模擬急進(jìn)高原過程對清醒和麻醉狀態(tài)大鼠血壓和呼吸的影響
[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.
【作者單位】: 青海大學(xué)醫(yī)學(xué)院;
【基金】:國家自然科學(xué)基金資助項(xiàng)目(No.81160012) 教育部新世紀(jì)優(yōu)秀人才項(xiàng)目(No.NCET-12-1022) 青海省自然科學(xué)基金資助項(xiàng)目(No.2012-Z-915Q) 青海大學(xué)醫(yī)學(xué)院中青年科研基金團(tuán)隊項(xiàng)目(No.2013-KT-4)
【分類號】:R594.3
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