摘要
目的观察纳洛酮(NAL)、山莨菪碱对休克失代偿期血管收缩反应性和一氧化氮(NO)的影响,探讨两者休克治疗的机制。方法(1)改良Wigger法建立兔失血性休克模型,测定休克失代偿期;(2)休克模型18只随机分为对照组(A组,n=6)、NAL组(B组,n=6)和山莨菪碱组(C组,n=6);在失代偿期前10min,B组静注NAL(1mg/kg)、C组静注山莨菪碱(2mg/kg)预处理,A组静注等容的0.9%氯化钠注射液;(3)记录休克前、休克30、60、90、120、150、180min注射去甲肾上腺素(NA)后平均动脉压(MAP)变化值;检测相应时点血清NO浓度。结果(1)Wigger模型在休克60min后进入休克的失代偿期;(2)B组休克60、90、120min的MAP升高幅度大于A组(P<0.05);(3)C组休克60min的MAP升高幅度大于A组(P<0.05);(4)B组休克60、120min的NO浓度低于休克前(P<0.05),休克60、120、180min的NO浓度低于A组(P<0.05);(5)C组NO浓度组内比较无统计学意义(P>0.05),与A组间比较亦无统计学意义(P>0.05)。结论(1)NAL提高失血性休克失代偿期血管收缩反应性,可能与NAL通过降低血清NO浓度有关;(2)山莨菪碱不提高失血性休克失代偿期血管收缩反应性,但延缓了失代偿期的出现。
Objective To investigate the effect of naloxone(NAL) and anisodamine on vascular response to norepinephrine(NA) and the change of nitric oxide(NO) during the period of vascular hyposensitivity in hemorrhagic shock(HS). Methods 18 HS model of rabbits were divided into three groups: GA (n = 6), served as control; GB (n = 6), as NAL treatment; GC (n = 6), as anisodamine treatment. The vascular responsibility of constriction was measured with NE injecting during the period of vascular hyposensitivity in HS. At the same time, the concentrations of NO in the plasma were detected. Results ( 1 ) The vascular responsibility of constriction in the GB was markedly increased compared with GA. Meanwhile, plasma NO was decline compared with GA. (2)In the GC, the vascular responsibility of constriction and the concentrations of NO in the plasma was same as GA. Conclusion ( 1 ) NAL improves the vascular responsibility of constriction during the period of vascular hyposensitivity in HS, maybe NO plays an important role in regulating the contractility of vessel. ( 2 ) Anisodamine can not improve the vascular responsibility of constriction during the period of vascular hyposensitivity in the HS.
出处
《海南医学》
CAS
2009年第5期32-34,共3页
Hainan Medical Journal
关键词
失血性休克
纳洛酮
山莨菪碱
一氧化氮
Hemorrhagic shock
Vascular hyposensitivity
Naloxone
Anisodamine
Nitric oxide