BACKGROUND: Activated fibrinolysis during cardiopulmonary bypass(CPB) is one of the causes of post CPB coagulopathy. Antifibirinolytics such as tranexamic acid have been administered prophylactically before CPB to decrease postCPB bleeding. However, their routinely application has been challenged as regarding it's thrombotic complication. This study was performed to evaluate the effect of tranexamic acid administered before CPB by thromboelastography. METHODS: 50 open heart surgical patients were randomly selected and devided into two groups, control(N=25) and tranexamic acid group(N=25). In tranexamic acid group. 125mg of tranexamic acid were singly infused before vena caval and aortic cannulation. All of parameters of thromboelastography (TEG) and fibrin degradation products measured before and after CPB were compared between two groups. RESULTS: There were no significant differences in fibrinolytic indexes of TEGs between control group and tranexamic group afte CPB. And there were also no changes in fibrinolysis index between before and after CPB in both groups. The concentration of FDP did not changed after CPB in both groups. CONCLUSIONS: It may be considered that prophylactic administration of tranexamic acid before CPB to reduce post-CPB bleeding would not be recommended routinely.
Catheterization ; Fibrin Fibrinogen Degradation Products ; Fibrinolysis* ; Heart* ; Hemorrhage ; Humans ; Thoracic Surgery* ; Thrombelastography ; Tranexamic Acid*

During hemorrhagic shock, liver is susceptible to ischemia and decreased hepatic energy charge results in decreasing arterial ketone body ratio(AKBR). Reperfusion after hemorrhagic shock can greatly amplify the generation of toxic oxygen metabolites. As a result, the fluxes of these highly toxic metabolites can overwhelm the endogenous antioxident defense mechanisms and lead to tissue injury. In order to observe the effect of glutathione(GSH) on the AKBR in hemorrhagic shock, dogs(n=16) were anesthetized with 1% enflurane in 02. We pretreated glutathione (100 mg/kg) intravenously before hemorrhagic shock in glutathione (GSH) group (n=8). Shock was induced with bleeding and mean arterial pressure was maintained 50 mmHg for 30 minutes. Recovery from shock was done with transfusion of preserved blood and maintained for 30 minutes. We measured arterial ketone bodies and ketone body ratio before, during and after shock, and compared them to control group (n=8) which was not pretreated with glutathione. AKBR during and after hemorrhagic shock in GSH group (0.8 and 1.0) were higher than those in control group (0.5 and 0.8). Light microscopic examination of liver biopsy revealed less portal degeneration during and after hemorrhagic shock in GSH group than control group. Pharmacologic modulation of hepatocytic function with glutathione before hemorrhagic shock has shown some beneficial effect with protection of decreased AKBR and histological change during and after hemorrhagic shock.
Animals ; Arterial Pressure ; Biopsy ; Defense Mechanisms ; Dogs* ; Enflurane ; Glutathione* ; Hemorrhage ; Ischemia ; Ketone Bodies ; Liver ; Oxygen ; Reperfusion ; Shock ; Shock, Hemorrhagic*

BACKGROUND: Portal triad clamping was first described by Pringle in 1908 as a mean of reducing bleeding from the cut surface of the liver during parenchymal resection. More recently some studies have reported that one period of portal triad clamping could be well tolerated for a longer duration, 60~90 minutes. The liver, generally, is believed to be very sensitive to anoxic damage and susceptible to ischemia and decreased hepatic energy charge results in decreasing arterial ketone body ratio (AKBR) during portal triad clamping. METHODS: In order to observe an adverse effects to liver in 30 minutes and 60 minutes of portal triad clamping on AKBR and histologic changes,rabbits were divided into thirty minutes of portal triad clamping in one group (Group I) and 60 minutes of that in the other group (Group II). RESULTS: During clamping, the mean AKBR of group I and II were 0.39 and 0.44, and decreased significantly compared with the mean AKBR (1.08 and 1.02) before clamping. Five minute after declamping, the mean AKBR of group II (0.49) was lower (P<0.05) than that of group I (0.63), but 30 minutes afterdeclamping, the AKBR of two groups had little difference (group I ; 0.57, group II 0.59, P>0.05). Under light microscopic examination of liver biopsy, there was no visible diffrences between two groups during clamping, 5 minutes and 30 minutes after declamping. CONCLUSIONS: It was concluded that there was no difference in hepatic energy change(AKBR) and histologic change under light microscopy after 30 minutes declamping between two groups.
Biopsy ; Constriction ; Hemorrhage ; Ischemia ; Liver ; Microscopy ; Rabbits*

During orthotopic liver transplantation (OLT), changes of hemodynamic, electrolytes and acid-base balance are frequently occurred. These changes may influence mortality and prognosis during and after surgery. The purpose of this study was to observe and evaluate the changes of hemodynamics and electrolytes occurring in 14 cases canine OLT. After insertion of endotracheal tube, anesthesia was maintained with 1%enflurane and pancuronium bromide. Swan-Ganz catheter(7.5 Fr.) was inserted into right external jugular vein and 20 gauge angiocatheter was also inserted into left femoral artery. Complete hemodynamic variables and electrolytes were measured 30 minutes after skin incision, anhepatic stage, 5 minutes before reperfusion, 5 and 30 minutes after reperfusion. The results were as follows; On reperfusion of grafted liver, 9 cases(64%) showed postreperfusion syndrome. In 9 cases showing Postreperfusion syndrome, cardiac output, systemic vascular resistance, mean pulmonary arterial pressure were decreased and serum potassium concentration was increased on reperfusion, but there were no significant changes in central venous pressure, pulmonary capillary wedge pressure, heart rate, body temperature and serum ionized calcium concentration when comparing with before reperfusion. Decreased mean arterial pressure during reperfusion in postreperfusion syndrome might be speculated through decrease of myocardial contractility and systemic vascular resistance.
Acid-Base Equilibrium ; Anesthesia ; Animals ; Arterial Pressure ; Body Temperature ; Calcium ; Cardiac Output ; Central Venous Pressure ; Dogs ; Electrolytes ; Femoral Artery ; Heart Rate ; Hemodynamics* ; Jugular Veins ; Liver Transplantation* ; Liver* ; Mortality ; Pancuronium ; Potassium ; Prognosis ; Pulmonary Wedge Pressure ; Reperfusion ; Skin ; Transplants ; Vascular Resistance