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白细胞在创伤后心功能不全中的作用 被引量:4

The role of leukocytes in post-traumatic cardiac dysfunction
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摘要 目的 探讨创伤后心肌组织是否存在着白细胞浸润 ,并研究白细胞在心脏功能不全中的作用。方法 麻醉后的雄性小鼠被随机分为创伤组和对照组 (2 5只 /组 ) ,在创伤后 6h测定两组小鼠平均动脉压(MAP)、心脏功能指标和心肌组织髓过氧化物酶 (MPO)活性。结果 创伤组小鼠出现了明显的低血压和心脏功能不全 [创伤组平均动脉压 (MAP)、等容收缩期室内压最大变化速率 (+dp dtmax) ,心脏指数(CI)分别为 (70± 9)mmHg ,(3492± 2 76 )mmHg/s ,(6 2± 6 )ml/min/ 10 0g ;对照组分别为 (90± 8)mmHg ,(474 5± 2 19)mmHg/s,(72± 7)ml/min/ 10 0g ,P <0 0 5 ];创伤组小鼠心肌组织MPO活性明显增高 [创伤组为 (8 4 6± 1 70 )U/ 10 0mg ,对照组为 (4 5 2± 0 94 )U/ 10 0mg,P <0 0 5 ],且MPO活性与心脏功能呈明显负相关。结论 创伤后心肌组织的炎症反应是导致创伤后心功能不全的一个重要因素 。 Objective To determine whether leukocyte infiltration in heart tissue,and to explore its role in post-traumatic cardiac dysfunction.Methods Aneasthetized male mice were randomly divided into traumatic group and sham group(n=25/group).Six hours after treatment,the mean arterial pressure and cardiac function parameters were measured,and the cardiac myeloperoxidase activity was assayed.Results In traumatic group,there existed a severe cardiac dysfunction manifested by reduced arterial blood pressure(70±9)mmHg (compared with sham group,P<0.05),decreased left ventricular (3492±276)mmHg/s (compared with sham group,P<0.05),and reduced cardiac contratility index(62±6) (compared with sham group,P<0.05).Traumatic group also significantly increased cardiac MPO activity(8.46±1.70) (compared with sham group,P<0.05).There was a significant negative correlation between MPO activity and cardiac funciton in traumatic.Conclusion The inflammatory reaction in cardiac tissue after traumatic injury may play an important role in cardiac dysfunction,this suggests that anti-inflammatory treatment may improve psot-traumatic cardiac dysfunction.
出处 《中华急诊医学杂志》 CAS CSCD 2003年第8期527-529,共3页 Chinese Journal of Emergency Medicine
关键词 白细胞 创伤 心功能不全 作用 麻醉 创伤性休克 中性粒细胞 多器官功能衰竭综合征 Shock,traumatic Nerutrophils Inflammation Multiple organ dysfunction syndrome
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  • 1Campbell B, Chuhran C, Lefer AM. Vascular endothlial growth factor attenuates trauma-induced injuty in rats. Br J Pharmacol, 2000, 129:71-76
  • 2Aldridge AJ. Role of the neutrophil in septic shock and the adult respiratory distress syndrom. Eur J Surg, 2002, 168:204-214.
  • 3Gao F, Yue TL, Shi DW, et al. P38MAPK ingibition reduces myocardial reperfusion injury via ingibithon of endothelial adhesion molecule expression and blockade of PMN accumulation. Cardiovase Res, 2002, 53: 414-22.
  • 4Hantaway RM. Tramatic shock alias psottrauma critical illness. Am Surg 2000, 66: 284-290.
  • 5Gando S. Disseminated intravaseular coagulation in trauma patients.Semin Thromb Hemost, 2001, 27: 585-592.
  • 6Zhao Z, Viten-Johansvn J. Myocardial apoptosis and ischemic preconditioning. Cardiovasc Res, 2002, 55: 438-455.
  • 7Suzuki K, Murtuza B, Smolenski RT, et al. Overexpression of interleukin-1 receptor antagonist provides cardioprotection against ischemia-repcrfusion ijury associated with reduction in apoptosis.Circulation, 2001, 104:1308-1313.
  • 8Pruefer D, Buerke U, Khalil M, et al. Cardioprotective effects of the serine protease inhibitor aprotinin after regional ischemia and repcrfusion on the beating heart. J Thorac Cardiovasc Surg, 2002, 124: 942-949.
  • 9Aardaway RM, Vasques Y. A shock toxin that produces diseminated intravascular coagulation and multiple organ failure. Am J Med Sci,2001, 322: 222-228.

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