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.

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.

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.

[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.

[Reproduction of a murine model of hyperthermic treatment].

OBJECTIVE: To find out the most suitable conditions for a whole body hyperthermia (WBH) model and the influence of these conditions on the blood brain barrier (BBB) disruption and brain edema in rats. METHODS: Forty male Sprague-Dawley (SD) rats were randomly assigned to four groups (n=10 in each group): control group, group A, group B and group C. After anesthesia with pentobarbital, rats were subjected to femoral artery and vein cannulation. Rats of control group were housed at a controlled room temperature (25-26 degrees C) for 4 hours. Rats of group A, group B and group C were exposed to WBH in a biological oxygen supply heated container (relative humidity 65%, wind velocity 25 cm/s) maintained at 34, 36 and 38 degrees C for 3 hours, respectively. Then the rats were removed from the heated container and their body temperature was cooled down for 1 hour. During heating, rectal temperature, heart rate (HR), mean arterial pressure (MAP), pH, partial pressure of oxygen in artery (PaO(2)), partial pressure of carbon dioxide in artery (PaCO(2)), the dosage of anesthetic, and the mortality rate in each group were recorded. Evans blue (EB) was administered into the femoral vein and allowed to circulate for 5 minutes. At the end of the experiment, the animals were perfused with 0.9% saline and heparin through the heart, and the brain was harvested for the examination of BBB permeability, water content and morphological alterations in brain tissues and neurons. RESULTS: The total dosage of pentobarbital was not significantly different among all groups. After WBH for 3 hours, the average rectal temperature was higher than rats without WBH, and the mortality rate was 0, 10%, 10% and 40% in groups control, A, B, C, respectively. HR of groups A, B and C were significantly higher than those of control group; MAP, pH of group A, B and C were significantly lower than those of control group (all P<0.05). Compared to that of control group, water content of the brain and permeability of EB in groups A, B and C were significantly increased (P<0.05 or P<0.01), but there was no marked difference on PaO(2), PaCO(2) and haematocrit (HCT) among groups A, B and C. Morphological investigation showed that there were different degrees of structural changes in brain tissue in groups A, B and C under light microscopy. Under transmission election microscopy, the structure of nerve cells and BBB in group B and group C showed moderate to profound alterations, but there were no changes in group A. CONCLUSION: Rats housed in a biological oxygen supply heat container with the temperature maintained at 36 degrees C for 3 hours could establish an ideal WBH model with notable BBB breakdown, moderate brain edema, and histological changes in brain.

Impact of invasive fungal infection on outcomes of severe sepsis: a multicenter matched cohort study in critically ill surgical patients.

INTRODUCTION: Fungal infection is increasingly common in critical illness with severe sepsis, but the influence of invasive fungal infection (IFI) on severe sepsis is not well understood. The aim of this study was to investigate the impact that IFI has on the outcomes of critically ill surgical patients with severe sepsis in China by means of matched cohort analysis; we also evaluated the epidemiologic characteristics of IFI in this population. METHODS: Records for all admissions to 10 university hospital surgical intensive care units (ICUs) from December 2004 to November 2005 were reviewed. Patients who met criteria for severe sepsis were included. IFI was identified using established criteria based on microbiologic or histological evidence. A matched cohort study was conducted to analyze the relationship between IFI and outcomes of severe sepsis. RESULTS: A total of 318 patients with severe sepsis were enrolled during the study period, of whom 90 (28.3%) were identified as having IFI. A total of 100 strains of fungi (58% Candida albicans) were isolated from these patients. Independent risk factors for IFI in patients with severe sepsis included mechanical ventilation (>3 days), Acute Physiology and Chronic Health Evaluation score, coexisting infection with both gram-positive and gram-negative bacteria, and urethral catheterization (>3 days). Compared with the control cohort, IFI was associated with increased hospital mortality (P < 0.001), high hospital costs (P = 0.038), and prolonged stay in the ICU (P < 0.001) and hospital (P = 0.020). CONCLUSION: IFI is frequent in patients with severe sepsis in surgical ICUs and is associated with excess risk for hospital mortality, longer ICU and hospital stays, and greater consumption of medical resources.

[Effects of hydroxyethyl-starch on hemorheology in patients with chronic liver disease].

OBJECTIVE: To investigate the effects of hemodilution with hydroxyethyl-starch (HES) on hemorheology in patients with chronic liver diseases in vitro. METHODS: Twenty-one healthy volunteers were selected as the control group and 21 patients with chronic liver disease as the study group. Both of the two groups were divided into HSE (n=11) and Ringer's solution (n=10) groups. Venous blood of 12 ml were collected from each subject and aliquoted into 4 samples, one of the 4 samples served as control (sample 1), and the other 3 (samples 2, 3, 4 respectively) were diluted with 6%; HES or Ringer's solution to cause the hematocrit (Hct) decrease to 30%;, 25%; or 20%;. The rheological parameters including Hct, blood viscosity, plasma viscosity, index of red blood cell aggregation (ARBC) and index of red blood cell rigidity (RRBC) were examined. RESULTS: The Hct of the study group was significantly lower than that of the control group (P<0.05), but plasma viscosity and ARBC were significantly higher. After being diluted by HES, the blood viscosity and ARBC decreased significantly in the study group (P<0.05), and were not significantly different from those of the control group (P>0.05) when Hct=25%; and 20%;. The RRBC of the study group was increased, but the increment was significantly higher than that of control group (P>0.05) only when Hct=20%;. CONCLUSION: The ARBC of patients with chronic liver diseases was significantly higher. Hemodilution with 6%; HES could significantly reduce the blood viscosity and ARBC.

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.

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.

[Inhibiting effect of intrathecal fentanyl on intraoperative vomiting during cesarean delivery under epidural anesthesia].

OBJECTIVE: To observe the inhibiting effect of intrathecal (IT) fentanyl on nausea and vomiting during cesarean delivery under epidural anesthesia. METHODS: Thirty healthy parturients (ASA grade I to II) were randomly assigned in equal numbers into control and fentanyl groups (n=15 each, patients in the latter group treated with IT fentanyl at the dose of 20 microgram/3ml). The incidence of nausea and vomiting during the elective cesarean delivery under epidural anesthesia between the 2 groups were compared and the neonates' Apgar scores assessed after the delivery. RESULTS: Intraoperative nausea and vomiting/retching were reduced in the IT fentanyl group as compared with the control group (6.7 % vs 33.3 % and 0 vs 26.7 %, P>0.05 and P<0.05 respectively). The neonates' Apgar scores were not significantly different between the 2 groups (P>0.05). CONCLUSION: IT fentanyl can decrease intraoperative vomiting during cesarean delivery performed under epidural anesthesia.

[Effects of fentanyl on EC50 of ropivacaine for postoperative epidural analgesia after gynecological surgery].

OBJECTIVE: To determine the effect of fentanyl on 50% effective concentration (EC50) of ropivacaine for postoperative epidural analgesia following gynecological surgery. METHODS: Sixty-five patients (ASA class I to II) scheduled for elective gynecological surgery were randomly divided into two groups to receive 20 ml ropivacaine (group R, n=33) or ropivacaine combined fentanyl (group RF, n=32) for postoperative epidural analgesia. The concentration of ropivacaine was adjusted according to double-blinded up-down sequential allocation. The efficacy was assessed using visual analog scores (VAS) and EC50 calculated using method of Dixon. RESULTS: The EC50 of ropivacaine was 0.098% in group R and 0.069% in group RF, showing significant difference (P<0.01). CONCLUSION: EC50 of ropivacaine for postoperative epidural analgesia determined by up-down sequential allocation is 0.098%, which can be decreased by the use of fentanyl.

[Effects of dexamethasone on epidural morphine-related nausea and vomiting].

OBJECTIVE: To observe the effect of intravenous dexamethasone injections in preventing nausea and vomiting resulted from epidural morphine for post-operation pain relief. METHODS: Eighty-four adult patients (ASA class I to II ) requiring epidural anesthesia for low abdominal surgical procedures were randomly divided into 2 groups, of which Group 1 (n=42) received intravenous dexamethasone injections at 10 mg and Group 2 (n=42) intravenous injection of 2 ml normal saline before administration of 2 mg epidural morphine for post-operation pain relief. The incidence of nausea and vomiting were recorded within 24 h after surgery. RESULTS: The incidence of nausea and vomiting were 12% and 7% in Group 1, while 31% and 21% in Group 2 respectively, showing significant difference between the 2 groups (P<0.05). The total incidence of nausea and vomiting were also significantly different (19% vs 52%, P<0.01). CONCLUSION: Intravenous dexamethasone injections at 10 mg can significantly decrease the incidence of epidural morphine-related nausea and vomiting.

[Determination of EC50 of ropivacaine and bupivacaine for postoperative epidural analgesia by up-down sequential allocation].

OBJECTIVE: To determine the median effective concentration (EC50) of ropivacaine and bupivacaine for postoperative epidural analgesia, and compare the efficacy of the 2 analgesics. METHODS: Sixty-five patients (ASA I to II) scheduled for elective gynaecological surgeries were randomly assigned into ropivacaine and bupivacaine groups to receive postoperative epidural analgesia with the indicated analgesics (20 ml). The concentration was determined by the response of a previous patient to a higher or lower concentration using double-blinded, up-down sequential allocation. The analgesic efficacy was assessed with 100 mm visual analog pain scores (VAS), and effectiveness was defined as having a VAS

Experimental study of in vitro buprenorphine hydrochloride transdermal permeation through hairless mouse skin.

OBJECTIVE: To investigate the in vitro transdermal permeation of buprenorphine hydrochloride gel through hairless mouse skin and the effect of permeation enhancers on the permeability of this transdermal drug delivery system. METHODS: Skin samples 1.0 cm in diameter were obtained from hairless mice for subsequent in vitro tests of the permeability of the drug. In permeation enhancer-free group, the permeability of buprenorphine hydrochloride at the concentrations of 0.5%, 1.0% and 2.0% was tested. The permeation enhancer group (all application containing 1% buprenorphine hydrochloride) was further divided into oleic group (including 3 subgroups with 2%, 4%, and 6% oleic), azone group (subdivided into 3 groups with 1%, 2%, and 4% azone) and mixed group (with 4% oleic plus 4% azone). The permeation parameters, namely steady state flux (Js) and Js enhancement ratio were evaluated. RESULTS: Js in permeation enhancer-free groups were 0.69+/-0.11, 0.90+/-0.14 and 1.18+/-0.10 microgram/cm2.h respectively, which differed only insignificantly (P>0.05). The mixed group showed the maximum permeation, with Js and ER of 13.22+/-1.27 microgram/cm2.h and 14.6 respectively. CONCLUSION: Permeation enhancers significantly increase Js of buprenorphine hydrochloride gel and renders its release kinetics approaching zero-order.

Effect of patient-controlled epidural analgesia for pain relief after thymectomy in patients with myasthenia gravis.

OBJECTIVE: To evaluate the effect of patient-controlled epidural analgesia (PCEA) with ropivacaine or bupivacaine in relieving pain after thymectomy in patients with myasthenia gravis. METHODS: Twenty adult ASA I-II patients with myasthenia gravis were randomized to receive either 0.125% ropivacaine (Group R, n=10) or 0.125% bupivacaine (Group B, n=10) with a PCEA device after transsternal thymectomy. PCEA (continuous infusion at 1 ml/h, bolus dose of 4 ml and lockout time of 30 min) was implemented via an epidural catheter inserted in the T3-4 intervertebral space. The vital signs and visual analogue scale (VAS), together with cumulative consumption (CC) of ropivacaine or bupivacaine were recorded within 48 h postoperatively. RESULTS: The vital signs, including systolic and diastolic blood pressure, heart rate, SpO2, pH and PaCO2, did not show any significant differences between the 2 groups. The CC of the local anesthetic was significantly higher in group R than that in group B at 24 and 48 h postoperatively, but VAS were not significantly different between the 2 groups which was less than 4 in both groups. CONCLUSIONS: PCEA with low concentration of ropivacaine or bupivacaine may provide effective and safe analgesia after transsternal thymectomy.

[Effects of intraperitoneal CO2 insufflation on hemodynamics and oxygen consumption during intravenous propofol anesthesia combined with epidural block].

OBJECTIVE: To investigate the effects of intraperitoneal CO2 insufflation on the hemodynamics, oxygen consumption (VO2) and carbon dioxide production (VCO2) during intravenous anesthesia with propofol in combination with epidural block. METHODS: Intratracheal intubation was performed after rapid induction of anesthesia and mechanical ventilation was given. Maintenance of anesthesia was achieved using continuous intravenous propofol infusion (2 mg/kg/h) ?N2O inhalation and intermittent epidural administration. Indices of hemodynamics and respiratory function were collected 5 min before induction, 1 min before CO2 insufflation, and 5, 10, 20, 30, 40, 50, 60 min after the start of insufflation and 5 min after the termination of insufflation. RESULTS: The mean arterial pressure (MAP), heart rate (HR), end-tidal PCO2 (P(ET)CO2), VO2 and VCO2 1 min before insufflation were markedly reduced(P<0.01), compared with those recorded before induction. MAP and HR did not undergo any conspicuous changes during CO2 insufflation and 5 min after insufflation termination. Compared with that 1 min before insufflation, PETCO2 was significantly increased 20 min after the start of insufflation (P<0.01), and subsequently carried on the increase though of a lesser scale. VO2 and VCO2 gradually rose after the start of insufflation, and VO2 presented a significantly elevation (P<0.01) 10 min after the insufflation while VCO2 did not show this marked increase(P<0.05) till 20 min after the insufflation in comparison with the levels before insufflation. Subsequently, VO2 continued to rise and VCO2 also retained the increase but of smaller magnitude. CONCLUSION: Intravenous propofol anesthesia combined with epidural block assisted by well-managed excessive ventilation before insufflation can alleviate the adverse effects of CO2 insufflation on respiratory and circulatory systems.

[Brain uptake of propofol during target-controlled infusion when effect compartment concentration is targeted].

OBJECTIVE: To study the correlation between the effect compartment concentration (ECC) and the brain uptake of propofol during sedation by target-controlled infusion (TCI). METHOD: Twelve ASA physical status I to II patients with neither cardiac nor intracranial diseases were scheduled for elective abdominal operation. Computer-assisted target-controlled infusion of propofol was performed for general anesthesia in all patients with the target ECC set at 4.0 microgram/ml. The plasma propofol concentrations were measured simultaneously from the radial artery and the jugular bulb at different time points by high performance liquid chromatography (HPLC), and the area under time-concentration curve (AUC(a-jv)) was calculated. RESULT: Before reaching the target propofol concentration of 4.0 microgram/ml (4.7+/-0.16 min), EEC was positively correlated with AUC(a-jv) (r(ECC-AUC)=0.977, P<0.001), but neither the arterial (Ca) nor jugular bulb propofol concentrations (Cjbv) showed such relation to AUC(a-jv) (r(Ca-AUC)= 0.054, P=0.92; r(Cjbv-AUC)=0.335, P=0.516). When ECC was controlled at 4.00 microgram/ml by TCI, Ca was comparable with Cjbv (P=0.512). Positive correlation was noted between AUCa-jv and ECC (r(ECC-AUC)=0.942, P<0.005) after the termination of infusion till the consciousness recovery of the patients, and Ca and Cjbv showed similar correlation with AUC(a-jv) (r(Ca-AUC)=0.986, P<0.001; r(Cjbv-AUC)=0.974, P<0.001). CONCLUSION: During TCI of propofol with ECC as the target concentration, ECC is significantly correlated with AUC(a-jv) to reflect the dynamic changes in cerebral propofol uptake.

[Management of hyperkalemia-induced cardiac arrest in anhepatic stage of orthotopic liver transplantation without venovenous bypass: report of 3 cases].

The causes of high serum potassium-induced cardiac arrest in anhepatic stage of orthotopic liver transplantation were analyzed in 3 cases without venovenous bypass, and the effectiveness of insulin was evaluated in correcting hyperkalemia during the anhepatic stage. To improve the survival rate of patients with such cardiac arrest, early cardiopulmonary resuscitation and timely defibrillation should be performed.

[Respiratory distress syndrome induced by immersion in seawater: a study of canine models].

OBJECTIVE: To study the mechanism of respiratory distress syndrome (RDS) induced by immersion in seawater to provide experimental evidence for its treatment. METHODS: Twelve normal hybrid dogs were randomly assigned into control group (n=4) and SDS model group (n=8). The changes in blood dynamics, blood gas analysis and histological changes in the lung tissues were compared between the 2 groups. The concentration of lactic dehydrogenase (LDH-L) and alkaline phosphatase (ALP) in the bronchoalveolar fluid and blood of the dogs in the model group were tested. RESULTS: The blood dynamics, blood gas analysis and histology of the dogs in the model group were significantly different from those in the control group, and LDH-L and ALP levels increased significantly in the bronchoalveolar fluid of the model group. CONCLUSION: Seawater aspiration into the lungs may lead to RDS, and the canine models used in this study may help explore the mechanism and management of RDS induced by immersion in seawater.

Effects of patient-controlled upper and lower epidural analgesias on postoperative respiratory and circulatory function.

OBJECTIVE: To compare the effects of patient-controlled high thoracic epidural analgesia (PCHEA) and low thoracic epidural analgesia (PCLEA) on respiratory and circulatory functions after operation. METHODS: Thirty-six patients were divided into 2 groups with 18 in each, and one group (Group H) received PCHEA during thoracic operations and the other (Group L) received PCLEA during abdominal operations. Postoperative patient-controlled analgesia (PCA) was performed in all the patients with 0.125% bupivacaine and 0.01% morphine delivered through the same epidural space for PCHEA or PCLEA. RESULTS: Postoperative analgesia did not produce significant differences in the respiration rate (Rr), tidal volume (Vt), vital capacity (VC) and oxygen saturation (SpO2) between the groups, but in both groups, Vt and VC were significantly improved compared with those before starting patient-controlled epidural analgesia (PECA) (P<0.01). In group H, its effects on systolic and diastolic blood pressure and heart rate were more obvious than in group L (P<0.05), and both groups showed these improvements after PCA started(P<0.01). CONCLUSION: PCHEA shows more marked effects on the respiratory and circulatory functions of the patients, which may mainly result from its blocking the cardiac sympathetic nerves. PCEA is able to improve postoperative respiratory function but both PCHEA and PCLEA necessitate individual-based adjustment of the PCA pump for the safety of the patient.