| PrefaceCardiopulmonary bypass surgery is often accompanied by a systemic inflammatory response, which can cause postoperaterateve complications , lengthened duration of hospital stay, and in the morst case scenario, multiole organ failure, the etiology of this inflammatory response has been trace to the stress of surgery and contact activation of platelets and leuckocyteswithin the bypass circuit, which leads to an increase in arvulating cytokine levels such as tumor necrosis factor (TNF -α) , interleukin - 1, interliukin - 6, and interliukin - 8. Inflammatory eytokines in turn cause endothelial cell ( EC) activation and exprecesion of vascular adhesion molecules involved in recruitment of leukocytes to sites of inflammation or tissue injury.Tree distinct phase have been described ( 1 ) initial attachment and roUing of leuckcytes along the vessel well. ( 2 ) firm adhesion , and ( 3 ) transmigration into the extravascular tissue. Aprotinin is a nonspecific serine protease inhibitor that has been used extensively in cardiac operations, it possesesbroad hemostatic properties that mediated by blocking pathways of complement activation and fibronolysis as well as by inhibiting the action of proteinases, such as trypsin, plasmin , ans kallikrein . we conducted this study to investigate whether aprotinin could exert anti - inflammatory effects.Materials and methodswenty - seven patients who underwent heart valve replacement from October 1,2001 ,to March 10,2002 were randomized in double - blind fashion into two groups: control group ( n =11) and aprotinin group (n = 16) , Aprotinin was given at 11200u during CPB in the aprotinin group. Exclusion criteria were impaired renal function, advanced hepatic dysfunction, and hematologic disease. The aprotinin group received 560u in 20 minute before the skin incision, 560u in the priming solution of the extracorporeal circuit, and continuors infusion during the operation. The control group didnt receive aprotinin. The anesthetic was standardized: each patient was premedicated with intramuscular scopolamine (0. 5mg) , intramuscular morphine (0. Img/ kg). Anesthesia was induced with fentanyl(0.02mg/kg) and midazo-lam(0. 15mg/kg) in patients . muscle relaxation was obtained with pancuronium bromide (0.1mg/kg). Anesthesia was maintained with fentanyl(up to o. o5mg/kg) , an infusion of midaxolam(0. 1 -0.2mg/ kg/h) in patient and isoflurane and pancuronium as needed. All patients were operated on through a median sternotomy. Before aortic cannulation, porcine mucous heparin(3mg/kg) was injected, and further heparin was administered to maintain a kaolinactivated coagulation time above 480 seconds. A hollow - fiber membrane oxygenator was used, and the priming solution of the circuit consisted of 1750 ml of a balanced crystalloid/colloid. Nonpulsatile blood flow was obtained with a roller pump(2.0-2.41/min/itf ) . Blood temperature was kept between 32℃ and 35℃. myocardial protection during aortic cross-clamping was achieved with the Buckberg method of blood cardiople-gia. The total dose of heparin administered during CPB was reversed with protamine sulfate(ratio 1:1). After anesthesia was induced, we performed radial puncture. We collected the blood as four times: the first sample was 4ml arterial blood which was drawed from radial after radial puncture. The blood was anti - cogulation with heparin. 0.5ml blood was sent to the center of check to analysis the blood routine. 3. 5ml blood was centufugated at 2400 rpm. The upper plasm was drawed and store in - 20℃. The second sample was collected during aortic crossclamping. The method was same as the first. The third sample was collected at sloping inventory. After operation the fourth sample was done. The method was as the first.When we fimished the sample. sICAM - 1 was determinated in ELISA. IL - 6 and TNF - awas detected by radio - immunity analysis. All data were expressed as X± S. All data were analyzed by T test (a =0.05) .ResultsThere was no significant differece in age, body weight, operation... |
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