体外循环中炎性反应对亚临床脑损伤的影响

Influence of inflammatory response during cardiopulmonary bypass on subclinical brain injury

目的:观察中低温体外循环期间脑循环中的炎性细胞因子肿瘤坏死因子α产生水平,并评价炎性反应与脑损伤标志性蛋白S100β蛋白水平的关系。方法:纳入四川大学华西医院心胸血管外科2003-01/06拟行人工心脏瓣膜置换术患者20例。麻醉诱导后经颈内静脉逆行放置导管至颈静脉球部,于体外循环前、稳定低温期、复温至33℃和体外循环后30min,分别成对抽取桡动脉和颈静脉球部血样检测肿瘤坏死因子α,于体外循环前和体外循环后30min,6,24,48h测量血浆S100β蛋白水平。结果:按实际处理分析,20例患者均进入结果分析。①血浆肿瘤坏死因子α水平:体外循环中较体外循环前明显增加(P<0.01),但仅在复温期和体外循环后30min观察到颈静脉和动脉肿瘤坏死因子α的差值,分别为(0.26±0.63)和(0.19±0.43)μg/L。②体外循环前后血浆S100β水平的变化:体外循环后30min达峰值,体外循环后48h恢复至体外循环前水平。③S100β与肿瘤坏死因子α水平关系:体外循环后30minS100β与肿瘤坏死因子α水平呈显著正相关(P<0.05,r=0.489);而S100β与颈静脉-动脉肿瘤坏死因子α差值和脑摄氧率均无显著相关性(P>0.05)。结论:中低温体外循环可激活脑的炎性反应,并引起血浆S100β蛋白水平增高;体外循环后血浆S100β水平与肿瘤坏死因子α水平只有一定的相关性。

AIM： To observe the level of tumor necrosis factor-α（TNF-α, a kind of inflammatory cytokines of cerebral circulation during hypothermic cardiopulmonary bypass （CPB）, and evaluate the correlation between inflammatory response and level of S100β protein（the marker protein of brain injury）. METHODS： Twenty patients who had scheduled to receive cardiac valve replacement in the Department of Cardiovascular ＆ Thoracic Suegery, Huaxi Hospital, Sichuan University were enrolled in our study from January to June 2003. After anesthesia induction, a retrograde internal jugular catheter was placed in the jugular bulb. Blood was sampled in radial artery and, jugular bulb to measure the level of TNF-α before CPB, in the stable hypothermic period, rewarming to 33 ℃ and 30 minutes after CPB. The level of serum S 100 β was measured before CPB, and 30 minutes, 6, 24 and 48 hours after CPB. RESULTS： Aeeording to the actual management, all the 20 patients were analyzed in the result. ①Although the serum level of TNF-α was increased significantly before CPB versus during CPB（P 〈 0.01）, the level of jugular arterial TNF-α gradients were only observed in re-warming period and 30 minutes after CPB,（0.26±0.63） and （0.19±0.43） μg/L respectively. ② Change of serum level of S 100 β： The serum level of S 100 β peaked 30 minutes after CPB, and returned to the basal level 48 hours after CPB. ③ Correlation between serum S 100 β level and TNF-α level： There was significantly positive correlation between serum S 100 β and TNF-α levels 30 minutes after CPB（P 〈 0.05, r=0.489）, However, There was no significant correlation of S 100 β with the jugular-arterial TNF-α gradient and cerebral oxygen extraction（P 〉 0.05）. CONCLUSION： The hypothermic CPB cam activate cerebral inflammatory response, and induce the serum level of S 100 β to increase. There is only some correlation between serum level of S 100 β and level of TNF-α after CPB.