V G Nielsen1, B T Geary. 1. Department of Anesthesiology, The University of Alabama at Birmingham, 35249, USA.
Abstract
PURPOSE: The purpose of this study was to determine if an increase in circulating heparinoid activity contributes to the hemostatic abnormalities associated with hepatoenteric ischemia-reperfusion. MATERIALS AND METHODS: Anesthetized rabbit (n = 18) underwent thoracic aorta occlusion for 30 minutes with a balloon catheter, followed by 30 minutes of reperfusion. Blood samples were obtained after 30 minutes of equilibration and 30 minutes of reperfusion. Hemostatic function was assessed by changes in the thrombelastographic variables R (reaction time), alpha (a measure of the speed of clot formation), and G (a measure of clot strength). Thrombelastography was performed on blood without platelet inhibition in the presence or absence of heparinase (n = 9 rabbits). Additional samples (n = 9) were exposed to cytochalasin D (platelet inhibitor) with or without heparinase. RESULTS: Compared with preischemic values, blood samples with intact platelet function obtained during reperfusion demonstrated a decrease in hemostatic function evidenced by a significant (P<.05) increase in R, decrease in alpha, and decrease in G. R, alpha, and G values of samples without platelet inhibition exposed to heparinase did not significantly change after ischemia. Blood samples exposed to cytochalasin D displayed a similar pattern. CONCLUSION: An increase in circulating heparinoid activity significantly contributes to the hemostatic disorder associated with hepatoenteric ischemia-reperfusion in rabbits.
PURPOSE: The purpose of this study was to determine if an increase in circulating heparinoid activity contributes to the hemostatic abnormalities associated with hepatoenteric ischemia-reperfusion. MATERIALS AND METHODS: Anesthetized rabbit (n = 18) underwent thoracic aorta occlusion for 30 minutes with a balloon catheter, followed by 30 minutes of reperfusion. Blood samples were obtained after 30 minutes of equilibration and 30 minutes of reperfusion. Hemostatic function was assessed by changes in the thrombelastographic variables R (reaction time), alpha (a measure of the speed of clot formation), and G (a measure of clot strength). Thrombelastography was performed on blood without platelet inhibition in the presence or absence of heparinase (n = 9 rabbits). Additional samples (n = 9) were exposed to cytochalasin D (platelet inhibitor) with or without heparinase. RESULTS: Compared with preischemic values, blood samples with intact platelet function obtained during reperfusion demonstrated a decrease in hemostatic function evidenced by a significant (P<.05) increase in R, decrease in alpha, and decrease in G. R, alpha, and G values of samples without platelet inhibition exposed to heparinase did not significantly change after ischemia. Blood samples exposed to cytochalasin D displayed a similar pattern. CONCLUSION: An increase in circulating heparinoid activity significantly contributes to the hemostatic disorder associated with hepatoenteric ischemia-reperfusion in rabbits.