D S Sulemanji1, A Dönmez, D Aldemir, A Sezgin, S Türkoglu. 1. Department of Anesthesiology, Başkent University Faculty of Medicine, Bahcelievler 06490, Ankara, Turkey. demets@baskent-ank.edu.tr
Abstract
BACKGROUND: In the present study, we aimed to determine whether during coronary artery bypass grafting (CABG) surgery, dexmedetomidine has protective effects against cerebral ischemic injury. METHOD: Twenty-four patients, aged 50-70 years, undergoing CABG surgery were randomized into two groups of 12 patients each: those receiving dexmedetomidine (group D) and those not receiving it (group C). As basal blood samples from arterial and jugular bulb catheters were drawn, dexmedetomidine (1 microg/kg bolus and infusion at a rate of 0.7 microg/kg/h) was administered to patients in group D. Arterial and jugular venous blood gas analyses, serum S-100B protein (S-100B), neuron-specific enolase (NSE) and lactate measurements were performed after induction, 10 min after the initiation of cardiopulmonary bypass (CPB), 1 min after declamping, at the end of CPB, at the end of the operation and 24 h after surgery. Mann-Whitney U- and Wilcoxon's tests were used for statistical analyses. RESULTS: No significant between-group differences were found regarding arterial and jugular venous pH, PO(2), PCO(2) and O(2) saturations. S-100B, NSE and lactate levels were also similar between groups D and C. During the post-operative period, there were no clinically overt neurological complications in any patient. CONCLUSION:Cerebral ischemia marker (S-100B, NSE, lactate) patterns were as expected during CPB; however, there were no differences between the groups, which led us to believe that during CABG surgery dexmedetomidine has no neuroprotective effects. Future studies with larger populations are recommended to further establish the effects of this drug.
RCT Entities:
BACKGROUND: In the present study, we aimed to determine whether during coronary artery bypass grafting (CABG) surgery, dexmedetomidine has protective effects against cerebral ischemic injury. METHOD: Twenty-four patients, aged 50-70 years, undergoing CABG surgery were randomized into two groups of 12 patients each: those receiving dexmedetomidine (group D) and those not receiving it (group C). As basal blood samples from arterial and jugular bulb catheters were drawn, dexmedetomidine (1 microg/kg bolus and infusion at a rate of 0.7 microg/kg/h) was administered to patients in group D. Arterial and jugular venous blood gas analyses, serum S-100B protein (S-100B), neuron-specific enolase (NSE) and lactate measurements were performed after induction, 10 min after the initiation of cardiopulmonary bypass (CPB), 1 min after declamping, at the end of CPB, at the end of the operation and 24 h after surgery. Mann-Whitney U- and Wilcoxon's tests were used for statistical analyses. RESULTS: No significant between-group differences were found regarding arterial and jugular venous pH, PO(2), PCO(2) and O(2) saturations. S-100B, NSE and lactate levels were also similar between groups D and C. During the post-operative period, there were no clinically overt neurological complications in any patient. CONCLUSION:Cerebral ischemia marker (S-100B, NSE, lactate) patterns were as expected during CPB; however, there were no differences between the groups, which led us to believe that during CABG surgery dexmedetomidine has no neuroprotective effects. Future studies with larger populations are recommended to further establish the effects of this drug.