临床误诊误治
臨床誤診誤治
림상오진오치
CLINICAL MISDIAGNOSIS & MISTHERAPY
2014年
10期
100-102
,共3页
张战波%王力军%范立斌%刘彩霞
張戰波%王力軍%範立斌%劉綵霞
장전파%왕력군%범립빈%류채하
血液稀释%脑损伤%休克,出血性%脑氧代谢%大鼠,Sprague-Dawley
血液稀釋%腦損傷%休剋,齣血性%腦氧代謝%大鼠,Sprague-Dawley
혈액희석%뇌손상%휴극,출혈성%뇌양대사%대서,Sprague-Dawley
Hemodilution%Brain injuries%Shock,hemorrhagic%Cerebral oxygen metabolism%Rats,Sprague-Dawley
目的:观察血液稀释对颅脑外伤合并失血性休克大鼠脑氧代谢的影响。方法选择雄性SD大鼠30只,常规方法造模,分为脑外伤组、单纯休克组及脑外伤合并休克组各10只。观察3组造模成功后和补液后15、30及45 min动脉血氧饱和度、动脉血氧含量、血红蛋白及脑组织氧分压。结果3组血氧饱和度不同时点组间及组内差异无统计学意义(P>0.05)。补液完成后15、30及45 min时,单纯休克组及脑外伤合并休克组血红蛋白、血氧含量及脑组织氧分压较造模成功后明显下降(P<0.05),但不在输血范围,且以补液后15 min下降最明显,30及45 min后恢复;造模成功后脑外伤合并休克组脑组织氧分压均低于其余两组(P<0.05,P<0.01);单纯休克组及脑外伤合并休克组与脑外伤组补液后相同时点比较,仅脑组织氧分压差异有统计学意义(P<0.05,P<0.01),且脑外伤合并休克组较单纯休克组下降更明显(P<0.01)。结论颅脑外伤合并失血性休克后即使正规补液也可能会加重缺氧性脑损伤。
目的:觀察血液稀釋對顱腦外傷閤併失血性休剋大鼠腦氧代謝的影響。方法選擇雄性SD大鼠30隻,常規方法造模,分為腦外傷組、單純休剋組及腦外傷閤併休剋組各10隻。觀察3組造模成功後和補液後15、30及45 min動脈血氧飽和度、動脈血氧含量、血紅蛋白及腦組織氧分壓。結果3組血氧飽和度不同時點組間及組內差異無統計學意義(P>0.05)。補液完成後15、30及45 min時,單純休剋組及腦外傷閤併休剋組血紅蛋白、血氧含量及腦組織氧分壓較造模成功後明顯下降(P<0.05),但不在輸血範圍,且以補液後15 min下降最明顯,30及45 min後恢複;造模成功後腦外傷閤併休剋組腦組織氧分壓均低于其餘兩組(P<0.05,P<0.01);單純休剋組及腦外傷閤併休剋組與腦外傷組補液後相同時點比較,僅腦組織氧分壓差異有統計學意義(P<0.05,P<0.01),且腦外傷閤併休剋組較單純休剋組下降更明顯(P<0.01)。結論顱腦外傷閤併失血性休剋後即使正規補液也可能會加重缺氧性腦損傷。
목적:관찰혈액희석대로뇌외상합병실혈성휴극대서뇌양대사적영향。방법선택웅성SD대서30지,상규방법조모,분위뇌외상조、단순휴극조급뇌외상합병휴극조각10지。관찰3조조모성공후화보액후15、30급45 min동맥혈양포화도、동맥혈양함량、혈홍단백급뇌조직양분압。결과3조혈양포화도불동시점조간급조내차이무통계학의의(P>0.05)。보액완성후15、30급45 min시,단순휴극조급뇌외상합병휴극조혈홍단백、혈양함량급뇌조직양분압교조모성공후명현하강(P<0.05),단불재수혈범위,차이보액후15 min하강최명현,30급45 min후회복;조모성공후뇌외상합병휴극조뇌조직양분압균저우기여량조(P<0.05,P<0.01);단순휴극조급뇌외상합병휴극조여뇌외상조보액후상동시점비교,부뇌조직양분압차이유통계학의의(P<0.05,P<0.01),차뇌외상합병휴극조교단순휴극조하강경명현(P<0.01)。결론로뇌외상합병실혈성휴극후즉사정규보액야가능회가중결양성뇌손상。
Objective To investigate the effect of hemodilution on cerebral oxyen metabolism in the rat model of trau-matic brain injury ( TBI) complicated by hemorrhagic shock. Methods A total of 30 male SD rats were randomly divided into 3 groups:TBI group (n=10), shock group (n=10), and TBI and shock group (n=10). SaO2, CaO2, hemoglobin and PbrO2 were determined after model establishment and 15 min, 30 min and 45 min after hemodilution. Results There were no signifi-cant differences of SaO2 at different time points among the three groups (P>0. 05). At 15 min, 30 min and 45 min after fluid infusion, the levels of hemoglobin, CaO2 and PbrO2 decreased significantly in shock group and shock and TBI group ( P <0. 05), especially at 15 min, but it rose again at 30 min and 45 min. Both groups were not at the range of blood transfusion. Af-ter successful molding, PbrO2 in TBI and shock group was lower than that in other two groups (P<0. 05, P<0. 01). Only PbrO2 showed significant differences between shock group and TBI and shock group at different time points after hemodilution (P<0. 05, P<0. 01), and it decreased significantly in TBI and shock group (P<0. 01). Conclusion The fluid resuscitation may aggravate hypoxic cerebral injury after traumatic brain injury (TBI) with hemorrhagic shock, although regular treatment.