中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2011年
12期
1259-1263
,共5页
急性颅脑损伤%心肌损伤%肿瘤坏死因子-α%ATP酶%Na+ -K+ -ATP酶%Ca2+-ATP酶%心肌肌钙蛋白Ⅰ%大鼠
急性顱腦損傷%心肌損傷%腫瘤壞死因子-α%ATP酶%Na+ -K+ -ATP酶%Ca2+-ATP酶%心肌肌鈣蛋白Ⅰ%大鼠
급성로뇌손상%심기손상%종류배사인자-α%ATP매%Na+ -K+ -ATP매%Ca2+-ATP매%심기기개단백Ⅰ%대서
Acute craniocerebral injury%Myocardial injury%Tumor necrosis factor-alpha%ATPase%Na + -K + -ATPase%Ca2 + -ATPase%Cardiac troponin%Rat
目的 观察大鼠急性颅脑损伤( ACI)后心肌ATP酶活性及血浆肿瘤坏死因子-α(TNF-α)含量的变化,探讨ACI后心肌损伤发生机制.方法 健康雄性SD大鼠64只随机(随机数字法)分为假手术对照组和模型组,每组分为2,6,24,72 h4个观察时相,每个时相8只大鼠.采用硬膜外自由落体打击法建立大鼠急性颅脑损伤模型,采用ELISA法测定血浆肌钙蛋白Ⅰ(cTnⅠ)和TNF-α含量及采用比色法测定心肌Na+-K+-ATP酶、Ca2+ -ATP酶活性,并观察心肌HE染色的病理形态学改变.结果 大鼠急性颅脑损伤后血浆cTnⅠ及TNF-α含量均升高(P＜0.05),心肌Na+ -K+ -ATP酶、Ca2+ -ATP酶活性均降低(P＜0.05)；心肌Na+ -K+ -ATP酶、Ca2+ -ATP酶活性与血浆cTnⅠ含量均呈负相关(r=0.357,r=0.557,P＜0.05),血浆TNF-α含量与cTnⅠ含量呈正相关(r =0.920,P＜0.05),HE染色可见心肌空泡变性、坏死伴有炎性细胞浸润等.结论 急性颅脑损伤可引起明显的心肌损伤,心肌ATP酶和TNF-α可能参与了急性颅脑损伤后的心肌损伤.
目的 觀察大鼠急性顱腦損傷( ACI)後心肌ATP酶活性及血漿腫瘤壞死因子-α(TNF-α)含量的變化,探討ACI後心肌損傷髮生機製.方法 健康雄性SD大鼠64隻隨機(隨機數字法)分為假手術對照組和模型組,每組分為2,6,24,72 h4箇觀察時相,每箇時相8隻大鼠.採用硬膜外自由落體打擊法建立大鼠急性顱腦損傷模型,採用ELISA法測定血漿肌鈣蛋白Ⅰ(cTnⅠ)和TNF-α含量及採用比色法測定心肌Na+-K+-ATP酶、Ca2+ -ATP酶活性,併觀察心肌HE染色的病理形態學改變.結果 大鼠急性顱腦損傷後血漿cTnⅠ及TNF-α含量均升高(P＜0.05),心肌Na+ -K+ -ATP酶、Ca2+ -ATP酶活性均降低(P＜0.05)；心肌Na+ -K+ -ATP酶、Ca2+ -ATP酶活性與血漿cTnⅠ含量均呈負相關(r=0.357,r=0.557,P＜0.05),血漿TNF-α含量與cTnⅠ含量呈正相關(r =0.920,P＜0.05),HE染色可見心肌空泡變性、壞死伴有炎性細胞浸潤等.結論 急性顱腦損傷可引起明顯的心肌損傷,心肌ATP酶和TNF-α可能參與瞭急性顱腦損傷後的心肌損傷.
목적 관찰대서급성로뇌손상( ACI)후심기ATP매활성급혈장종류배사인자-α(TNF-α)함량적변화,탐토ACI후심기손상발생궤제.방법 건강웅성SD대서64지수궤(수궤수자법)분위가수술대조조화모형조,매조분위2,6,24,72 h4개관찰시상,매개시상8지대서.채용경막외자유락체타격법건립대서급성로뇌손상모형,채용ELISA법측정혈장기개단백Ⅰ(cTnⅠ)화TNF-α함량급채용비색법측정심기Na+-K+-ATP매、Ca2+ -ATP매활성,병관찰심기HE염색적병리형태학개변.결과 대서급성로뇌손상후혈장cTnⅠ급TNF-α함량균승고(P＜0.05),심기Na+ -K+ -ATP매、Ca2+ -ATP매활성균강저(P＜0.05)；심기Na+ -K+ -ATP매、Ca2+ -ATP매활성여혈장cTnⅠ함량균정부상관(r=0.357,r=0.557,P＜0.05),혈장TNF-α함량여cTnⅠ함량정정상관(r =0.920,P＜0.05),HE염색가견심기공포변성、배사반유염성세포침윤등.결론 급성로뇌손상가인기명현적심기손상,심기ATP매화TNF-α가능삼여료급성로뇌손상후적심기손상.
Objective To investigate the changes of myocardial ATPase activity and plasma tumor necrosis factor- alpha (TNF- a) levels in rats with acute craniocerebral injury (ACI).Methods Sixtyfour male SD rats were randomly (random number) divided into sham group and model group.The observation intervals were set at 2 h,6 h,24 h and 72 h after ACI (n =8,at each interval).ACI model was established in rats by free falling objects hitting skull.Plasma levels of cardiac troponin Ⅰ (cTnⅠ) and TNF-αwere determined by using enzyme -linked immunosorbent assay (ELISA).And the myocardial Na +-K+ -ATPase and Ca2+ -ATPase activity changes were determined by colorimetric method.Then the pathological change of myocardium with HE staining were observed under light - microscopy.Results Plasma cTnⅠ and TNF-α levels increased (P ＜ 0.05),while myocardial Na+-K+-ATPase and Ca2+- ATPase activity decreased in the rats with ACI (P ＜ 0.05 ); There was a negative correlation between myocardial Na + -K + -ATPase、Ca2 + -ATPase activity and plasma Ievels of cTnI ( r =0.357,r =0.557,P ＜ 0.05),and positive correlation between plasma levels of TNF-α and cTnⅠ ( r =0.920,P ＜ 0.05 ).Vacuolar degeneration and necrosis with inflammatory cell infiltrates of myocardium were observed under light -microscopy.Conclusions ACI can lead to myocardial injury,resulting in increase in plasma cTnⅠ and TNF-αand decrease in myocardial ATPase activity.Decrease in myocardial ATPase and increase in TNF-αmay involve in the pathogenesis of myocardial injury after ACI.
