模拟急进高原过程对清醒和麻醉状态大鼠血压和呼吸的影响

发布时间：2018-10-12 09:26

【摘要】：目的:为了全面地反映急进高原过程中机体的一些真实改变,本实验通过动态监测清醒和麻醉2种不同状态下大鼠血流动力学指标,旨在探讨清醒和麻醉状态大鼠在急性缺氧时血流动力学的差异,并以此进一步探讨其可能的机制。方法:实验将SD大鼠随机分为麻醉组、清醒组、5 000 m麻醉对照(A-5000-control)组、5 000m麻醉氨基胍(A-5000-AG)组、5 000 m清醒对照(C-5000-control)组和5 000 m清醒氨基胍(C-5000-AG)组。麻醉组和清醒组大鼠在低压氧舱从2 260 m开始,以2 m/s模拟急进高原5 000 m过程;其余4组均在模拟5 000 m海拔条件下进行。实验期间通过Power Lab生理记录仪实时、动态地监测整个过程中大鼠的系统动脉压(system arterial pressure,Psa)、中心静脉压(central venous pressure,CVP)、心率(heart rate,HR)和呼吸频率(breathing rate,BR)。结果:清醒组大鼠的HR和BR明显高于麻醉组,但MAP明显低于麻醉组。随着海拔的逐渐升高,清醒组和麻醉组大鼠均出现平均动脉压(mean arterial pressure,MAP)降低,且清醒组大鼠降低更为显著。另外,在5 000 m时,清醒组大鼠HR明显降低,而整个过程中2组大鼠的BR均无明显改变。静脉注射诱导型一氧化氮合酶(inducible nitric oxide synthase,i NOS)抑制剂氨基胍后,C-5000-AG组和A-5000-AG组大鼠动脉血压均明显升高,而HR和BR未见明显变化。结论:在急进高原过程中,血压和心率会明显下降,而呼吸频率变化不大。该现象可能的机制为:急性缺氧早期机体启动自我保护机制,活化i NOS,大量产生并释放NO,使血管舒张,可调节肺通气、引起血压下降;达到海拔5 000 m左右甚至更早时,机体可能出现失代偿,使心率减慢,引起血压进一步降低。由于受麻醉药物戊巴比妥钠的影响,麻醉状态的大鼠血压下降出现得较为迟缓,而清醒大鼠对急进高原性低氧反应迅速,能够更真实全面地反映急进高原过程中低氧引起的血流动力学改变。
[Abstract]:Objective: in order to reflect the real changes of the body in the course of rapid advance into high altitude, the hemodynamic indexes of rats under two different states of wakefulness and anaesthesia were monitored dynamically in this experiment. The purpose of this study was to explore the difference of hemodynamics between conscious and anesthetized rats during acute hypoxia, and to further explore its possible mechanism. Methods: SD rats were randomly divided into anaesthesia group, awake group, 5 000 m anesthetic control group (A-5000-control), 5 000 m anesthetic aminoguanidine (A-5000-AG) group, 5 000 m awake control group (C-5000-control) and 5 000 m clear aminoguanidine (C-5000-AG) group. The anaesthetized and awake rats in the hypobaric oxygen chamber began at 2 260 m and simulated the rapid advance to the altitude of 5 000 m with 2 m / s, while the other 4 groups were all simulated at 5 000 m altitude. During the experiment, the systemic arterial pressure (system arterial pressure,Psa), central venous pressure (central venous pressure,CVP), heart rate (heart rate,HR) and respiratory frequency (breathing rate,BR) were dynamically monitored by Power Lab physiological recorder. Results: the HR and BR of conscious group were significantly higher than that of anesthesia group, but MAP was significantly lower than that of anesthesia group. With the increase of altitude, the mean arterial pressure (mean arterial pressure,MAP) decreased in both awake group and anesthetic group, and the decrease was more significant in awake group. In addition, at 5 000 m, the HR of the conscious group decreased significantly, but the BR of the two groups did not change significantly during the whole process. After intravenous injection of aminoguanidine, an inhibitor of inducible nitric oxide synthase (inducible nitric oxide synthase,i NOS), arterial blood pressure was significantly increased in both C-5000-AG and A-5000-AG groups, but HR and BR did not change significantly. Conclusion: the blood pressure and heart rate decreased significantly, but the respiratory frequency did not change. The possible mechanism of this phenomenon is that during the early stage of acute hypoxia, the body starts to protect itself by activating I NOS, to produce and release NO, in large quantities, which can relax blood vessels, regulate pulmonary ventilation and cause blood pressure to decrease, and reach 5 000 m or earlier at altitude. Decompensation may occur, slowing the heart rate and further lowering blood pressure. Under the influence of pentobarbital sodium, the blood pressure of anesthetized rats decreased slowly, while the conscious rats reacted quickly to the acute altitude hypoxia. It can more truly reflect the hemodynamic changes caused by hypoxia during the rapid advance into the plateau.
【作者单位】：青海大学医学院;
【基金】：国家自然科学基金资助项目(No.81160012) 教育部新世纪优秀人才项目(No.NCET-12-1022) 青海省自然科学基金资助项目(No.2012-Z-915Q) 青海大学医学院中青年科研基金团队项目(No.2013-KT-4)
【分类号】：R594.3

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