小型猪特异性麻醉颉颃剂对小型猪血浆RAAS的影响

Effects of the specifically antagonistic agent of XFM on plasma R-A-A-S in Miniature Pigs

为了研究小型猪特异性麻醉拮抗剂对小型猪血浆肾素-血管紧张素-醛固酮系统(RAAS)的影响,将14头中国实验用小型猪,随机分为单纯麻醉组(X/S组)和麻醉-催醒组(X/W组),肌肉注射小型猪特异性麻醉剂(XFM),记录麻醉前及麻醉后5 min、10 min、20 min、30 min无创血压和心率(HR);麻醉后30 min即刻,麻醉-催醒组肌肉注射小型猪特异性麻醉颉颉抗剂,单纯麻醉组肌肉注射相同量的生理盐水,并记录麻醉后32 min、35 min、40 min、60 min、90 min、120 min小型猪的无创血压及心率(HR),并于以上时间点采取前腔静脉血样。采用ELISA方法测定小型猪血浆中RAAS含量,并分析它们与心率和血压之间的相关性。结果显示,与对照组相比,在肌肉注射小型猪特异性麻醉颉颃剂后,无创血压、HR均明显的升高(P<0.01或P<0.05);小型猪血浆血管紧张素(AⅡ)浓度发生明显变化(P<0.05);血浆AⅡ的浓度与HR呈现显著负相关(P<0.05)。表明血浆中R-A-A-S参与了小型猪血流动力学变化的调节。

[Objective] The aim of this study was to investigate the effects of specificity Antagonist for Miniature Pigs Combined Anaesthetic on the plasma RAAS in miniature pigs. [ Method ] Fourteen Chinese experimental miniature pigs were anaesthesized with XFM intramuscularly, then animals were randomly divided into anesthesia group（X/S group） and anesthesia-wake-up group（X/W group）. Thirty minutes after the treatment, the X/W group was awakened with the specifically antagonistic agent of XFM, but the X/S group was administered with the same dosage of saline as the X/W group. Blood samples were collected before anaesthesia（O min） and at 5,10,20,30,32,35,40,60,90, and 120 min after injection of anaesthesic agents, and non-invasive arterial blood pressure and HR were monitored at the same timepoint. Plasma PRA. AII , ALD were determined by ELISA. and analyzed for the correlation with HR and blood pressure. [ Results ] After being injected with the specific antagonist for miniature pigs combined anaesthetic the Blood pressure and HR in X/W group increased significantly （P 〈0.05） compared with the X/S group in addition concentrations of A Ⅱ in plasma increased significandy and a negative correlation was observed between the A Ⅱ and HR （P 〈0.05）. [ Conclusion ] RAAS participated in the process of hemodynamic changes caused by specific antagonistic agent of XFM, and A Ⅱ may be one of the main reasons for these changes changing in the HR, which was caused by specific antagonistic agent of XFM.