摘要
目的建立兔急性脑挫伤实验模型,观察实施不同程度急性等容血液稀释(ANH)对血清S-100B蛋白和脑氧代谢指标的影响。方法实验兔24只随机分为对照组(C组)、轻度血液稀释组(H1组)、重度血液稀释组(H2组),每组8只。参照Feeneys自由落体打击方法建立急性脑挫伤模型。C组不进行血液稀释,H1、H2组于脑挫伤后行ANH,目标红细胞压积(Hct)分别为30%和15%。于打击脑组织前(T0)、打击后30 min(ANH前,T1)、ANH后2 h(T2)分别采集颈静脉血检测S-100B蛋白浓度、乳酸浓度(VLAC)、静脉血氧饱和度(SjvO2)及Hct。结果 T0时各组S-100B蛋白浓度、SjvO2、VLAC比较差异无统计学意义(P>0.05);T1时3组S-100B蛋白、VLAC较T0时升高,SjvO2降低(P>0.05),组间比较差异无统计学意义(P>0.05);T2时3组S-100B蛋白、VLAC较T0时明显升高,SjvO2降低(P<0.05),但H1组的升降幅度明显小于H2组和C组(P<0.05)。结论以Hct=30%为目标实施ANH有利于兔急性脑挫伤后脑组织的氧供和氧利用,减少继发性脑组织损害发生,而以Hct=15%为目标实施ANH反而加重继发性脑损害。
Objective To investigate the effects of acute normovolemic hemodilution on serum S-100B protein and cerebral oxygen metabolism in brain contusion rabbits.Methods Twenty four rabbits were randomly divided into control group（Group C）,mild hemodilution group（Group H1）,and severe hemodilution group（Group H2）.The acute brain contusion model was established according to Feeney＇s method.Hemodilution was carried out in Group H1 and Group H2 after brain contusion until target hematocrits（Hct） of 30% and 15% were reached,respectively,while no hemodilution was given in Group C.Blood samples were drawn at baseline（T0）,30 minutes（T1）,and 2 hours for determination of plasma level of S-100B protein,venous blood lactate concentration（VLAC）,O2 saturation of jugular venous blood（SjvO2） and Hct.Results There was no significant difference in S-100B,SjvO2 or VLAC among the three groups at T0.S-100B and VLAC was elevated while SjvO2 was reduced at T1 without significant difference（P〉0.05）.There was significant increase of S-100B and VLAC and reduction of SjvO2 T2（P〈0.05）,with significantly smaller changes in Group H1 comparing to Group H2 and group C（P〈0.05）.Conclusion ANH target Hct of 30% benefits oxygen supply and consumption of brain tissue in acute contusion so as to prevent secondary injury.
出处
《广东医学》
CAS
CSCD
北大核心
2010年第12期1505-1507,共3页
Guangdong Medical Journal
基金
广东省科技计划项目(编号:2006B36004011)
关键词
急性等容血液稀释
脑挫伤
S-100B蛋白
脑氧代谢
acute normovolemic hemodilution
brain contusion
S-100B protein
cerebral oxygen metabolism
