Study on the cerebral protective effects of dexmedetomidine during anesthesia for surgical correction of congenital heart disease with cardiopulmonary bypass

Objective: To evaluate the cerebral protective effects of dexmedetomidine (DMED) during anesthesia for surgical correction of congenital heart disease (CHD) with cardiopulmonary bypass (CPB). Methods: One hundred patients who would undergo elective surgery for CHD with CPB were included in this study. According to the method of random number table, they were divided into two groups: DMED group and control group, with 50 cases in each group. In DMED group, patients received intravenous injection of 1.0 mu g/kg DMED within 10 min before the routine anesthesia induction, followed by an intravenous infusion of 0.5 mu g/kg/h DMED until the end of surgery; while in control group, patients were given the same volume of normal saline at the same rate. The heart rate and blood pressure were measured respectively at the beginning (T1) and end (T2) of CPB, 12 h (T3) and 24 h after CPB (T4). The value of jugular venous oxygen saturation (SjvO2), arterial venous oxygen content difference (Da-jvO2) and cerebral oxygen extraction ratio (CERO2) at these four time points were analyzed. The concentration of plasma S-100 beta protein, TNF-alpha and serum neuron-specific enolase (NSE) were also detected using ELISA across different time points. The levels of postoperative agitation and pain in patients were scored according to the Sedation-Agitation Scale (SAS) and the Visual Analogue Scale (VAS). Emergence from anesthesia was assessed for comparison between two groups. Results: There was no significant difference between two groups in terms of general information, such as age, gender, body mass index (BMI), preoperative left ventricular ejection fraction (LVEF), and time spent on CPB, aortic cross-clamping and operation (P > 0.05). No intergroup difference was observed in heart rate and blood pressure at T1, T2, T3 and T4 during the perioperative period (P > 0.05). Compared with T1, both groups showed an evident decrease in Da-jvO2 and CERO2, as well as increase in SjvO2 (P = 0.000). However, compared with control group at T2, the decrease in Da-jvO2 and CERO2 and increase in SjvO2 were much greater in DMED group (all P = 0.000). The values of TNF-alpha, S-100 beta protein and NSE at T2 and T3 were also higher in both groups compared to those at T1 (all P = 0.000), but the levels of these markers at T2 and T3 in DMED group were much lower than those in control group (all P = 0.000). The incidences of moderate and severe agitation, total occurrences of agitation, and VAS score were also much lower in DMED group than those in control group (P = 0.000). No significant difference was found in regard to the time for awakening and full recovery of consciousness, extubation time and length of stay in CICU between two groups (P> 0.05). Conclusion: DMED has cerebral protective effect in some degree during anesthesia for the surgical correction of CHD with CPB. It could significantly improve the balance between cerebral oxygen supply and consumption, reduce the expression of markers of brain injury, as well as ameliorate the agitation and pain during the emergence after general anesthesia. Besides, it would barely affect the hemodynamics and awakening. These findings might be related to the fact that DMED could reduce the cerebral oxygen metabolism and inhibit inflammatory response.