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Objective To evaluate premature clopidogrel cessation,intraoperative tranexamic acid and their interaction on bleeding and transfusion outcomes in on-pump CABG patients.Methods The current study is a prospective and randomized trial with 2 × 2 factorial design.The first factor is preoperative clopidogrel with 2 levels,clopidogrel ingestion within 7 days preoperatively (group E) and nave to clopidogrel (group B).The second level is antifibrinolytic therapy with 2 level,tranexamic acid (group T) and placebo (group P).A total of 333 patients receiving selective on-pump CABG were recruited.The tranexamic acid regimen was a bolus of 10 mg · kg-1 followed by a maintenance of 10 mg · kg 1 · h-1 throughout the surgery.Results Baseline characteristics were fairly balanced among the groups.Tranexamic acid significantly reduced postoperative blood loss.major bleeding,the volume of erythrocyte and plasma transfused,the exposure of erythrocyte,plasma and any allogeneic products (ET vs EP,P ＜ 0.01 ; BT vs BP,P ＜ 0.01).Clopidogrel within 7 days preoperatively significantly increased blood loss (EP vs BP,P＜0.05),major bleeding,the volume of erythrocyte (EP vs BP,P＜0.01) and the exposure of erythrocyte and plasma (EP vs BP,P ＜ 0.05) and any allogeneic products (EP vs BP,P ＜ 0.01).Under the protection of tranexamic acid,the bleeding and transfusion outcomes were comparable between the patients with premature clopidogrel cessation and those nave to clopidogrel (ET vs BP,P ＞0.05).Perioperative mortality,morbidity and the incidence of adverse events were comparable among the groups except for IABP.Conclusion Comparing with nave to clopidogrel,premature cessation within 7 days preoperatively deteriorated bleeding and transfusion outcomes in on-pump CABG patients.Intraoperative tianexamie acid could reduce the risk.
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Objective To investigate the effect of full-dose and half-dose aprotinin on perioperative inflammatory response in patients undergoing off-pump coronary artery bypass grafting (CABG) .Methods Thirty-nine patients aged 50-65 yrs undergoing off-pump CABG were randomly divided into 3 groups (n = 13 each):Ⅰcontrol group (C);Ⅱfull-dose aprotinin group (A-full) andⅢhalf-dose aprotinin group (A-half) . In groupⅡ( A-full) aprotinin 2?106 KIU in 100 ml normal saline (NS) was infused over 30 min after induction of anesthesia followed by aprotinin infusion at 0.5?106 KIU?h-1 until the end of surgery. In group A-half, half the amount of aprotinin administered in group A-full was given. In control group only NS was administered. Blood samples were taken before operation (T1,baseline) , 0.5 h after completion of vascular anastomosis (T2) and 2, 6, 18 h after operation (T3-5), for determination of plasma concentrations of IL-10, IL-6 and troponin (TnI) .Results The 3 groups were comparable with respect to age, M/F ratio, duration of operation and the number of bypass grafts. Plasma concentrations of IL-10, IL-6 and TnI were significantly increased after operation as compared to the baseline values (T0) in all 3 groups. The plasma concentrations of IL-10, IL-6 and TnI were significantly lower and postoperative blood loss smaller in the 2 aprotinin groups than in the control group; but they were not significantly different between the two aprotinin groups. Conclusion Both full-dose and half-dose aprotinin can inhibit the inflammatory response to CABG, reduce myocardial injury and postoperative blood loss. Half-dose aprotinin is recommended in patients undergoing off-pump CABG.
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Objective To investigate the protective effects of cardiomyopeptidin (CMP) pretreatment against hippocampal neuronal injury caused by anoxia-reoxygenation and the underlying mechanism. Methods Hippocampal neurons were isolated from neonatal SD rats and cultured for 9-10 days. The cultured primary hippocampal neurons were randomly divided into 4 groups: ( I ) control group; ( II ) anoxia-reoxygenation group (A-R); (I) CMP 10?g?ml-1 group (CMP1) and (IV) CMP 100 ?g?ml-1 group (CMP2). In A-R group hippocampal neurons were subjected to 4 h anoxia (cultured in 95 % N2 + 5 % CO2 ) and 48 h reoxygenation (cultured in aerobic environment). In group III and IV CMP was added to culture media with end-concentration of CMP 10 ?g?ml-1 or 100?g?ml-1 before oxygen-deprivation. Neuronal viability was assessed by MTT method and Bcl-2 protein expression was determined by immune-cytochemistry.Results The optical density (OD) value of hippocampal neurons and the Bcl-2 expression were significantly higher in group IV (CMP2) than those in group Q (A-R) and III (CMP1) (P
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Objective To investigate the effects of propofol on the survival rate of and the expression ofinducible nitric oxide synthase (iNOS) in the cultured hippocampal neurons.Methods Hippocampal neuronsisolated from new-born SD rats were dispersed and cultured in B27 culture medium for 9-10days.The culturedhippocampal neurons were randomized to one of 4 groups: (1)control group; (2) anoxia group; (3)propofol 4?g?ml~(1) + anoxia group; (4) propofol 12 ?g?ml~(-1)+ anoxia group. For anoxia the cultured hippocampal neurons wereplaced in a tightly closed vessel filled with 95 % N_2～5% CO_2 at 37℃ for 4h,followed by 24 h reoxygenation. Inthe propofol groups (group 3 and 4) propofol was added before anoxia. Survival rates were measured by MTTassay The levels of iNOS expression were determined by immunocytochemistry method.Results In the twopropofol groups (group 3 and 4) propofol attenuated the levels of iNOS expression in the cultured hippocampalneurons and increased the survival rates as compared with anoxia group (group 2). Depofol reduced the levels ofiNOS expression in a concentration-dependent manner.Conclusion Propofol can decrease the level of iNOSexpression in cultured hippocampal neurons induced by anoxia-reoxygenation and increase the survival rate ofhippocampal neuron after anoxia-reoxygenation. Inhibition of iNOS expression may explain partly the mechanism ofcerebral protective effects of propofol.