Objective To investigate the correlation between arterial carbon dioxide partial pressure (PaCO2 )and end-tidal carbon dioxide partial pressure (PET CO2 )in prone position operation and calculate the value of PaCO2 according to the PET CO2 .Methods Forty patients with ASA Ⅰ orⅡ undergoing spinal surgery were selected,and the values of PaCO2 and PET CO2 as basic value (T0 ) after induction of general anesthesia in supine position monitor and record the value of PET CO2 and PaCO2 in prone position after 30 min (T1 ),60 min (T2 )and 90 min (T3 ).The correlation between PaCO2 and PET CO2 in each time point were analyzed,and the equation of PaCO2 (y)and PET CO2 (x) with curve fitting and difference of PaCO2 and PET CO2 were calculated.Results There was significant correlation between PaCO2 and PET CO2 in the supine and prone position,their correlation coefficients were r 0 =0.84,r 1 =0.88,r 2 =0.84,r 3 =0.82 (P <0.01).The Pa-ET CO2 was (5.3±2.1)(T0 )in supine position and (6.6± 2.1 )mm Hg (T1 ),(5.8 ± 2.2 )mm Hg (T2 ),(5.9 ± 2.1 )mm Hg (T3 )in prone position.The equation in each time point PaCO2 (y)and PET CO2 (x)were y0 =1.1 x0 +2.5,y1 =1.1 x1 +2.3,y2 =1.1 x2 +2.4,y3 =1.1 x3 +4.6,and the Pa-ET CO2 was 3.7-8.7 mm Hg. There was no significant difference between PaCO2 and PET CO2 at T1-T3 .Conclusion Whenever in prone position or supine position,PET CO2 and PaCO2 have significant correlation in prone position and supine position.The overall range of Pa-ET CO2 is 3.7-8.7 mm Hg,and the PET CO2 can be as indica-tor to estimate PaCO2 in prone position.

Objective To investigate the effects of remifentanil on lipid peroxidation druing hemorrhagic shock-induced acute lung injury (ALI) in rabbits. Methods Thirty-two healthy adult rabbits weighing 2.0-2.5 kg were randomly divided into 4 groups (n = 8 each): sham operation group (group S); ALI group; low-dose remifentanil group (group LR); high-dose remifentanil group (group HR). The left femoral artery was cannulated for blood-letting and blood sampling. The right femoral artery was cannulated for remifentanil administration. The model of hemorrhagic shock was established by modified Wigger' s methods. In group S, only cannulation was performed. In group LR and HR, remifentanil was infused intraperitoneally at 0.66 and 1.32 μg·kg-1 ·min-1 15 min before blood-letting respectively, while group ALI received equal volume of normal saline instead. Arterial blood samples were taken at 0, 20,70 and 100 min after blood-letting (T1-4) for blood gas analysis. The animals were then sacrificed and the lungs were immediately removed for histological examination with light microscope and determination of W/D lung weight ratio, MDA content and SOD activity. Results W/D ratio and MDA content were significantly increased, while SOD activity was significantly decreased in group ALI compared with group S (P ＜0.05). The pH value at T2 and PaO2 at T2-4 in group LR and the pH value and PaCO2 at T2-4 in group HR were significantly higher than those in group ALI (P ＜ 0.05). W/D ratio and MDA content were significantly lower,while SOD activity was significantly higher in group LR and HR than in group ALI, and in group HR than in group LR (P ＜ 0.05). Remifentanil infusion significantly attenuated the pathologic changes in a dose-dependent manner. Conclusion Remifentanil pretreatment can attenuate hemorrhagic shock-induced ALI through inhibiting lipid peroxidation in rabbits.

Objective To investigate the effects of intrathecal (IT) lidocaine on propofol-induced sedation and content of lidocaine in brain tissues in rats.Methods Twenty male Sprague-Dawley rats,aged 2-3 months,weighing 250-350 g,were equally and randomly assigned to one of four groups:control group (group C),iv lidocaine group (group IV-L),IT normal saline group (group IT-NS) and IT lidocaine group (group IT-L).Groups IT-NS and IT-L received IT normal saline 15μl and 2％ lidocaine 15 μl,respectively.Group IV-L received iv 2％ lidocaine 15 μl.Propofol was infused starting from 10 min after IT or iv administration.When the eyelash reflex disappeared,the infusion of propofol was stopped and the dose of propofol consumed was recorded.The rats were sacrificed in IT-L and IV-L groups and brains were removed for determination of lidocaine level in brain tissues (by RP-HPLC).Results Compared with groups C,IV-L and IT-NS,the dose of propofol consumed when the eyelash reflex disappeared was significantly decreased in group IT-L (P ＜ 0.05).No significant difference was found in the propofol requirement when the eyelash reflex disappeared between groups C,IV-L and IT-NS and in the content of lidocaine in brain tissues between groups IV-L and IT-L (P ＞ 0.05).Conclusion Sedation induced by lidocaine administered intrathecally is not due to a direct action of lidocaine on the brain in rats.

Objective To investigate the effect of liver cirrhosis on the potency of propofol for sedation in rats. Methods Fifty-eight male SD rats, aged 10-12 weeks, weighing 180-220 g, were randomly divided into 3 groups: control group (group C, n = 18), mild liver cirrhosis group (group M1, n =20) and severe liver cirrhosis group (group M2, n = 20). The model of liver cirrhosis was established using four factors described by Chen et al. After successful establishment of the model, propofol was injected intravenously. The dose of propofol was determined by up-and-down sequential method for loss of righting reflex. The dose of propofol was 5.912 mg/kg in the first rat and the ratio of the doses between the two consecutive rats was 0.85. ED50 of propofol was calculated using up-and-down sequential method. Results ED50 of propofol was significantly lower in group M1 and M2 than in group C and in group M2 than in group M1 ( P ＜ 0.05 or 0.01 ). Conclusion The liver cirrhosis can enhance the potency of propofol for sedation in rats.

Objective To investigate the acute toxicity of intravenous isoflurane in Beagles.Methods Six healthy adult Beagles of both sexes aged 6-8 months weighing 6-8 kg were used in this study.Isoflurane injectio (120 mg/ml) in 30% hpid emulsion was injected intravenously. Femoral artery was cannulated for direct BP monitoring.ECG was continuously monitored.The maximal tolerance dose (MTD) and approximate lethal dose (ALD) were determined by up-and-down technique. The initial dose was 3.0 ml/kg. The dose was decreased/increased by 0.3 ml/kg if the previous animal died/survived.The survived dogs were observed for 2 weeks.Autopsy and histopathological examination were performed on all dead Beagles.Results The ALD and MTD of intravenous isoflurane were 252 and 216 mg/kg. Autopsy and histopathological examination did not show any abnormality.Conclusion Cardiopulmonary depression is the main manifestation of the acute toxicity of intravenous isoflurane in Beagles.