Effect of Gingkgo biloba leaf extract induced delayed preconditioning on cytochrome c oxidase expression during myocardial ischemia-reperfusion in rats / 中南大学学报(医学版)

OBJECTIVE@#To determine the effect of Gingkgo biloba leaf extract (EGb761) induced delayed preconditioning on cytochrome c oxidase (CcO) expression during myocardial ischemia-reperfusion in rats.@*METHODS@#Four groups (10 in each) of Sprague-Dawley male rats were studied. In the sham group, the rats received no treatment. Rats in the ischemia-reperfusion (IR) group were treated with NS (1.0 mL/kg intravenously) 24 h before ischemia. Rats in the M group were treated with EGb761 (100 mg/kg intravenously) 24 h before the ischemia. In the D group , EGb761-treated rats that received the 5-hydroxydecanoate (5-HD), an inhibitor of mitochondrial KATP channels 15 min before the ischemia. The IR, M, and D groups were subjected to ischemia by 30 min of coronary artery occlusion before 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size was measured. CcO was measured by Western blot. The myocardial ultrastructure was observed under the electron microscope.@*RESULTS@#The infarct size was significantly smaller in the M group [(23.78 ± 4.82)%] than in the I/R group [(37.87 ± 5.92)%] (P0.05).@*CONCLUSION@#EGb761 induced delayed preconditioning attenuates myocardial ischemia-reperfusion injury possibly through up-regulating CcO expression in rats.

Limb ischemic preconditioning reduces rabbit hepatic ischemia-reperfusion injury through inhibition the phosphorylation of proteins in the MAPK signal pathway in the late phase / 中南大学学报(医学版)

OBJECTIVE@#To investigate the liver protection mechanisms of MAPK signaling pathway of limb ischemia preconditioning in the late phase.@*METHODS@#Thirty-six adult male New Zealand white rabbits, weighing 1.8-2.0 kg, were randomly divided equally into 3 groups: group C (sham operation), group L (liver ischemia-reperfusion 24 h after limb ischemia preconditioning), group IR (liver ischemia-reperfusion without limb ischemia preconditioning). Serum alanine transaminase (ALT) was measured during ischemia reperfusion. The tissue and cell injury of liver were examined by optical and electron microscopy. Activation of P38MAPK, P44/P42MAPK, and JNK in hepatic tissue was assessed by western blot after 30 min of reperfusion.@*RESULTS@#Serum ALT and cell injury in the liver as examined by optical and electron microscopy was decreased in group L as compared with the group IR. Phosphorylation of P38MAPK, P44/ P42MAPK, and JNK were all increased significantly after 30 min of reperfusion. Phosphorylation of P38MAPK and JNK was reduced by limb ischemia pre-treatment.@*CONCLUSION@#Limb ischemia pre-treatment can induce the late phase of preconditioning in rabbit liver through the inhibition of the phosphorylation of P38MAPK and JNK.

Retrograde changes in the dorsal motor nuclei of rat vagus nerve after vagotomy / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the retrograde changes in the dorsal motor nuclei (DMV) of the vagus nerve after vagotomy in rats.</p><p><b>METHODS</b>Nissl staining and immunohistochemistry were used to observe the morphological and quantitative changes of the DMV and alterations of the expression of iNOS and NADPH after severing of the vagus nerve in adult male Wistar rats.</p><p><b>RESULTS</b>Compared with the control group, the rats with right vagotomy showed obvious morphological changes and a significantly decreased number of neurons in the right DMV (P<0.05). Numerous iNOS- and NADPH-immunopositive cells were detected in the right DMV 5 and 10 days after right vagotomy.</p><p><b>CONCLUSION</b>Vagotomy causes obvious retrograde changes in rat DMV shown by a significantly decreased number and obvious morphological changes of the neurons in the DMV.</p>

Effect of high concentration carbon dioxide preconditioning on lipid peroxidation daring myocardial ischemia-reperfusion in rabbits / 中华麻醉学杂志

Objective To investigate the effect of high concentration carbon dioxide preconditioning on lipid peroxidation during myocardial ischemia-reperfusion (I/R) in rabbits. Methods Twenty-four New Zealand white rabbits weighing 2.0-3.9 kg were randomly divided into 3 groups ( n = 8 each): sham operation group (group S) , I/R group, high concentration carbon dioxide preconditioning group (group H) . The amimals were tracheal intubated and mechanically ventilated. In groups S and I/R, fresh gas flow was set at 0.3 L/min (100% O2 ), respiratory rate 30-40 bpm and tidal volume IS ml/kg, and PETCO2 was maintained at 40-50 mm Hg for 30 min. In group H, fresh gas flow was set at 0.3 L/min (100% O2), respiratory rate 20-30 bpm and tidal volume 10 ml/kg, PETO2 was maintained at 75-85 mm Hg for 5 min, and then all the ventilatory parameters were adjusted to the same as those in groups S and I/R. Myocardial I/R was produced by occlusion of left anterior descending branch of coronary artery for 30 min followed by 3 h reperfusion after preconditioning in groups I/R and H. The animals were sacrificed at the end of reperfusion and myocardial tissues obtained for determination of the superoxide dismutase (SOD) activity and malondialdehyde (MDA) content and examination of the ultrastnicture of myocardium with the transmission electron microscope. Results The SOD activity was significantly lower, while MDA content higher in group I/R than in group S ( P ＜ 0.01) . The SOD activity was significantly higher, while MDA content lower in group H than in group I/R ( P ＜ 0.01) . The myocardial injury was attenuated in group H compared with group I/R. ConclusionHigh concentration carbon dioxide preconditioning can reduce myocardial I/R injury in rabbits through inhibiting lipid peroxidation.

Proteomics analysis of adenosine A1 receptor agonist-induced delayed myocardial protection in rabbits / 中南大学学报(医学版)

OBJECTIVE@#To investigate the changes of myocardial protein expression profiles in 2-chloro-N6-cyclopentyladenosine (CCPA), an adenosine A1 receptor agonist-induced delayed myocardial protection in New Zealand rabbits .@*METHODS@#A total of 8 rabbits were randomly divided into a CCPA group (CCPA group) and a normal saline group (NS group). CCPA and NS were infused into rabbits in the CCPA group and the NS group respectively. Twenty-four hours later, the rabbits were subjected to 30 min left anterior descending coronary artery occlusion and were reperfused for 2 hours, then the ischemic zone tissues of left ventricle were sampled for proteomic analysis.A total of 12 other New Zeland rabbits were divided into a sham group (Sham group), a normal saline group (NS group) and a CCPA group (CCPA group). The expression of αB-crystalline, one of the differential proteins, was confirmed by Western blot.@*RESULTS@#Analysis of two dimensional gel electrophoresis showed that the expression of 55 protein spots were different between the two groups, 17 protein spots were preliminarily identified with the matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS) and Mascot and Expasy bioinformatics software. These proteins included stress proteins, metabolism-associated proteins, signal transduction pathway-related proteins, ionophorous proteins, immunity-associated proteins, and so on. Western blot showed that the expression of αB-crystalline was significantly up-regulated in the CCPA group.@*CONCLUSION@#The myocardial protein expression profiles are changed markedly in the preconditioning late phase of CCPA .The differential proteins might be involved in the delayed cardioprotection induced by CCPA.

KATP Channel Mediate the Protective Effect of Hypercarbonic Preconditioning on Myocardial Cells / 天津医药

Objective: To investigate the function of the ATP-sensitive K+(KATP) channel activation on the protective effect of hypercarbonic acidosis preconditioning on rabbit myocardial cells. Methods: Thirty-two rabbits were randomly divided into 4 groups (n = 8 for each group): pseudo-operation group (group P), ischemia and reperfusion group(group IR), hypercarbonic acidosis group(group H) and hypercarbonic acidosis+ glybenzcyclamide group (group H+G). Animals were ventilated normally in group IR and group P, tidal volume 15 mL/kg, breathing rate 35 bpm .The PETCO_2 was maintained at the level of 40-50 mm Hg for 30 minutes. Animals received low-frequency, low volume ventilation in group H group H+G, tidal volume 10 ml/kg, breathing rate 25 bpm to achieve hypercarbonic acidosis. The target value of PETCO_2 was 75-85 mm Hg. This value was maintained for 5 minutes. The animals then were ventilated normally to make the PETCO_2 return to 40-50 mm Hg. Animals were injected with 0.3 mg/kg glybenzcyclamide 10min before achieving hypercarbonic acidosis with hypoventilation in group H+G. Animals received ligation of left anterior branch artery for 30 minutes and reperfusion for 180 minutes in each group except P group. The myocardial ischemia area, the myocardial infarction area and their ratios were calculated by the ismaeil methods. Results: The ratio of the myocardial infarction area to the myocardial ischemia was significantly less in group H than those of group IR and group H+G (P 0.05). Conclusion: Hypercarbonic acidosis preconditioning can protect the cardiomyocytes by activating the KATP channel.

Effect of esmolol on bispectral index in patients undergoing orotracheal intubation during induction of anesthesia / 中华麻醉学杂志

Objective To evaluate the effect of esmolol on bispectral index (BIS) in patients undergoing orotracheal intubation during induction of anesthesia and to investigate the mechanism of inhibiting the cardiovascular responses to tracheal intubation.Methode Forty patients in physical status of ASA Ⅰ or Ⅱ and aged 20-60 years were randomly divided into 2 groups ( n = 20 each): esmolol group (group E) and control group (group C). Anesthesia was induced with midazolam 0.1 mg/kg, fentanyl 5 μg/kg and vecuronium 0.1 mg/kg. In group E, esmolol 1 mg/kg was given intravenously before anesthesia induction and followed by an infusion of esmolol 250 μg· kg- 1·min-1, while a comparable volume of saline was given for group C. Mean arterial pressure (MAP), heart rate (HR) and BIS were recorded before esmolol administration, before induction of anesthesia, before orotracheal intubation, and at 1, 2 and 5 min after intubation, respectively.Results There were no significant differences in HR, MAP and BIS between the two groups before tracheal intubation. HR and MAP significantly increased after tracheal intubation in both groups, but BIS only in group C significantly increased after intubation.HR, MAP and BIS were significantly lower after intubation in group E than in group C ( P＜ 0.05).Conclusion Esmolol can decrease BIS during tracheal intubation and its antinociceptive property is related to the mechanism of inhibiting cardiovascular responses to tracheal intubation.

Role of mitochondrial permeability transition pore in attenuation of myocardial ischemia-reperfusion injury by delayed preconditioning with sevoflurane in rats / 中华麻醉学杂志

Objective To investigate the role of mitochondrial permeability transition pore (mPTP) in attenuation of myocardial ischemia-reperfusion (I/R) injury by delayed preconditioning with sevoflurane in rats.Methods Eighty male SD rats, weighing 250-300 g, were randomly assigned into 5 groups ( n = 16 each): Ⅰsham operation group (group S), Ⅱ group I/R, Ⅲ sevoflurane delayed preconditioning group (group SP), Ⅳ the mPTP opener atractyloside + sevoflurane delayed preconditioning group (group A + SP), and Ⅴ atractyloside group (group A). Myocardial I/R was induced by ligation of anterior descending branch of left coronary artery for 30 min followed by 120 min of reperfusion in group I/R, SP, A + SP and A. In group SP and A + SP, 2.5%sevoflurane was inhaled for 1 h, while pure oxygen was inhaled for 1 h in the other groups, and then myocardial ischemia was performed 24 h later. In group A + SP and A, atractyloside 5 mg/kg was injected intravenously via caudal vein 15 min before ischemia. Blood samples were taken from carotid arteries for detection of serum cardiac troponin-Ⅰ (cTnI) concentrations at the end of reperfusion. Then the rats were sacrificed and hearts removed. The myocardial infarct size (IS) and expression of Bcl-2 and Bax in the myocardium were determined. Myocardial ultrastructure was examined with the electron microscope. Results Serum cTnI concentrations and Bax expression were significantly higher, the myocardial IS was significantly larger and Bcl-2 expression was significantly lower in the other groups than in group S ( P ＜ 0.05). Serum cTnI concentrations and Bax expression were significantly lower, the myocardial IS was significantly smaller and Bcl-2 expression was significantly higher in group SP than in group I/R ( P ＜ 0.05). Microscopic examination showed less damage in group SP than in group I/R. The protection provided by sevoflurane preconditioning was abolished by atractyloside. Conclusion Inhibition of mPTP opening can result in an up-regulation of Bcl-2 expression and down-regulation of Bax expression, which plays a role in attenuation of myocardial I/R injury by delayed preconditioning with sevoflurane in rats.

Proteomic analysis of morphine rabbit myocardium with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry / 中南大学学报(医学版)

OBJECTIVE@#To analyze the morphine rabbit myocardium with matrix-assisted laser desorption/ ionization time-of-flight mass spectrometry (MALDI-TOF-MS).@*METHODS@#Six New Zealand white rabbits were randomly assigned to a control group (Group C) and a morphine group (Group M). Group C were pretreated with bolus injection of saline 1 mL/kg. Group M were pretreated with bolus injection of morphine 3 mg/kg. The myocardium tissue proteins of the rabbits 24 hours after the injection of morphine or saline preconditioned were extracted and separated by two dimensional gel electrophoresis(2-DE), and the images were analyzed and different proteins were found. Some of the different proteins were determined with MALDI-TOF-MS.@*RESULTS@#There were 51 protein spots that displayed quantitative changes in expression (P < 0.05), 15 protein spots were chosen for MS analysis, and 8 proteins were preliminarily identified.They were aldose reductase, zinc finger protein 312, src related tyrosine kinase, carbonic anhydrase 12 precursor, electron transfer flavoprotein beta-subunit, glyceraldehyde-3-phosphate dehydrogenase, tumor necrosis factor ligand superfamily member 11 and transmembrane emp24 domain-containing protein.@*CONCLUSION@#These proteins may be involved in the cardioprotection of morphine preconditioning.

Effect of isoflurane delayed preconditioning on the expression of Bcl-2 and caspase-3 in myocardium during ischemia reperfusion in rabbits / 中南大学学报(医学版)

OBJECTIVE@#To investigate the effect of isoflurane delayed preconditioning on the activation of caspase-3 and the expression of Bcl-2 in rabbit myocardium during ischemia reperfusion and the possible mechanism.@*METHODS@#Forty New Zealand male white rabbits were randomly divided into 4 groups: a sham group (Group C), an I/R group, an isoflurane group (Group S), and an isoflurane + opioid recepters inhibitor group (Group N). Group S was exposed to 2.0% isoflurane for 2 h. Group N was given naloxone (6.0 mg/kg) before exposing to 2.0% isoflurane. Group C and Group I/R were exposed for 2 h to 100% oxygen, serving as untreated controls. Twenty-four hours later, Group S and Group N underwent 40 min of coronary occlusion followed by 2 h of reperfusion. At the end of the reperfusion, infarct size(IS) and area at risk(AAR) were defined by Evans and TTC staining. The myocardial ultrastructure was observed by electron microscopy. The levels of the myocardial Bcl-2 and caspase-3 expression were determined by Western blot.@*RESULTS@#The caspase-3 activity of Group S was significantly lower than that of Group I/R(P<0.05). The IS was significantly reduced in Group S(19.7%+/-2.8%) as compared with Group I/R(37.8%+/-1.7%) (P<0.05). Microscopic examination showed less myocardial damage in Group S than in Group I/R.@*CONCLUSION@#Isoflurane delayed preconditioning can inhibit the apoptosis of myocardium by up-regulating the expression of Bcl-2 and down-regulating the activation of caspase-3, which may be part of the molecular mechanism of isoflurane delayed preconditioning on myocardial preservation.

Effects of isoflurane delayed preconditioning on myocardial proteome in rabbits with myocardial ischemia-reperfusion injury / 中华麻醉学杂志

Objective To investigate the effects of isoflurane delayed preconditioning(IDP) on myocardial proteomin rabbits with myocardial ischemia-reperfuaion(I/R).mjury.Methods Eight New Zealand white rabbits of both sexes weighing 2.0-2.5 kg were randomly divided into 2 groups(n=4 each):I/R group and IDP group.Myocardial I/R Wgg induced by occlusion of left anterior descending artery for 40 min followed by 120 min repednsion.In group IDP.the animals inhaled 2%isoflurane for 2 h,undergoing I/R 24 h later.At the end of 120 min reperfusion,the myocardium of left ventricle anterior wall was removed for two-dimensional gel electrophorvsis.The different protein spots were analyzed by means of mass chromatography.Results There were 13 different protein spots between group I/R and IDP.Of the 13 proteins,the expression of 10 spots Was up-regulated and 3 spots down-regulated in quantity.Eleven protein spots of all spots were identified by means of MALDI-TOF-MS.Conclusion IDP can aNenuate myocardial I/R injury in rabbits and it may be related to the alteration in proteome of myocardium.

Metallothionein mediates cardioprotection induced by delayed preconditioning with adenosine A1 receptor agonist in rabbits / 中南大学学报(医学版)

Objective To investigate the protective effect of adenosine A1 receptor agonist (2-chloro-N6-cyclopentyladenosine, CCPA) delayed preconditioning on myocardial ischemia reperfu-sion injury and the potential mechanism in rabbits. Methods Thirty New Zealand male white rabbits were randomly assigned to 3 groups:a control group, an I/R group, and a CCPA group. CCPA group was given CCPA 0.1 mg/kg before the myocardial ischemia. Twenty-four hours later I/R group and CCPA group underwent 40 min of coronary occlusion followed reperfusion for 2 h. At the end of the reperfusion, blood samples were taken from the arterial line for determining the plasma level of malondialdhyde and superoxide dismutase activity. The infarct size and area at risk were de-fined by Evans and TIC staining. The heart was harvested and levels of metallothionein (MT) were determined by Western blot, and ultrastructures were observed under the electron microscope. Results The MT level of CCPA group was significantly higher than that of the I/R group (P<0.05). CCPA significantly reduced the infarct size (22.1%±3.8% in the CCPA group) of the left yen-tricular area at risk as compared with the control (41.8%±4.3% in the I/R group,P<0.05). The injury of I/R group was worse than that of the CCPA group under the light microscope. CCPA group had higher superoxide dismutase and lower malondialdhyde than those of the I/R group. Con-clusion CCPA can increase the level of metallothionein during ischemia-reperfusion, which may be part of the molecular mechanism of CCPA delayed preconditioning on cardioprotection.

Role of opioid receptors in protective effects of isoflurane- induced delayed preconditioning against myocardial ischemia-reperfusion injury in rabbits / 中华麻醉学杂志

Objective To investigate the role of opioid receptors in the protective effects of isoflurane-induced delayed preconditioning against myocardial ischemia-reperfusion (I/R) injury in rabbits. Methods Forty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 4 groups ( n = 10 each) : group I sham operation (S); group II I/R; group Ⅲ isoflurane + I/R (Iso) and group IV Iso + naloxone + I/R (Nal). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group Ⅲ (Iso) 2% isoflurane in 100% O2 was inhaled for 2 h and I/R was produced 24 h later. In group IV (Nal) naloxone 6 mg/kg was given iv 10 min before 2 h of 2% isoflurane inhalation and I/R was produced 24 h later. At the end of 120 min reperfusion, infarct size (IS) and area at risk (AAR) were determined by Evan's blue and TTC staining. Myocardial ultrastructure was examined by electron microscopy. The phosphorylated p38MAPK protein expression in myocardium was determined by Western blot. Results The IS was significantly smaller in group Iso ( Ⅲ ) ( 19.7% ± 2.8%) than in I/R group ( II ) (37.8% ±1.7%) (P<0.05). The phosphorylated p38MAPK protein expression in myocardium was significantly lower in group Iso than in group I/R. Microscopic examination showed less myocardial damage in Iso group than in group I/R. The protective effects of delayed preconditioning by isoflurane was prevented by naloxone pretreatment. ConclusionOpioid receptors may be involved in the protective effects of delayed preconditioning by isoflurane against myocardial I/R injury.

The effect of octreotide acetate on plasma ETX and serum inflammatory cytokine of the rabbit with hepatic Ischemia-reperfusion Injury / 中国医师杂志

Objective To observe the effect of octreotide acetate on plasma ETX and serum inflammatory cytokine of the rabbit with hepatic ischcmia reperfusion injury. Methods Pringle's maneuver rabbit hepatic ischemia-repeffusion models were established. 24 adult New Zealand rabbits were random divided into equal 3 groups: sham operative group(group A), iacbemia reperfusion group(group B)and octreotide acetate preconditioning group(group C). Endotoxin (ETX) in the plasma, tumor necrosis factor-alpha (TNF-α) and intcdeukin-1beta (IL-1β) were detected in every rabbit at the time before iachemia (T1), 30min after ischemia (T2), 30min (T3) and 120min (T4) after reperfusion. Results From T2 to T4, the ETX in group B and C were higher than that in group A (P < 0.05), the ETX of group C were lower than that in group B (P<0.05). From T2 to T4, the TNF-α of group B and C were higher than that of group A(P<0.05). From T3 to T4 the TNF-α of group C were higher than that of group A(P<0.05). From T2 to T4,the IL-1β of group B and group C were higher than that of group A(P<0.05), and the IL-1β of group C were lower than that of group B (P<0.05). Conclusion Octreotide acetate can decrease plasma ETX and down-regulate inflammation factors, such as TNFαand IL-1β, in serum of the rabbit with hepatic iacbe-mia-reperfusion injury, which may be the protective mechanism of oetreotide acetate on rabbit hepatic isehemia-reperfusiun injury.

Effects of isoflurane delayed preconditioning on nuclear factor-κB during myocardial ischemia reperfusion injury in rabbits / 中华急诊医学杂志

Objective To explore the mechanism of the catdioprotection of isoflurane delayed preconditioning on myocardial ischemia reperfusion injury in rabbits.Method Thirty male New Zealand white rabbits,weighing 2.0 to 2.5 kg,were randomly divided into three groups(ten for each group):Control group(group C),I/R group(I/R group) ,2.0% isoflurane group(group S) .Group S was exposed to 2.0% isoflurane-100% oxygen for2 h.Group C and I/R group were exposed 2 h to 100% oxygen served as untreated controls.Twenty-four hours later I/R group and group S underwent 40 rain of coronary occlusion followed by 2 h of reperfusion.Blood samples were taken from arterial line at 20 min before occlusion(T1) ,20 rain after occlusion(T2) ,40 rain after occlusion(T3) ,1 h after reperfusion(T4) and 2 h after reperfusion(TS) for determination of plasma IL-10 levels and TNF-alevels by ELISA.At the end of the reperfusion,infarct size and area at risk were defined by Evans and TTC staining.The heart was harvested and levels of the nuclear factor kappa β(NF-κB)activity were determined by Western Blot,and ultrastructures were observed by electron microscopy.The data was expressed as,and were analyzed by using oneway ANOVA test with SPSS 13.0.P value less than 0.05 indicated statistical significance.Results The NF-κB activity of group S was significantly lower than that of group I/R(P<0.05).Group S significantly(P<0.05)reduced infarct size(19.7%±2.8% in group S) of the left ventricular area at risk as compared with control (37.8 %±1.7 % in I/R group).The injury of I/R group was worse than that of group S from the changes of the cellular structure under light microscope.Group S had a lower levels of TNF-α and also had a higher level of IL-10.Conclusions Isoflurane can inhibit NF-κB activity during myocardial ischemia reperfusion and modulate the cytokine expression,which may be one of molecular mechanisms of Isoflurane delayed preconditioning on cardioprotection.

Blood-saving effect of low central venous pressure combined with acute hypervolemic hemodilution in patients undergoing hepatic lobectomy / 中华麻醉学杂志

Objective To evaluate the blond-saving effect of low central venous pressure(CVP) combined with acute hypervolemic hemedilution(AHHD)in patients undergoing hepatic lobectomy.Methods sixty ASA I orⅡpatients of both sexes aged 32-48 yr weighing 47-72 kg undergoing hepatic lobectomy for primary malignant hepatonm under epidural combined with general anesthesia were randomly divided into 3 groups(n=20 each);group I control(C);group 1I AHHD and group Ⅲ low CVP+AHHD.Group C received crystalloid and coloid in a ratio of 1.5:1 during operation.In groupⅡ4% suecinylated gelatin was infused at 50 ml·kg-1·h-1 for 30 min after tracheal intubation (AHHD);while inⅢ group low CVP was induced and maintained by epidural administration of a mixture of 1.5% lidnoaine +O.2% bupivacaine 6-8 ml combined with intravenous infmion of propofol at 6 mg·kg-1·h-1 until 10 min after hepatic lobectomy was completed.then 4% succinylated gelatin was infused at 50 ml·kg-1·h-1 for 30 min.Blood glucose,Hb,Hct, WBC count,blood coagulation (PT,AVIT,Fib),shtmic-pyruvic transaminase (GPT) and renal function (BUN,Cr) were determined before operation (baseline),immediately before skin incision,immediately before and 10 min after liver lobe was removed,at the end of operation and 7 d after operation.Urine output,intraoperative blood loss and blood transfusion and complications were recorded.Results The glood glucose concentration.WBC count and GPT levd were significantly lower;the amount of fluid infused and urinary output before hepatic lobe resection and the percentage of the patients with allogeneic blood transfusion during operation were less;Hb,Hct and the amounl of fluid infused and urinary output after hepatic lobe resection were uigher in grolp Ⅲ than in group I and ⅡⅡⅡ.There were no significant differences in blood coagulation,renal function,the total amount of fluid infused and urine output among the 3 groups.No patient developed any complication.Conclusion The low CVP hefor combined with AHHD after hepatic resection can decrease intraoperative blood loss and allogeneic blood transfusior and is safe.

The effect of hypercapnic acidosis preconditioning on rabbit myocardium / 华中科技大学学报（医学）（英德文版）

This study observed the protective effect of hypercapnic acidosis preconditioning on rabbit heart suffered from ischemia-reperfusion injury. Hypercapnic acidosis was established in animals with mechanical hypoventilation before ischemia-reperfusion. Thirty-two rabbits were randomly divided into 4 groups, with each having 8 animals in term of the degree of acidification: hypercapnic acidosis group A (group A), hypercapnic acidosis group B (group B), hypercapnic acidosis group C (group C), ischemia and reperfusion group (group IR). Animals in group IR were ventilated normally (tidal volume: 15 mL/kg, breathing rate 35 bpm). The PETCO(2) was maintained at the level of 40-50 mmHg for 30 min. Animals in groups A, B, C received low-frequency, low-volume ventilation to achieve hypercarbonic acidosis and the target levels of PETCO(2) were 75-85,65-75, 55-65 mmHg, respectively, with levels being maintained for 5 min. The animals then were ventilated normally to lower PETCO(2) to 40-50 mmHg. The left anterior branch artery of all the animals was ligated for 30 min and reperfused for 180 min. Then the infarct size was calculated. The cardiomyocytes were morphologically observed and ECG and hemodynamics were monitored on continuous basis. Acid-base balance was measured during procedure. Our results showed that the infarct size was (48.5+/-11.5)% of the risk area in the control group and (42.4+/-7.9)% in group C (P>0.05). Mean infarct size was significantly smaller in group B (34.5%+/-9.4%) (P<0.05 vs control group) and group A (31.0%+/-9.1%) (P<0.01 vs control group). It is concluded that HA-preconditioning can effectively protect the myocardium.

Cardioprotective effects of morphine on rat heart suffering from ischemia and reperfusion / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the cardioprotective effects of morphine on ischemic reperfused rat heart in vitro and its mechanism.</p><p><b>METHODS</b>The isolated rat heart was perfused in a Langendorff apparatus. Infarct myocardium was determined by TTC. Coronary flow (CF), heart rate (HR), left ventricular pressure (LVP), the first derivative of ventricular pressure (LVP/dtmax) and infarct size after ischemia and reperfusion in rat heart given 0.3 micro mol/L morphine were observed. The effects of naloxone and glibenclamide on the cardioprotection of morphine were also measured.</p><p><b>RESULTS</b>After ischemia and reperfusion, CF, HR, LVP and LVP/dtmax of isolated rat hearts decreased significantly (P < 0.01). After morphine preconditioning, HR, LVP and LVP/dtmax increased (P < 0.01) and infarct size was reduced significantly (P < 0.01), while no significant change in CF (P > 0.05). The cardioprotective effects of morphine were abolished by naloxone or glibenclamide completely.</p><p><b>CONCLUSIONS</b>Morphine can reduce ischemia-reperfusion injuries in isolated rat heart. The cardioprotective effects of morphine are mediated by a local opioid receptor-K(ATP) channel linked mechanism in rat hearts.</p>

Protection of propofoi against ischemia-reperfusion injury in isolated rat hearts / 中华麻醉学杂志

Objective: To investigate the effect of propofol on ischemia reperfusion injury in isolated rat heart with the modified Langredorff model. Method: Thirty rats were divided equally into five groups at random. Rat hearts were perfused with Krebs-Henseleik(K-H)buffer for 70 min at a constant pressure of 7.84kPa and constant temperature of 37℃ in control group (group C)and in the other four groups,a three-phase protocal was performed: (1)20-minute preperfusion, (2)30-minute global normothermic(37℃)ischemia, (3)30-minute reperfusion. Treatment with 50?mol/L propofol(group P1),25?mol/L propofol(group P2), 90?g/ml intralipid (group IN )dissolved in K H buffer started 10 minutes before ischemia and throughout the experiment. Only K-H buffer was perfused in the ischemia-reperfusion group(group I-R). The heart rate(HR),left ventricular pressure (IVP)and it's first derivative(?dp/dtmax) and coronory flow (CF)were recorded at the tenth and twentieth minute of preperfusion, and the 30th minute of reperfusion. Creatin kiuase (CK)activity was measured in the coronory effluent at the 30th minute of reperfusion. Result: After 30-minute reperfusion, recovery of hears treated with propofol were better than that of group I-R and group IN,indicated by better contractivity, higher coronory flow and lower CK level (P

Protective effects of midazolam and propofol on myocardial ischemic reperfusion injury in patients undergoing open heart surgery / 中华麻醉学杂志

Objective To compare the protective effects of midazolam and propofol at equivalent dose on myocardial ischemia reperfusion injury during open heart surgery Methods Thirty six patients,scheduled for elective open heart surgery, were divided into midazolam (M), propofol (P) and no occluding (N) groups Before induction, a bolus of midazolam 0 2mg?kg -1 was given in group M or N , and a bolus of propofol 2 0mg?kg -1 in group P; after induction, midazolam was infused at 0 4mg?kg -1 ?h -1 in group M or N , and propofol at 4 0mg?kg -1 ?h -1 in group P The arterial blood samples were taken to measured the activities of serum enzymes ,at the beginning of CPB, 30min, 4, 12 and 24h after release of the aortic cross clamp Results As compared with those at at the beginning of CPB, the activities of serum enzymes increased significantly in three groups following declamping (P