Alterations of epinephrine-induced gluconeogenesis in aging

The effects of glucagon and epinephrine on gluconeogenesis in young (4 month) and old (24 month) Fisher 344 rat hepatocytes were compared. In contrast to glucagon, which had a similar effect on gluconeogenesis in both young and old cells, epinephrine caused a smaller increase in gluconeogenesis in old rat hepatocytes than in young hepatocytes. beta2 adrenergic receptor (beta2-AR) expression slightly decreased in aged rat liver, and there were differences between young and old hepatocytes in their patterns of G protein coupled receptor kinases, which are involved in the activation of beta2-AR receptor signal desensitization. The major isoform of the kinase changed from GRK2 to GRK3 and the expression of beta-arrestin, which is recruited by the phosphorylated beta2-AR for internalization and degradation, increased in aged rat liver. GRK3 overexpression also decreased the glucose output from young rat hepatocytes. We conclude that an age-associated reduction in epinephrine-induced gluconeogenesis occurs through the epinephrine receptor desensitizing system.

Alterations of epinephrine-induced gluconeogenesis in aging

The effects of glucagon and epinephrine on gluconeogenesis in young (4 month) and old (24 month) Fisher 344 rat hepatocytes were compared. In contrast to glucagon, which had a similar effect on gluconeogenesis in both young and old cells, epinephrine caused a smaller increase in gluconeogenesis in old rat hepatocytes than in young hepatocytes. beta2 adrenergic receptor (beta2-AR) expression slightly decreased in aged rat liver, and there were differences between young and old hepatocytes in their patterns of G protein coupled receptor kinases, which are involved in the activation of beta2-AR receptor signal desensitization. The major isoform of the kinase changed from GRK2 to GRK3 and the expression of beta-arrestin, which is recruited by the phosphorylated beta2-AR for internalization and degradation, increased in aged rat liver. GRK3 overexpression also decreased the glucose output from young rat hepatocytes. We conclude that an age-associated reduction in epinephrine-induced gluconeogenesis occurs through the epinephrine receptor desensitizing system.

The Influences of 6% HES (130/0.4) Solution on Hemostasis / 대한마취과학회지

BACKGROUND: Hydroxyethyl starches (HES) solutions are the most commonly used colloids for treating hypovolemia and expanding plasma, but they compromise platelet function and reduce the level of coagulation factors. As opposed to other HES solutions, 6% HES (130/0.4) solution may influence hemostasis minimally due to its low mean molecular weight and degree of substitution. This study was designed to establish the safety of HES (130/0.4) infusion in the presence of massive blood loss. METHODS: Twelve healthy adult patients scheduled for spine surgery were enrolled in this study. Before the induction of general anesthesia, all patients underwent acute normovolemic hemodilution (ANH), which was independent of surgical stress and other confounding factors. While approximately 30% of the estimated blood volume was procured, the blood deficit was replaced with the same volume of 6% HES (130/0.4) solution. Hematocrit, platelet count, factor VIII activity and plasma fibrinogen concentration were determined and thrombelastography was performed to evaluate the hemodilution effect and hemostatic impairment before and after ANH. Statistical testing was conducted to analyze the effect of HES on hemostasis. RESULTS: Hematocrit, platelet count, factor VIII activity and plasma fibrinogen concentrations decreased significantly (P < 0.05 respectively) after the ANH. On comparing pre-ANH and post-ANH thrombelastographic findings, the R time was shortened (P = 0.045), the alpha angle increased (P = 0.01) and MA decreased (P = 0.003) significantly. CONCLUSIONS: Summarizing, little effect was observed on the hemostatic system when 20 ml/kg of 6% HES (130/0.4) solution was infused. HES (130/0.4) solution as used to maintain normovolemia during ANH may be free from bleeding risk.

The Changes of Coagulation State among ABO Blood Types during Acute Normovolemic Hemodilution / 대한마취과학회지

BACKGROUND: Improvement of coagulation function by acute normovolemic hemodilution (ANH) is well evidenced in modern medical practice. It has been reported that there are fixed differences in the plasma concentrations of von Willebrand factor and factor VIII according to ABO blood types. Therefore, the changes of coagulation state among ABO blood types during ANH are expected but have not yet been studied. This study was designed to establish the changes of coagulation state among ABO blood types during ANH by intraoperative thrombelastography (TEG). METHODS: Fifty one healthy adult patients scheduled for spine surgery were enrolled in this study. All patients were grouped by ABO blood types and underwent ANH after the induction of general anesthesia. While autologous blood (25% of EBV) was procured, warmed 0.9% saline, 3 times the blood volume deficit, was infused to maintain normovolemia. Platelet count, prothrombin time (PT), activated partial thromboplastin time (APTT), factor VIII activity and TEG were performed to evaluate coagulation state before and after ANH. Statistical analysis was conducted to determine the dilutional effects and intergroup differences. RESULTS: Improvement of coagulation function after ANH was visible only by TEG, and not by PT, APTT or factor VIII activity. Fourteen of fifteen patients with type O blood showed decreased factor VIII activity to under the normal limit after ANH. In patients with blood type O, changes of APTT (P = 0.093, P = 0.086) and factor VIII activity (P = 0.001, P = 0.004) during ANH were remarkable in comparison with blood type B and AB. CONCLUSIONS: ANH enhances coagulation function evaluated by means of TEG. No difference was observed in terms of the changes of coagulation state among ABO blood types during ANH. However, ANH should be instituted cautiously in patients with type O blood because there is a possibility of impairing factor VIII activity.