摘要
目的:探讨PEEP及失血性休克(HS)对内源性NO的影响。方法:健康杂种犬6只在PEEP〔0.98kPa,(10cmH2O)〕及失血性休克前后分别测定血浆中的NO浓度及肺动脉压,肺及全身血管阻力。结果:NO在PEEP后呈增加趋势,停止PEEP10分钟后升高约2.49μmol/L(P<0.05),30分钟后恢复至基础水平。失血性休克初始,血浆NO水平,与休克前相比差异不显著,休克30分钟时分别比休克前及休克初始下降约3μmol/L(P<0.01)和2μmol/L(P<0.05)。结论:PEEP导致PVRI及PAP升高,引起NO释放增加,有利于降低PEEP所致的肺动脉高压。失血性休克时,在循环指标显著降低的同时,NO浓度亦逐步下降,提示此时血压及血管阻力的降低并非由NO介导。NO的变化并不与循环指标的变化同步。
Objective:To investigate the effects of PEEP and hemorrhagic shock (HS) on endogenous NO production in six anesthetized healthy mongrel dogs Methods:After surgical preparation,all the dogs were ventilated (Simens 900B ventilator,FiO 2 0 3,20 bpm) with 10 cmH 2O PEEP lasting 20 min After spontaneous breath of 30 min,the dogs were bleeded from femoral artery to induce HS (MAP 6 kPa) The concentration of plasma NO was detected with luminol chemiluminecence technique Result:During 10 cmH 2O PEEP,pulmonary artery pressure(PAP),pulmonary vascular resistance index(PVRI) and systemic vascular resistance index(SVRI) increased significantly from 1 6±0 2 to 2 4±0 3 kPa,125 4±38 4 to 234 5±58 1 and 1974 0±333 9 to 3145 4±658 4 dyn sec -1 ·cm -5 ·m 2,respectively(P<0 01) The concentration of plasma NO unchanged significantly After withdrawal of PEEP,plasma NO level increased by 2 5 μmol/L(P<0 05)at 10 min and returned to the baseline at 30 min During HS,PAP decreased significantly(P<0 01) Plasma NO level remained stable (P>0 05) at the begining of HS,and decreased to 2 8±1 3 μmol/L(P<0 01) 30 min following HS Conclusion:The changes of endogenous NO level can play an important role in modulating pulmonary and peripheral vascular tension so as to maintain the steadiness of homeostasis during PEEP(>10cmH 2O) and HS,moreover,the changes of NO level and circulation parameters are not synchronous
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
1997年第5期279-281,共3页
Chinese Journal of Anesthesiology
关键词
休克
失血性休克
一氧化氮
Positive pressure respiration Shock,hemorrhagic Nitric oxide