纳络酮对失血性休克失代偿期血管收缩低反应性影响与血一氧化氮浓度变化的研究

目的研究纳络酮（NAL）对失血性休克低反应期儿茶酚胺类缩血管药物升压效应及对一氧化氮（NO）的影响。探讨抗休克的机制。方法建立兔的失血性休克模型，间断静注去甲肾上腺素（NA），通过平均动脉压改变的幅度来测定失血性休克低反应期时段。大白兔12只，建立失血性休克模型后随机分成对照组6只，NAL治疗组6只。通过静脉注射NA，研究休克低反应期的血管收缩反应性；检测两组模型在休克前、后多个时点血清中NO浓度。结果失血性休克低反应期，NAL组的血管收缩反应性高于对照组；随着NAL作用的减退，血管收缩反应性也随之降低。NAL治疗组血清中NO浓度在低反应期明显低于对照组。结论NAL能够提高失血性休克低反应期的血管收缩反应性，NAL可能是通过降低血浆NO浓度来改善血管收缩反应性。

Effect of naloxone on vascular response to norepinephrine and the change of nitric oxide during the period of vascular hyposensitivity in hemorrhagic shock rabbit

Objective The purppse of the study is to investigate whether naloxone effects at the vascular hypo-responsiveness to norepinephrine and the change of nitric oxide in hemorrhagic shock. Methods Twelve hemorrhagic shock rabbits were prepared by withdrawing blood. Rabbits were divided in two groups：group A （n =6） ,served as control,group B （n =6）,as naloxone treatment. In the group B,naloxonc was given at 50 minutes after hemorrhagic shock. In the group A, same volume saline was given. The vascular responsibility of constriction was measured by monitoring the changes of the mean arterial pressure after the norepinephrine was injected. At the same time,the activity of plasma nitric oxide were detected at 60 minutes, 120 minutes, 180 minutes after hemorrhagic shock. Results The vascular response was hyper-responsive to norepincphrine at 30 minutes after hemorrhagic shock and hypo-responsive after one hour of hemorrhagic shock. 60 minutes after treatment with naloxone. The vascular responsibility of constriction in the group B was markedly increased compared with group A. Meanwhile, plasma nitric oxide was declined compared with group A, and it was closely related to the significant elevation of the mean arterial pressure. Conclusion naloxone improve the vascular response to norepinephrine during the period of vascular hyposensitivity in hemorrhagic shock rabbits and nitric oxide plays an important role in vascular hyposensitivity.