TEG Assessment of The Effect of Tranexamic Acid on Fibrinolysis during Open Heart Surgery / 대한마취과학회지

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.

Study on Hepatic Injury following Occlusion of Hepatic Inflow in Rabbits / 대한마취과학회지

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 (P0.05). 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.

Protection of Hepatic Dysfunction during and after Hemorrhagic Shock with Intravenous Glutathione in Dogs / 대한마취과학회지

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.