood flow of uterine artery (BFUA) and plasma concentrations of norepinephrine (NE) and nitric oxide (NO) in rats with pregnancy hypertension (PIH) . Methods Forty pregnant Wistar rats weighing 240-270 g were randomly divided into 5 groups with 8 animals in each group: control group( group C) , L-NAME induced hypertension groupl and 2 (group Bl, B2); TCST group and sham operation group. In control group no hypertension was induced. In group Bl and B2 hypertension was induced with L-NAME 12.5 mg.100-1 or 6.25 mg. 100-1 injected subcutaneously from 14 th to 20 th day of gestation. In TCST group TCST was performed on the 14th day of gestation and hypertension was induced as in group B1. In sham operation group cervical sympathetic trunk was exposed but not transected on the 14 th day of gestation and hypertension was induced as in group Bl. BFUA was measured and blood samples were taken from abdominal aorta for determination of plasma NE and NO concentrations on the 21 st day of gestation. Results (1) The mean BFUA during systole and systole + diastole was significantly lower in group Bl and B2 than that in group C ( P 0.05). (2) The plasma NE levels in group Bl and B2 were significantly higher than in that in group C (P
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Objective To investigate the effects of propofol on ketamine-induced HSP 70 mRNA and protein expression in the rat posterior cingulate cortex and to explore the possibility of using propofol to prevent or treat ketamine-induced psychotomimetic effects and neuronal damage. Methods Thirty male Wistar rats weighing 250-300 g were randomly divided into 5 groups with 6 animals in each group: group 1 received normal saline intraperitoneally ip (NS); group 2 received ketamine 100 mg? kg-1 ip (K); group 3 received propofol 100 mg ? kg-1 ip (P); group 4 received propofol 50 mg?kg-1 + ketamine 100 mg?kg-1 ip (P1 K) and group 5 received propofol 100 mg?kg + ketamine 100 mg?kg-1 ip (P2K) . In group 4 and 5 the interval between propofol and ketamine administration was 15 min. Twenty-four hours after ketamine and/or propofol administration, the animals were decapitated and brain was removed. HSP 70 mRNA expression in the posterior cingulate cortex was detected by using semi-quantitative RT-PCR technique; HSP 70 protein expression in posterior cingulated cortex was determined by immuno-histochemical method. Results The levels of HSP 70 mRNA and HSP 70 protein expression were significantly different among the 5 groups. Ketamine induced marked HSP 70 mRNA and HSP 70 protein expression in the posterior cingulated cortex. Propofol itself did not induce HSP 70 gene expression in this brain region. Propofol significantly inhibited ketamine-induced HSP 70 mRNA and HSP 70 protein expression in the posterior cingulate cortex in a dose-dependent manner. Conclusions Propofol pretreatment can significantly inhibit ketamine-induced HSP 70 mRNA and protein expression in the posterior cingulated cortex. It may be one of the mechanisms of inhibition of ketamine-induced psychotomimetic effect and neuronal damage by propofol.
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Objective To study the effects of intrathecally administered morphine and ketamine on nitric oxide synthase (NOS) activity and nitric oxide content in the spinal cord.Methods Thirty-two male Wistar rats weighing 220-260 g were anesthetized with intraperitoneal chloral hydrate 300 mg?kg-1 . A catheter was implanted in subarachnoid space at lumbal region. Sciatic constriction injury (SCI) was produced by loose ligation of right sciatic nerve trunk with 4-0 cutgut. On the 4th postoperative day the animals were randomly divided into four groups of 8 animals :(1) control group (C); (2) morphine group (M);(3) ketamine group (K) and morphine-ketamine group (KM) . Morphine 20 ?g / ketamine 20 ?g / morphine 10 ?g + ketamine 10 ?g were injected intrathecally every day for 7 consecutive days in group M, K and KM. In control group normal saline was injected intrathecally instead of morphine and / or ketamine. The withdrawal latenvies to radiant heat focused on plantar surface were measured as radiant heat threshold before intrathecal administration of the analgesic (baseline) and 30 min after intrathecal administration of ketamine and / or morphine every day for 7consecutive days. The percentage of maximal possible effect ( MPE % ) was calculated : MPE % = (latency after intrathecal administration-baseline latency) / (radiant heat cut-off time-baseline latency) X 100% . After 7 days of intrathecal administration the animals were decapitated and the spinal cord was immediately removed and the lumbal spinal cord was dissected on ice. NOS activity and nitric oxide ( NO) content were measured by spectrophotometry. Results MPE % was significantly higher in group M and KM than in group C and K ( P
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The management system of work attendance is developed by the support of local area network of No.1 Military Medical Project and by the use of PowerBuilder. The system is applied to record work attendance on net, by which the management department can check work attendance of all departments of our hospital at any time. The application of the system realizes the management of work attendance on network, enhances work efficiency and avoids trivial manual work of count and collection.