Background: Despite remarkable progress in surgical, cardiopulmonary bypass (CPB) and anesthetic tecniques, neurocognitive damage still remains an important cause of postoperative morbidity in cardiac surgery. The aetiology of neurocognitive damage is likely to be multifocal; including macro and microemboli, cerebral hypoperfusion, inflammation and nonpulsatile flow. N-methyl-D-asparticAcid (NMDA) receptors play an important role during neurocognitive damage. Ketamine is a non-competitive antagonist to the phencyclidine site of NMDA receptor for glutamate and directly suppresses proinflammatory cytokine production. The aim of the present study was to evaluate whether ketamine has neuroprotective effects during open-heart surgery through the use of neurocognitive tests.
Methods: We considered all patients aged between 58-76 years who were referred to a single cardiothoracic surgical team for elective, primary coronary revascularization. Patients were excluded from the study for the following reasons: a history of neurological, psychiatric, gastrointestinal, hepatic, renal, hematologic and clotting systems disorder and repeat procedures. Undergoing CPB were randomized 2 groups: Group1 (ketamine)(n=25) or Group2 (propofol)(n= Patients 25) In the propofol group, anesthesia was induced with 3mg/kg propofol, 1µg/kg remifentanyl, 0.1mg/kg vecuronium. Remifentanyl 0.5-1μg/kg/min was infused intravenously throughout the whole procedure. In the ketamine group, anesthesia was induced with 1-2mg/kg propofol, 1-2mg ketamin, 0.1mg/kg vecuronium. Ketamin 1mg/kg/hour was infused intravenously. Pressors, inotropic agents and antiarrhythmics were used as needed. The Mini-Mental State Examination(MMSE) was administered the day before surgery and three days later. The change in scores for MMSE was calculated for each patient and all the group. The results were compared statistically with paired simple t-test.
Results: The mean age, CBP duration, lowest temperature was not statistically significant (Table1). Peroperative and postoperative blood pressures and pulse rates showed differences between groups. There were no preoperative differences between the groups on any of the mean MMSE score (Table2). The ECG monitoring revealed that most patients remained in sinus rhythm, with no difference between groups.
Conclusions: We could not demonstrate that intraoperatively administered ketamine resulted in greater neuroprotective effects compared with propofol. Ketamine in combination with propofol during cardiac surgery is associated with a stable hemodynamic profile. Propofol may reduce the delivery of microemboli to the cerebral circulation by decreasing the cerebral blood flow. Propofol has a direct neuroprotective effect in vitro, although Roach et al. could not demonstrate a protective effect of propofol during open-heart surgery. Propofol enhances the antiinflammatory response to surgery by several mechanisms. This might have masked a neuroprotective effect of ketamine because propofol was administered in both groups in our study.
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