中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2013年
4期
368-371
,共4页
胡四平%汪卫星%刘洋%吴鹤芬%余亮%刘鹤
鬍四平%汪衛星%劉洋%吳鶴芬%餘亮%劉鶴
호사평%왕위성%류양%오학분%여량%류학
肺损伤%休克,出血性%高渗溶液
肺損傷%休剋,齣血性%高滲溶液
폐손상%휴극,출혈성%고삼용액
Lung injury%Shock,hemorrhagic%Hypertonic solutions
目的 探讨高渗高胶液(4.5g/ml氯化钠联合6.0 g/ml羟乙基淀粉,简称HHS)对肺创伤合并失血性休克兔脑保护作用及其可能机制. 方法 30只新西兰大耳白兔按随机数字表法分为三组:A组为对照组,B组为乳酸林格液(LRS)组,C组为HHS组;每组10只.B、C组建立肺创伤合并失血性休克模型,休克维持60 min后,以3倍失血量的LRS和5ml/kg的HHS分别对两组兔进行液体复苏.复苏后4h处死各组动物并取脑组织,荧光显微镜下观察各组脑组织顶叶皮层伊文蓝渗出情况,称量并计算脑含量水,TUNEL法检测凋亡神经元,Western blot检测Bcl-2和Bax蛋白表达. 结果 与A组比较,B组顶叶皮层有大量伊文蓝渗出,脑含水量显著增加,并出现大量凋亡神经元,Bcl-2和Bax蛋白表达增加,但Bcl-2/Bax比例降低(P<0.01);与B组比较,C组顶叶皮层伊文蓝渗出明显减少,脑含水量显著降低,凋亡神经元数量减少,Bcl-2/Bax比例显著增高(P<0.05). 结论 HHS通过改善血脑屏障功能、抑制神经元凋亡对肺创伤合并失血性休克兔脑起到一定的保护作用.
目的 探討高滲高膠液(4.5g/ml氯化鈉聯閤6.0 g/ml羥乙基澱粉,簡稱HHS)對肺創傷閤併失血性休剋兔腦保護作用及其可能機製. 方法 30隻新西蘭大耳白兔按隨機數字錶法分為三組:A組為對照組,B組為乳痠林格液(LRS)組,C組為HHS組;每組10隻.B、C組建立肺創傷閤併失血性休剋模型,休剋維持60 min後,以3倍失血量的LRS和5ml/kg的HHS分彆對兩組兔進行液體複囌.複囌後4h處死各組動物併取腦組織,熒光顯微鏡下觀察各組腦組織頂葉皮層伊文藍滲齣情況,稱量併計算腦含量水,TUNEL法檢測凋亡神經元,Western blot檢測Bcl-2和Bax蛋白錶達. 結果 與A組比較,B組頂葉皮層有大量伊文藍滲齣,腦含水量顯著增加,併齣現大量凋亡神經元,Bcl-2和Bax蛋白錶達增加,但Bcl-2/Bax比例降低(P<0.01);與B組比較,C組頂葉皮層伊文藍滲齣明顯減少,腦含水量顯著降低,凋亡神經元數量減少,Bcl-2/Bax比例顯著增高(P<0.05). 結論 HHS通過改善血腦屏障功能、抑製神經元凋亡對肺創傷閤併失血性休剋兔腦起到一定的保護作用.
목적 탐토고삼고효액(4.5g/ml록화납연합6.0 g/ml간을기정분,간칭HHS)대폐창상합병실혈성휴극토뇌보호작용급기가능궤제. 방법 30지신서란대이백토안수궤수자표법분위삼조:A조위대조조,B조위유산림격액(LRS)조,C조위HHS조;매조10지.B、C조건립폐창상합병실혈성휴극모형,휴극유지60 min후,이3배실혈량적LRS화5ml/kg적HHS분별대량조토진행액체복소.복소후4h처사각조동물병취뇌조직,형광현미경하관찰각조뇌조직정협피층이문람삼출정황,칭량병계산뇌함량수,TUNEL법검측조망신경원,Western blot검측Bcl-2화Bax단백표체. 결과 여A조비교,B조정협피층유대량이문람삼출,뇌함수량현저증가,병출현대량조망신경원,Bcl-2화Bax단백표체증가,단Bcl-2/Bax비례강저(P<0.01);여B조비교,C조정협피층이문람삼출명현감소,뇌함수량현저강저,조망신경원수량감소,Bcl-2/Bax비례현저증고(P<0.05). 결론 HHS통과개선혈뇌병장공능、억제신경원조망대폐창상합병실혈성휴극토뇌기도일정적보호작용.
Objective To investigate effect of hypertonic-hyperoncotic solution (HHS,namely 4.5 g/ml NaCl plus 6.0 g/ml hydroxyethyl starch) on brain protection in rabbits with pulmonary trauma combined with hemorrhagic shock and the possible mechanism.Methods Thirty New Zealand white rabbits were randomly divided into control group (Group A),lactated Ringer' s solution (LRS) treatment group (Group B) and HHS treatment group (Group C),with 10 rabbits per group.Models of pulmonary trauma with hemorrhagic shock were established in Groups B and C.Later,fluid resuscitation,including LRS at 3-fold the volume of blood loss and HHS at dose of 5 mL/kg,was respectively given for Groups B and C at 60 minutes after shock.Rabbits in each group were sacrificed at 4 hours after resuscitation for brain tissue harvest.Evan blue exudation in the parietal cortex of rabbit brain in each group was observed by fluorescence microscope.Brain water content was weighed and calculated.Neuron apoptosis was tested by TUNEL method.Expressions of Bcl-2 and Bax proteins were detected by Western blot.Resalts Group B showed massive exudation of Evan blue,notable increase of brain water content,large apoptosis of neurons,up-regulation of Bcl-2 and Bax proteins,but a decline of Bcl-2 to Bax ratio,as compared with Group A (P < 0.01).However,Group C showed significant decrease regarding Evan blue exudation,brain water content and apoptotic neurons,and significant increase of ratio of Bcl-2 and Bax,as compared with Group B (P < 0.05).Conclusion HHS improves blood brain barrier,inhibits neuron apoptosis and thus protects brain function.