The Effects Of Carbon Dioxide Field Flooding On Cerebral Protective In Patients Undergoing Cardiac Valve Replacement With Cardiopulmonary Bypass

Objective: It has been well established that there is an incidence of braininjury after cardiac surgery with cardiopulmonary bypass （CPB）. Severaletiologies are hypothesized and include embolism, ischemia-reperfusioninjury, hypoperfusion and the systemic inflammatory response that can occurduring surgery. Gaseous micro embolism, occurring particularly during openchamber surgery, is one of emboli in brain. Some researches showed thatcarbon dioxide （CO₂） field flooding could markedly decreases the incidenceof air microemboli, but its effect on brain injury after cardiac surgery withCPB is uncertain now. The goal of the present study was to observe thedynamic change of blood plasma S-100β protein and neuron specific enolase（NSE） in the process of cardiac surgery with CPB; to observe the effect ofcarbon dioxide （CO₂） field flooding on the level of S-100β protein and NSE,and eventually to find the potential cerebral protective effect on patientsundergoing cardiac valve replacement with CPB after CO₂field floodingduring this surgery.Methods: Forty patients with rheumatic heart disease undergoingcardiac valve replacement surgery were randomly designed into CO₂fieldflooding group （group Ⅰ, n=20） and control group （group Ⅰ, n=20）. Thepatients with a history of neurologic events or carotid stenosis were excludedfrom the trial. All patients were anaesthetized by intravenous combined withinhalation, and CPB was conducted with mild hemodilution and hypothermia. In group Ⅰ, at the time of establishing CPB, a gas diffuser （left atriumdrainage tube） with CO2was insufflated into the cardiothoracic wound whichwas placed5cm below the wound opening adjacent to the diaphragm, and theCO2flow was set at4or5L/min. The CO2was insufflated into thecardiothoracic wound before opening right atrium, and was closed when atrialseptal closed. Blood samples was collected following5time points: beforeanesthesia induction （T1）, immediately release of the aortic crossclamp （T2）,2h after the end of CPB （T3）,6h after the end of CPB（T4） and24h after theend of CPB （T5）. The concentration of blood plasma S-100β protein and NSEwere detected by chemiluminescence immunoassay.Results: All patients survived the procedure. There were no significantdifference between the general information of patients in the two groups（P>0.05）. The level of S-100β protein and NSE changed in different timepoint. The density of blood plasma S-100β protein and NSE of two groupswere normal before anesthesia induction, and which reached a peak atimmediately release of the aortic crossclamp （T2）, then gradually declined atthe T3, T4and T5. Immediately release of the aortic crossclamp,6hour and24hour after the end of CPB, the level of blood plasma S-100β protein andNSE were deceased than those before anesthesia induction in the controlgroup. The level of blood plasma S-100β protein and NSE in the group Ⅰwere lower than those in the group Ⅰ at2hours and6hours after CPB （P＜0.05）, furthermore, NSE protein in the group Ⅰwere lower than those in thegroup Ⅰ at24hours after CPB （P＜0.05）.Conclusions:1. the level of S-100β protein and NSE changed indifferent time point. The density of blood plasma S-100β protein and NSE oftwo groups were normal before anesthesia induction, reached a peak at immediately release of the aortic crossclamp, then gradual declined.2carbondioxide field flooding can decrease the release of blood plasma S-100βprotein and NSE, and finally attenuate cerebral injury during cardiac valvereplacement with CPB.