Comparison of Pain Thresholds and Analgesic Effects of Parecoxib Sodium in Surgical Patients of Different Racial and Religious Backgrounds.

OBJECTIVE: To explore the differences of the thresholds of pain and analgesic effects of parecoxib sodium among patients with different racial and religious backgrounds. METHODS: A total of 48 male patients aged 18 to 38 years who had undergone elective laparoscopic appendectomy under general anesthesia in our centers were enrolled in our study and then divided into 6 groups(n=8 in each group)based on their racial backgrounds(three levels:Mongoloid,Negroid,and Europoid)and religious backgrounds(two levels:without religion background,with religion background).All subjects received the same anesthesia,surgical procedure,and postoperative analgesia with parecoxib sodium. The temperature pain threshold and electrical pain threshold were detected 1h before and after analgesia. RESULTS: The threshold of pain was higher in Europoids than in Negroids and Mongoloids before and after treatment. The temperature pain threshold and electrical pain threshold were not significantly different between subjects with or without religious background(before analgesic therapy:F=251.119,P=0.130,F=275.861,P=0.059;after analgesic therapy:F=308.531,P=0.086,F=180.062,P=0.078). Also,there was no interaction between the racial and religious backgrous in terms of temperature pain threshold and electrical pain threshold(F=13.553,P=0.091,F=22.001,P= 0.089;after analgesic therapy:F=4.624,P=0.089,F=15.935,P=0.094). CONCLUSIONS: The threshold of pain differs among individuals with different racial background:it is highest in Europoids,followed by Negroids and Mongoloids. It shows no obvious difference in people with different religious backgrounds.

Propofol up-regulates expression of ABCA1, ABCG1, and SR-B1 through the PPARγ/LXRα signaling pathway in THP-1 macrophage-derived foam cells.

BACKGROUND: ATP-binding cassette transporter A1 (ABCA1), ATP-binding cassette transporter G1 (ABCG1), and scavenger receptor-B1 (SR-B1) promote cholesterol efflux from cells to lipid-poor apolipoprotein A-I and play an important role in the development of atherosclerosis. Liver X receptor (LXRα) and peroxisome proliferator-activated receptor-gamma (PPARγ) operate as cholesterol sensors, which may protect from cholesterol overload by stimulating cholesterol efflux from cells to high-density lipoprotein through ABCA1, ABCG1, and SR-B1. Propofol administration is associated with cardiovascular protective effects, including anti-inflammatory and antioxidant properties. Here, we examined the effect of propofol on ABCA1, ABCG1, and SR-B1 expression and explored whether PPARγ and LXRα were involved in the regulation of propofol-induced ABCA1, ABCG1, and SR-B1 expression in THP-1 macrophage-derived foam cells. METHODS AND RESULTS: Propofol significantly increased expression levels of ABCA1, ABCG1, and SR-B1 in a time-dependent manner. Cellular cholesterol content was decreased while cholesterol efflux was increased by propofol treatment. Moreover, PPARγ and LXRα were up-regulated by propofol treatment. In addition, the up-regulated expression of ABCA1, ABCG1, and SR-B1 by propofol was significantly abolished by both PPARγ siRNA and LXRα siRNA in THP-1 macrophage-derived foam cells. CONCLUSION: These results provide evidence that propofol up-regulates expression of ABCA1, ABCG1, and SR-B1 through the PPARγ/LXRα pathway in THP-1 macrophage-derived foam cells.

Propofol Attenuates Lipopolysaccharide-Induced Monocyte Chemoattractant Protein-1 Production Through Enhancing apoM and foxa2 Expression in HepG2 Cells.

Monocyte chemoattractant protein-1 (MCP-1) is a cytokine that mediates the influx of cells to sites of inflammation. Our group recently reported that propofol exerted an anti-inflammatory effect and could inhibit lipopolysaccharide (LPS)-induced production of pro-inflammatory cytokines. However, the effect and possible mechanisms of propofol on MCP-1 expression remain unclear. LPS-stimulated HepG2 cells were treated with 50 µM propofol for 0, 6, 12, and 24 h, respectively. The transcript and protein levels were measured by real-time quantitative PCR and Western blot analyses, respectively. We found that propofol markedly decreased both MCP-1 messenger RNA (mRNA) and protein levels in LPS-stimulated HepG2 cells in a time-dependent manner. Expression of apolipoprotein M (apoM) and forkhead box protein A2 (foxa2) was increased by propofol treatment in HepG2 cells. In addition, the inhibitory effect of propofol on MCP-1 expression was significantly abolished by small interfering RNA against apoM and foxa2 in LPS-stimulated HepG2 cells. Propofol attenuates LPS-induced MCP-1 production through enhancing apoM and foxa2 expression in HepG2 cells.

Atorvastatin Attenuates TNF-alpha Production via Heme Oxygenase-1 Pathway in LPS-stimulated RAW264.7 Macrophages.

OBJECTIVE: To assess the effect of atorvastatin on lipopolysaccharide (LPS)-induced TNF-α production in RAW264.7 macrophages. METHODS: RAW264.7 macrophages were treated in different LPS concentrations or at different time points with or without atorvastatin. TNF-α level in supernatant was measured. Expressions of TNF-α mRNA and protein and heme oxygenase-1 (HO-1) were detected by ELISA, PCR, and Western blot, respectively. HO activity was assayed. RESULTS: LPS significantly increased the TNF-α expression and secretion in a dose- and time-dependent manner. The HO-1 activity and HO-1 expression level were significantly higher after atorvastatin treatment than before atorvastatin treatment and attenuated by SB203580 and PD98059 but not by SP600125, suggesting that the ERK and p38 mitogen-activated protein kinase (MAPK) pathways participate in regulating the above-mentioned effects of atorvastatin. Moreover, the HO-1 activity suppressed by SnPP or the HO-1 expression inhibited by siRNA significantly attenuated the effect of atorvastatin on TNF-α expression and production in LPS-stimulated macrophages. CONCLUSION: Atorvastatin can attenuate LPS-induced TNF-α expression and production by activating HO-1 via the ERK and p38 MAPK pathways, suggesting that atorvastatin can be used in treatment of inflammatory diseases such as sepsis, especially in those with atherosclerotic diseases.

WITHDRAWN: Propofol reduces MMPs expression by inhibiting PI3K/AKT activity in human HepG2 cells.

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Anti-inflammatory effects of propofol are mediated by apolipoprotein M in a hepatocyte nuclear factor-1α-dependent manner.

Propofol (2,6-diisopropylphenol) is probably the most widely used intravenous hypnotic agent in daily practice. However, its anti-inflammatory properties have seldom been addressed. In this study, we evaluated the anti-inflammatory activity and mechanisms of propofol on lipopolysaccharide (LPS)-induced inflammation in vivo and in vitro and found that propofol markedly inhibited LPS-induced production of pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6, and expression of inducible nitric oxide synthase (iNOS). At the same time, the expression of hepatocyte nuclear factor-1α (HNF-1α) and apolipoprotein M (APOM) was inhibited by treatment with LPS and LPS-induced down-regulation of HNF-1α expression and APOM expression could be compensated by propofol treatment. However, propofol could not compensate LPS-induced down-regulation of APOM expression by treatment with HNF-1α siRNA and the suppressive effect on LPS-induced pro-inflammatory cytokines production by propofol was significantly compensated by treatment with APOM siRNA. These results provide evidence that propofol may first up-regulate APOM expression by enhancing HNF-1α expression and then inhibit pro-inflammatory cytokine production in LPS-stimulated cells. Therefore, our study may be useful in understanding the critical effect of propofol in patients with systemic inflammatory response syndrome.

Propofol induces rat embryonic neural stem cell apoptosis by activating both extrinsic and intrinsic pathways.

Propofol has previously been shown to have detrimental effects on the developing brain. Neural stem cells, identified in the embryonic brain as well as in the adult brain, are multipotent, self-renewing cells, which are capable of differentiating into different phenotypes of the nervous system. The present study was designed to investigate propofol-induced rat embryonic neural stem cell apoptosis and its potential mechanisms. Rat embryonic neural stem cells were isolated, cultured and characterized. Treatment of these cultured stem cells with different doses of propofol was carried out and cell proliferation was assessed by MTT assay and apoptosis by flow cytometric analysis. Cellular levels of active forms of caspase-3 and caspase-8, which regulate the extrinsic apoptotic pathway, and of caspase-9 and cytochrome C, which regulate the intrinsic apoptotic pathway, were detected by western blotting. Over 95% of isolated rat embryonic neural stem cells expressed the Nestin protein, as detected by immunofluorescence staining. Using an in vitro cell culture system, we showed that propofol inhibited cell growth and induced cell apoptosis in a dose-dependent manner. Furthermore, western blot analysis showed that propofol treatment significantly elevated levels of active forms of caspase-3, caspase-8, caspase-9 and cytochrome C in the embryonic neural stem cells. Propofol induced rat embryonic neural stem cell apoptosis and activated caspase-3, caspase-8, caspase-9 and cytochrome C, suggesting that propofol-induced stem cell apoptosis may be regulated through both the extrinsic and intrinsic apoptotic pathways.

[Effect of propofol at uptake equilibrium on γ-aminobutyric acid in different cerebral regions in dogs].

OBJECTIVE: To investigate the effect of propofol at doses for different anesthesia depths on γ-aminobutyric acid (GABA) in different cerebral regions at propofol uptake equilibrium in dogs. METHODS: Twelve 12-18-month-old healthy hybrid dogs weighing 10-12 kg were randomly divided into light anesthesia group (n=6) and deep anesthesia group (n=6) with a single bolus dose of propofol (5.5 and 7.0 mg/kg, respectively) completed in 15 s followed by intravenous propofol infusion at a constant rate (55 and 70 mg·kg(-1)·h(-1), respectively). Blood samples (2 ml) were taken from the internal carotid artery and jugular vein to measure plasma propofol concentrations 50 min after the start of the infusion. The dogs were then sacrificed and tissues were taken from different brain regions and the cervical cord to measure GABA concentrations using high-pressure liquid chromatography (HPLC). RESULTS: The plasma propofol concentrations in internal carotid artery and jugular vein were similar in both light anesthesia group (3.00 ± 0.31 and 3.10 ± 0.51 µg/ml, respectively, P>0.05) and deep anesthesia group (6.41 ± 0.05 and 6.40 ± 0.11 µg/ml, respectively, P>0.05). GABA concentrations in the brain regions were significantly higher in deep anesthesia group than in light anesthesia group (P<0.05). The dorsal thalamus and hypothalamus showed greater GABA variations [(83.83 ± 2.230%) and (85.83 ± 1.72)%] compared to other brain regions at different anesthesia depths (P<0.05). CONCLUSIONS: In both groups, plasma propofol concentrations in the internal carotid artery and internal jugular vein reach equilibrium at 50 min of propofol infusion. The variation of GABA is associated with the anesthesia depth of propofol, and GABA variation in the dorsal thalamus and hypothalamus plays an important role in propofol anesthesia.

[Effects of hypertonic sodium chloride hydroxyethyl starch 40 on brain histopathology in rats with whole body hyperthermia].

OBJECTIVE: To investigate the effects of hypertonic sodium chloride hydroxyethyl starch 40 (HSH) on brain edema and morphological changes during whole body hyperthermia (WBH) in rats. METHODS: Sixty adult male SD rats were randomized into control group, WBH group without fluid infusion (group HT), WBH group with Ringer's infusion (group RL), WBH group with HAES + Ringer's infusion (group HRL) and WBH group with HSH infusion (group HSH). WBH was induced by exposure to 36 degrees celsius; for 3 h to achieve a rectal temperature of 41-42 degrees celsius;, and the corresponding fluids were administered intravenously within 30 min at the beginning of WBH. The control rats were housed at a controlled room temperature (22∓1) degrees celsius; for 4 h. After cooling at room temperature for 1 h, the rats were sacrificed and brain water content and morphological changes were evaluated. RESULTS: Compared with the control group, all the WBH groups had significantly increased brain water content (P<0.05 or 0.01), but group HSH showed a significantly lower brain water content than group HT (P<0.05). The rats in groups HT, RL and HRL showed serious to moderate structural changes of the brain tissue and nerve cells, but HSH group had only mild pathologies. CONCLUSION: HSH can reduce brain edema and ameliorate the damages to brain cells in rats exposed to WBH.

[Effect of methylprednisolone pretreatment on pulmonary permeability and dipalmitoylphosphatidylcholine content in rabbits with reexpansion pulmonary edema].

OBJECTIVE: To investigate the effects of methylprednisolone pretreatment on pulmonary lung permeability index and the content of the pulmonary surfactant dipalmitoylphosphatidylcholine (DPPC) in a rabbit model of reexpansion pulmonary edema. METHODS: Twenty-one male New Zealand white rabbits were randomly divided into control group, reexpansion, and reexpansion+methylprednisolone pretreatment groups. The rabbit model of reexpansion pulmonary edema was established using Sakaos method. A bolus dosage of methylprednisolone (3 mg/kg) in reexpansion+methylprednisolone group group or 2.0 ml/kg normal saline in the other two groups was administered intravenously 20 min before reexpansion pulmonary edema. Bronchoalveolar lavage fluid (BALF) and arterial blood samples were collected for measurement of the total protein (TP) and DPPC contents 4 h after reexpansion, and the pulmonary permeability index was calculated. RESULTS: The pulmonary permeability index in methylprednisolone pretreatment group was significantly lower than that in the reexpansion group (0.007∓0.002 vs 0.177∓0.004, P<0.05). Methylprednisolone pretreatment significantly increased DPPC concentration in the BALF as compared with saline treatment in the reexpansion group (61.815∓28.307 vs 101.955∓24.544 µg/ml, P<0.05). CONCLUSION: Methylprednisolone pretreatment can increase pulmonary surfactant content and improve pulmonary permeability in the rabbit model of reexpansion pulmonary edema.

[Protective effects of penehyclidine hydrochloride against acute renal injury induced by hemorrhagic shock and lipopolysaccharides in rats].

OBJECTIVE: To investigate the effect of penehyclidine hydrochloride (PHC) in a rat model of renal injury induced by hemorrhagic shock and lipopolysaccharides (LPS). METHODS: Forty-five healthy Wistar rats were randomized into sham operated group, model group, and 3 penehyclidine hydrochloride (PHC) dose (1, 2 and 3 mg/kg) groups (PHC1, PHC2, and PHC3 groups, respectively). The arterial blood samples were collected to determine the concentrations of serum tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), interleukin-1 (IL-1), urine creatinine (Cr) and blood urine nitrogen (BUN), and the renal tissues were collected to measure the expressions of ICAM-1 and nuclear factor-κB (NF-κB) and observe the pathological changes. RESULTS: TNF-α, IL-8, IL-1, Cr, BUN, ICAM-1 and NF-κB in the 3 PHC groups were significantly lower than those in the model group (P<0.05). TNF-α, IL-8, IL-1, Cr and BUN were significantly lower in PHC1 (P<0.05) than in the PHC2 and PHC3 groups, and ICAM-1 and NF-κB were similar between 3 PHC groups (P>0.05). Compared with the model group, the 3 PHC groups showed lessened pathological changes in the renal tubules. CONCLUSION: PHC has protective effects against renal injury induced by hemorrhagic-endotoxin shock in rats, and treatment with 1 mg/kg PHC produces the most significant protective effect.

[Effects of parecoxib on morphine dosage in postoperative patient-controlled analgesia following thoracoscope-assisted thoracotomy].

OBJECTIVE: To observe the effect of parecoxib on morphine dosage in patient-controlled analgesia (PCA) following thoracoscope-assisted thoracotomy. METHODS: A consecutive series of 100 patients undergoing thoracoscope-assisted thoracotomy were randomized into 5 groups and received PCA with morphine doses at 0, 5, 10, 15, and 20 mg given in 200 ml saline (groups P(1), P(2), P(3), P(4), and P(5), respectively). Parecoxib (40 mg) was given in all the patients immediately before the operation, and the mixture (4-5 ml) of lidocaine and ropivacaine was administered into the 3 intercostal spaces upper and lower to the incision before chest closure. PCA was administered for each patient. The visual analogue scale (VAS) at rest and coughing and the respiratory functional parameters were recorded at 1, 2, 4, 8, 12, 24, 36, and 48 h after the start of PCA, and the actual and effective button-pressing times (D(1)/D(2)) in PCA were also recorded. RESULTS: No patients showed signs of respiratory inhibition within 24 h after the operation, and the resting VAS was comparable between the groups within the initial 6 postoperative hours. At 8 to 24 h postoperatively, the VAS scores at rest and coughing were significantly higher in P(1) group than in the other groups (P<0.05), and no significant differences were found between the groups at 36 to 48 h. D(1)/D(2) in groups P(1) and P(2) were significantly different from those in the other 3 groups at 4-24 h, but no such difference was found between groups P(3), P(4), and P(5). CONCLUSION: The application of parecoxib may reduce the dosage of morphine in PCA following thoracoscope-assisted thoracotomy and results in good analgesic effect without affecting the patients respiratory function and sputum elimination.

[Application of subclinical doses of pentazocine and propofol in painless vaginal egg retrieval].

OBJECTIVE: To assess the feasibility of using subclinical doses of pentazocine in painless egg retrieval. METHODS: Eighty-one patients undergoing painless egg retrieval were randomized into the observation group and the control group to receive 0.4 mg/kg pentazocine with 1.5 mg/kg propofol and 0.5 mg/kg pentazocine with 1.5 mg/kg propofol, respectively. The mean arterial pressure (MAP), heart rate (HR), SPO(2), respiratory rate (RR), unconsciousness time, awake time, hospital stay, complications, consciousness during the operation and adverse effects were compared between the two groups. RESULTS: The two groups showed no significant differences in the analgesic effect, dosage of propofol, adverse effects, unconsciousness time, awake time, or hospital stay. But compared with the control group, the observation group showed greater intraoperative consciousness but with more stable respiration. CONCLUSION: Subclinical doses of pentazocine can be used in the painless egg retrieval, but the dose of propofol should be increased to reduce the body activity during the operation.

[Effect of propofol on proliferation and differentiation of rat embryonic neural stem cells in vitro].

OBJECTIVE: To investigate the effect of propofol on the proliferation and differentiation of rat embryonic neural stem cells in vitro. METHODS: Embryonic neural stem cells of fetal Wistar rats (gestational age of 14-16 days) in primary culture, after identification for nestin expression, were divided into control group, introlipid group, and propofol groups (treated with propofol at the doses of 5, 25, 50, and 100 µmol/L). The changes in the proliferation of the embryonic neural stem cells after the treatments were observed using Brdu incorporation assay. In the course of induced differentiation of the embryonic neural stem cells, 50 µmol/L propofol was added in the cells to assess its impact on the differentiation of the cells by immunohistochemical detection of NeuN and GFAP expressions. RESULTS: More than 95% of the embryonic neural stem cells in primary culture were Nestin-positive. The percentages of Brdu-positive cells showed no significant changes after treatment with different concentrations of propofol, whereas the addition of 50 µmol/L propofol resulted in a significant increase of NeuN-positive cell percentage to (23.1∓0.9)% as compared with that of (13.4∓0.8)% in the control group (P<0.05) without affecting the GFAP-positive cells. CONCLUSION: Clinically relevant doses of propofol have no obvious effect on the proliferation of rat neural stem cells cultured in vitro, but can induce their differentiation into neuron-like cells.

Sevoflurane inhibits proliferation, induces apoptosis, and blocks cell cycle progression of lung carcinoma cells.

PURPOSE: Sevoflurane, an inhalational anesthetic, is used extensively during lung cancer surgery. However, the effect of sevoflurane on growth of lung carcinoma cells remains unclear. The purpose of this study is to investigate effects on proliferation, apoptosis, and cell cycling in the A549 human lung adenocarcinoma cell line. METHODS: A549 cells were treated with 1.7%, 3.4%, and 5.1 % sevoflurane for 2, 4, and 6 hours. Cell proliferation was evaluated by the MTT assay and colony formation assay. Apoptosis and cell cycle was analyzed by flow cytometry. Expression of X-linked inhibitor of apoptosis protein (XIAP), survivin, Bcl-2, Bax, caspase-3, cyclin A, cyclin B1, and cdc2 was measured by Western blotting. RESULTS: Significant inhibition of cell proliferation and induction of apoptosis were found in A549 cells after sevoflurane treatment. Simultaneously, expression of XIAP and survivin was supressed, while that of caspase-3 increased significantly, but Bcl-2 and Bax were not altered. Sevoflurane caused cell cycle arrest at the G2/M phase. At the same time, data revealed that cyclin A, cyclin B1, and cdc2 expression was down-regulated after sevoflurane treatment. CONCLUSION: This study demonstrated that sevoflurane inhibited proliferation, and induced apoptosis in human lung adenocarcinoma A549 cells, associated with down-regulated expression of XIAP and suvivin, and activating caspase-3.

[A proteomic study of peripheral blood mononuclear cells in patients undergoing cardiopulmonary bypass].

OBJECTIVE: To explore the effect of cardiopulmonary bypass (CPB) on the profile of protein expression in peripheral blood mononuclear cells (PBMCs). METHODS: Eleven patients undergoing cardiac surgery under cardiopulmonary bypass were enrolled in the study. Peripheral blood samples were collected before CPB (T0), 1 h after CPB (T1) and at the end of operation (T2), and PBMCs were obtained by gradient centrifugation. The profile of protein expression was analyzed using 2-D gel electrophoresis (2-DE) and mass spectrometry. The candidate proteins were further identified by Western blotting. RESULT: Compared to protein profile at T0, 12 protein spots were identified to be up-regulated in PBMCs at T1 (P <0.05), among which S100A9 reached the peak level at T1 and decreased after operation,but not returned to its initial level. CONCLUSION: Results indicate that 12 proteins are likely to be involved in CPB, however, their roles need to be elucidated.

The effects of preloading infusion with hydroxyethyl starch 200/0.5 or 130/0.4 solution on hypercoagulability and excessive platelet activation of patients with colon cancer.

Hypercoagulability and excessive platelet activation account for a significant percentage of mortality and morbidity in cancer patients. In order to test the hypothesis that preloading infusion (PLI) with 6% hydroxyethyl starch 200/0.5 (HES 200), or 6% hydroxyethyl starch 130/0.4 (HES 130) solution can attenuate the hypercoagulable state and inhibit excessive platelet activation of patients with colon cancer, we selected 35 colon cancer patients undergoing laparoscopic-assisted radical colectomy. They were received randomly a test of 15 ml/kg of either HES 200 (n=17), or HES 130 (n=18) over a 30-min period preoperatively. In addition, fifteen healthy volunteers were selected as normal control group. Coagulation function was assessed by thrombelastography (TEG), platelet glycoprotein IIb/IIIa and CD62P was analyzed by flow cytometry before PLI, the end of PLI, 1 h after PLI, and 1 h after the end of surgery. Results demonstrated that hypercoagulable state indicated by TEG and excessive platelet activation was found in patients with colon cancer. We found that preloading infusion with HES 200/0.5 can inhibit platelet activation, and the two solutions, especially HES 200/0.5, compromised TEG parameters that indicated hypercoagulability of patients with colon cancer during perioperative period.

[Narcotrend index monitoring can predict the recovery of consciousness in patients undergoing abdominal surgery].

OBJECTIVE: To investigate the value of Narcotrend (NT) index monitoring versus standard hemodynamic parameters in predicting the recovery of consciousness in patients undergoing abdominal surgery. METHODS: Forty ASA I or II patients undergoing elective abdominal surgery were randomized into two groups to receive sevoflurane-sufentanil anesthesia monitored by NT index or solely by clinical parameters. Anesthesia was induced with the inhalation of 8% sevoflurane and sufentanil target-controlled infusion at 0.2-0.5 ng/ml. The values of NT stage (NTS), NT index (NTI), and hemodynamic parameters (MAP and HR) were recorded during the period of recovery. The prediction probability (Pk) of each parameter was calculated and compared. RESULTS: NTS and NTl were closely correlated to the changes of consciousness during the recovery from general anesthesia. The Pk values of NTS and NTI in predicting eye opening and orientation recovery were 0.95, 0.92, and 0.92, 0.89, respectively, obviously higher than the Pk values of MAP and HR (P<0.05). CONCLUSION: NT monitoring can be used to effectively predict the recovery of consciousness in patients undergoing abdominal surgery and facilitates a significant reduction of the recovery time and sufentanil dosage during a sevoflurane-sufentanil anesthesia.

[Effect of noxious stimulation on regional distribution of propofol in canine spinal cord].

OBJECTIVE: To observe the regional distribution of propofol in canine spinal cord under noxious stimulation. METHODS: Twelve healthy hybrid dogs (12-18 months old, weighing 10-12 kg) were randomly divided into control group (n=6) and stimulation group (n=6). All the dogs were anesthetized with a single bolus dose of propofol (7 mg/kg) in 15 seconds followed by propofol infusion at a constant rate of 70 mg/kg/h via the great saphenous vein of the right posterior limb. In the stimulation group, the tails of the dogs were clamped for 5 min after 45 min of propofol infusion. Blood samples were taken from the internal carotid artery and internal jugular vein at 50 min after propofol infusion to detect plasma propofol concentrations by high-pressure liquid chromatography (HPLC). The dogs were then immediately sacrificed by decapitation and the frontal horn, posterior horn, intermediate zone, frontal funiculus, posterior funiculus and lateral funiculus of the spinal cord were dissected for determination of propol content by HPLC. RESULTS: The plasma concentrations of propofol in the internal carotid artery and internal jugular vein were 5.07-/+0.23 and 5.03-/+0.10 microg/ml in the stimulation group, respectively showing no significant differences from those in the control group (5.09-/+0.03 and 5.08-/+0.03 microg/ml, P>0.05). In the control group, the propofol concentration was 5.09-/+0.08 microg/g in the frontal horm, 5.10-/+0.08 microg/g in the posterior horn, 5.05-/+0.19 microg/g in the intermediate zone, 5.06-/+0.14 microg/g in the frontal funiculus, 5.06-/+0.15 microg/g in the posterior funiculus and 5.06-/+0.41 microg/g in the lateral funiculus, showing no significant differences (P>0.05). The propofol concentrations in the frontal horn (7.65-/+0.47 microg/g) and posterior funiculus (7.06-/+0.82 microg/g) in the stimulation group were significantly higher than those in the other spinal cord tissues (P<0.05) and those in the control group (P<0.05). CONCLUSION: At 50 min after intravenous injection of propofol at a constant rate of 70 mg/kg/h, plasma propofol concentrations in the internal carotid artery and internal jugular vein reaches equilibrium with a balanced distribution in all the spinal cord regions. Propofol concentration can be higher in the frontal horn and posterior funiculus under noxious stimulation.

[Prophylactic effect of acupuncture on nausea and vomiting after laparoscopic operation].

OBJECTIVE: To explore the prophylactic effect of acupuncture Neiguan (PC 6) on nausea and vomiting after laparoscopic operation. METHODS: One hundred patients with laparoscopic gastrointestinal operation were randomly divided into an acupuncture group and a control group, 50 patients in each group. The operation was carried out with the combined infusion and inhalation anesthesia. The patients in the acupuncture group were being punctured at bilateral Neiguan (PC 6) before anesthesia and during the operation. The needles were extracted after operation, and the acupoints were covered with opaque tape. In contrast, the patients in the control group only accepted tape covering without acupuncture. After operation, all patients were given the self-controlled intravenous analgesia, and followed up at 6 h, 12 h, 24 h, 48 h for recording the incidence rate of the nausea, retching and vomiting, then scoring with VAS. RESULTS: At 6 h, 12 h, 24 h, 48 h after operation, in the acupuncture group, the incidence rates of the nausea were 12.0%, 6.0%, 6.0% and 2.0%, and the incidence rates of the retching were 0, 0, 2.0% and 2.0%, respectively; in the control group, the incidence rates of the nausea were 28.0%, 20.0%, 12.0% and 2.0%, and the incidence rates of the retching were 2.0%, 6.0%, 2.0% and 0, respectively. At 6 h, 12 h after operation, the incidence rates of the nausea and retching in the acupuncture group were lower than those of the control group (P < 0.05, P < 0.001). The vomiting was not happened in both groups. There was no difference between the two groups according to the scoring with VAS. CONCLUSION: Acupuncturing at Neiguan (PC 6) can reduce the incidence rates of the patients' nausea and retching after laparoscopic operation, especially in 24 h.