摘要
目的:作者探讨高原(海拔3080m)缺氧对脓毒败血症性肺损伤的影响.方法:采用盲肠结扎穿孔方法复制脓毒败血症模型,采用 ̄125Ⅱ放免测定方法测定家兔静脉血中血栓素A_2(TXA_2),前列腺环素(PGI_2)和动脉壁内亮氨酸脑啡肽(L-ENK)的含量及小鼠死亡率的变化.结果:高原缺氧使动物24h累积死亡率(97.1%)显著增加;TXB_2含量是对照组的4倍,6-keto-PGF_(1α)含量也有增加;花生四烯酸代谢的改变可以被消炎痛所阻断;肠、肾及肺动脉壁内L-ENK含量明显降低(P<0.01);支气管肺泡灌洗液中白蛋白含量明显增加(P<0.01).结论:结果表明环氧酶代谢产物不是肺通透性的主要介质,TXA_2和L-ENK的变化可能是脓毒败血症时肺动脉压增高、肺血管阻力增加的机制之一.
Objective: The aim is to explore the effects of altitude(3080 m above sea level) hypoxia on septicpulmonary injury. Methods :A model of septicemia induced by cecal ligation and puncture,thromboxane A_2(TXA_2),prostacyclin (PGI_2 ) of the venous plasma and leucine-enkephalins (L-ENK)in the arterial wallswere measured by using radioimmunoassay in 31 rabbits,and mouse mortality was observed.Results : 24-haccumulative mortality of mouse(97.1%)was greater than that of control(35%); TXB_2 was as 4 timesmuch as the concentration of control group and 6-keto-PGF_(1α) was elevated too. These changes of arachidonicmetabolism could be blocked by indomethasin. The content of L-ENK in arterial walls of pulmonary,mesen-teric and renal arteries decreased significantly compared with control group(P<0.01).The albumin contentof the bronchoalveolar lavage fluid increased significantly compared with control group(P<0.01 ).Conclu-sion: The results demonstrate that the metabolites of cyclooxygenase are not the major mediators to increasepulmonary permeability in the experiment.The content alteration of TXA_2 and L-ENK may be one of themechanisms,by which the pulmonary artery pressure and pulmonary vascular resistance increased during sepsis.
出处
《第四军医大学学报》
1995年第1期36-38,共3页
Journal of the Fourth Military Medical University
关键词
缺氧
高原
脓毒败血症
肺损伤
血栓素A2
PGI2
altitude
hypoxsia
septicemia
lung injury
thromboxane A_2
prostacyclin
leu-enkephalins