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

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.

Objective To investigate the effects of ulinastatin on cerebral injury during cardiac valve replacement and the possible mechanisms involved. Methods Twenty-four NYHA Ⅱ or Ⅲ patients of both sexes (13 male, 11 female) aged 23-45 yr undergoing cardiac valve replacement with hypothermic cardiopulmonary bypass (CPB) were randomly divided into two groups: control group (group C, n = 12) and ulinastatin group (group U, n = 12) . In group U ulinastatin 12 000 U?kg-1 was given i.v. after induction of anesthesia, 6 000 U? kg-1 was added to the priming solution and another 6 000 U?kg-1 was given at 5 min before aortic unclamping. In group C normal saline was given instead of ulinastatin. Internal jugular vein was cannulated and the catheter was advanced in a cephalad direction till jugular bulb. Blood samples were taken from jugular bulb after induction of anesthesia(T1) , when rewarming to 36℃(T2), 30 min (T3 ) and 6 h (T4 ) after discontinuation of CPB for determination of plasma S100? protein, neuron specific evolase (NSE) , MDA concentrations and SOD activity. Plasma TNF-?, IL-6, IL-8 and IL-10 levels were also determined at T1, T3 and T4.Results Plasma levels of S100? protein, NSE and MDA were significantly increased during and after CPB (T2-4) compared to the baseline values before CPB (T1), but were significantly lower in group U than in group C (P

Objective To investigate the effects of chloroquine (CQ) on the acute lung injury (ALI) induced by total hepatic ischemia-reperfusion (I/R) .Methods Ninety SD rats of both sexes weighing 300-350g were randomly divided into 3 groups (n=30 each) : group A sham operation; group B total hepatic I/R and group C CQ + total hepatic I/R. The animals were anesthetized with 3% pentobarbital 45 mg?kg-1. Total hepatic I/R was produced by occlusion of hepatic hilum, supra-and infra-hepatic inferior vena cava for 20 min and the occlusion was then released for reperfusion. In group C CQ 10 mg?kg-1 in normal saline (NS) 1 ml?kg-1 was injected via right femoral vein 10 min before abdomen was opened. In group A and B NS 1 ml?kg-1 was given Ⅳ instead of CQ. The animals were killed at the end of 20 min ischemia (T0); 4 h of reperfusion (T1) and 48 h of reperfusion (T2) (n=10 at each time point). Blood samples were taken at T0 and T1 from portal vein of liver for determination of plasma D-lactate, endotoxin (ETX) and TNF-? concentrations. 48 h survival rate was recorded and the animals were then killed for microscopic examination of the lung.Results Portal vein plasma D-lactate, ETX and TNF-? concentrations at T0 and T1 in group B were significantly higher than those in group A. In group C pretreatment significantly attenuated the increases induced by hepatic I/R. The 48-hour survival rate was significantly higher in group C than in group B. The histologic damage was significantly lighter in group C than in group B. Conclusion CQ has protective effects on the lung against injury induced by total hepatic I/R.

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

Objective To investigate the effect of isoflurane on lung ischemia reperfusion injury in rabbit in vivo Methods Thirty two healthy New Zealand white rabbits of either sex weighing 2 0 2 5kg were randomly divided into four groups of eight each:sham operation (group A): chest was opened and left main bronchus and pulmonary artery and vein were isolated but not clamped The lungs were ventilated for 120min; ischemia reperfusion (group B): left hilum was isolated and clamped for 60min, after declamping the lungs were ventilated for another 60min Isoflurane+ischemia reperfusion(group C): the lungs were first ventilated with 1MAC isoflurane for 15min then the left hilum was clamped for 60min, after declamping the lungs were ventilated with 1MAC isoflurane for another 60min Isoflurane(group D): left hilum isolated but not clamped The lungs were ventilated with 1MAC isoflurane for another 60min Animals were then killed by blood letting, left lung was excised for microscopic examination and measurement of wet/dry weight(W/D) ratio and MDA content Results The W/D ratio and MDA content of left lung were significantly higher in group B and group C than those in group A and group D, while W/D ratio and MAD content in group B were significantly higher than those in group C Microscopic examination showed that there were severe leukocyte infiltration and edema formation in alveolar spaces and alveolar structure was destroyed in group B and group C, but the changes were less severe in group C Conclusions Inhalation of 1MAC isoflurane before ischemia and during reperfusion protects the lungs against ischemia reperfusion injury in rabbit in vivo

Objective To investigate the effects of different doses of propofol on erythrocyte lipid peroxidation in patients undergoing open heart surgery Methods Twenty seven adult patients with rheumatic heart disease undergoing elective value replacement were divided randomly into three groups of nine patients each: control group (group C), low dose propofol group (group LP) and high dose propofol group (group HP) The patients were premedicated with intramuscular morphine 0 08mg/kg and scopolamine 0 06mg/kg Anesthesia was induced with propofol 2 0 mg?kg -1 (group LP and HP) or midazolam 0 2mg?kg -1 (group C), fentanyl 5 0 ?g?kg -1 and vecuronium 0 1mg?kg -1 After tracheal intubation the patients were mechanically ventilated Anesthesia was maintained with propofol 5mg?kg -1 ?h -1 (group LP) or 10mg?kg -1 ?h -1 (group HP) or Isoflurane inhalation (group C) in addition to fentanyl (total dose 40 60?g?kg -1 ) and vecuronium Blood samples were taken from internal jugular vein before operation (T 1), 60min after initiation of CPB(T 2), 15min (T 3) and 60min (T 4) after aorta declamping and 24h after termination of CPB (T 5) for determination of plasma and erythrocyte LPO (P LPO and E LPO) and erythrocyte SOD (E SOD) The shape of erythrocyte was also viewed under electron microscope Results The levels of P LPO and E LPO increased significantly after initiation of CPB and the level of E SOD was higher than baseline level at T 2, then decreased from T 3 to T 5 in the three groups (P

Objective To investigate the effects of pretreatment with volatile anesthetics on myocardial apoptosis induced by myocardial ischemia-reperfusion. Methods Forty-eight healthy New Zealand white rabbits of both sexes weighing 3.2-3.5kg were anesthetized with intramuscular ketamine 70mg?kg-1. The animals were tracheotomized and intubated and mechanically ventilated. PaCO2 was maintained at 4-4.5kPa. Sternum was longitudinally splitted. Left anterior descending branch of coronary artery was exposed and mobilized and a fine rubber tube was placed around it for occlusion of the artery. The occlusion of the artery was confirmed by cynosis of the area of myocardium involved and ECG which showed elevation of S-T segment. The animals were randomly allocated to one of 6 groups of 8 animals in each group: sham-operation group (P) ; ischemia / preconditioning group (IP) ; and three groups pretreated with isoflurane (I), sevoflurane (S) and desflurane (D) . Each group except group P was subjected to 3h occlusion of left anterior descending artery followed by 3h reperfusion. Group I, S and D were pretreated with inhalation of 1.1% isoflurane, 2% sevoflurane or 6% desflurane for 30 min followed by 15 min washout. The heart was then removed after ischemia-reperfusion. Infarct size and ischemic area were determined by dual staining with triphenyltetrazolium chloride and Evan' s blue. DNA laddering in the border zone of myocardial ischemic area was revealed by agarose gel electrophoresis. Apoptosis index (A I ) was obtained by flow cytometry. Results The infarct size, expressed as the percentage of the ischemic area was (60.8?10.8)% in ischemia-reperfusion group and was greatly reduced in group IP (33.1 ?4.9)%, group I (39.0?5.9)%, group S (30.9 ?6.8)% and group D (32.2? 7.5)% (P

Objective To investigate the effect of ulinastin on the gastro-intestinal circulation and systemic inflammatory response during open heart surgery with cardiopulmonary bypass( CPB) .Methods Thirty adult patients undergoing valve replacement with mild hypothermic CPB were randomly divided into two groups: ulinastin group (U ,n = 15) and control group (C , n = 15). In ulinastin group patients received ulinastin 6000 IU?kg-1iv after induction of anesthesia and another 6000 IU?kg-1 was added into the priming solution. In control group patients received equal volume of normal saline, instead of ulinastin. The patients were premedicated with morphine 0.2 mg?kg-1 and scopolamine 0.06 mg?kg-1 .Ranitidine 1 mg?kg-1 was given iv before induction of anesthesia. Anesthesia was induced with midazolam 0.1 mg?kg-1 , fentanyl 10?g?kg-1 and vecuronium 0.1 mg?kg-1 and maintained with fentanyl 50-60?g?kg-1, midazolam, isoflurane and vecuroinum. The patients were intubated and mechanically ventilated. PET CO2 was maintained at 35-45 mm Hg during operation. Gastric intramucosal PCO2 (PiCO2 ) was measured (pHi was calculated) and blood concentrations of TNF-?and IL-6 were determined before CPB (T0), 30 min after aorta was cross-clamped (T1), 60 min after termination of CPB(T2 ) and 6 h after operation (T3 ) .Results The two groups were comparable with regard to age, sex, body weight, ejection fraction, duration of CPB and cross-clamping time. (1) pHi decreased significantly at T1-2 as compared with the baseline value at T0 (P

Objective To investigate the effects of pretreatment with different inhalational anesthetic agents on myocardial Bcl-2, Bax and p53 gene expression during ischemia-reperfusion ( I/R) in rabbits. MethodsForty New Zealand white rabbits of both sexes were anesthetized with intramuscular ketamine 70 mg kg-1 tracheotomized and mechanically ventilated with 100% O2. PETCO2 was maintained at 4.0-4.5 kPa. Carotid artery and external jugular vein were cannulated for BP monitoring, fluid administration and medication. Anesthesia was maintained with midazolam 0.05-0.1 mg kg-1?h-1 , ketamine 2-5 mg? kg-1?h-1and vecuronium 0.05-0.1 mg? kg -1 ? h-1 . Myocardial ischemia was induced by occlusion of anterior descending branch of left coronary artery. Ischemia was confirmed by cyanosis of local myocardium and elevation of S-T segment. The animals were randomly allocated to one of five groups with 8 animals in each group : group C sham operation; group I/R; group I isoflurane pretreatment; group S sevoflurane pretreatment and group D desflurane pretreatment. In guoup C animals underwent no I/R. In group I/R animals were subjected to 3h of ischemia followed by 3 h reperfusion. In group I, S and D animals inhaled 1.1% isoflurane or 2% sevoflurane or 6% desflurane for 30 min followed by 15 min of wash-out before I/R. Intravenous anesthetic infusion was suspended while inhalational anesthetic was being inhaled. Myocardium 100 mg was obtained from marginal zone of ischemic area and made into cell suspension for determination of apoptosis index ( AI) and expression of Bcl-2, Bax and p53 genes, using flow cytometry.ResultsAI was (14)% in group I/R and was significantly reduced to (6.7 ? 1.8)% ( group Ⅰ ), (6.7 ? 1.6)% ( group S) and (7.4?2.0)% ( group D) (P