【摘要】：目的:為了全面地反映急進高原過程中機體的一些真實改變,本實驗通過動態(tài)監(jiān)測清醒和麻醉2種不同狀態(tài)下大鼠血流動力學指標,旨在探討清醒和麻醉狀態(tài)大鼠在急性缺氧時血流動力學的差異,并以此進一步探討其可能的機制。方法:實驗將SD大鼠隨機分為麻醉組、清醒組、5 000 m麻醉對照(A-5000-control)組、5 000m麻醉氨基胍(A-5000-AG)組、5 000 m清醒對照(C-5000-control)組和5 000 m清醒氨基胍(C-5000-AG)組。麻醉組和清醒組大鼠在低壓氧艙從2 260 m開始,以2 m/s模擬急進高原5 000 m過程;其余4組均在模擬5 000 m海拔條件下進行。實驗期間通過Power Lab生理記錄儀實時、動態(tài)地監(jiān)測整個過程中大鼠的系統(tǒng)動脈壓(system arterial pressure,Psa)、中心靜脈壓(central venous pressure,CVP)、心率(heart rate,HR)和呼吸頻率(breathing rate,BR)。結果:清醒組大鼠的HR和BR明顯高于麻醉組,但MAP明顯低于麻醉組。隨著海拔的逐漸升高,清醒組和麻醉組大鼠均出現(xiàn)平均動脈壓(mean arterial pressure,MAP)降低,且清醒組大鼠降低更為顯著。另外,在5 000 m時,清醒組大鼠HR明顯降低,而整個過程中2組大鼠的BR均無明顯改變。靜脈注射誘導型一氧化氮合酶(inducible nitric oxide synthase,i NOS)抑制劑氨基胍后,C-5000-AG組和A-5000-AG組大鼠動脈血壓均明顯升高,而HR和BR未見明顯變化。結論:在急進高原過程中,血壓和心率會明顯下降,而呼吸頻率變化不大。該現(xiàn)象可能的機制為:急性缺氧早期機體啟動自我保護機制,活化i NOS,大量產(chǎn)生并釋放NO,使血管舒張,可調(diào)節(jié)肺通氣、引起血壓下降;達到海拔5 000 m左右甚至更早時,機體可能出現(xiàn)失代償,使心率減慢,引起血壓進一步降低。由于受麻醉藥物戊巴比妥鈉的影響,麻醉狀態(tài)的大鼠血壓下降出現(xiàn)得較為遲緩,而清醒大鼠對急進高原性低氧反應迅速,能夠更真實全面地反映急進高原過程中低氧引起的血流動力學改變。
[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】： 青海大學醫(yī)學院;
【基金】：國家自然科學基金資助項目(No.81160012) 教育部新世紀優(yōu)秀人才項目(No.NCET-12-1022) 青海省自然科學基金資助項目(No.2012-Z-915Q) 青海大學醫(yī)學院中青年科研基金團隊項目(No.2013-KT-4)
【分類號】：R594.3

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