CAJ | 학술논문

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、5000 m麻醉对照（ A-5000-control）组、5000 m麻醉氨基胍（ A-5000-AG）组、5000 m清醒对照（ C-5000-control）组和5000 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2260 m开始，以2 m／s模拟急进高原5000 m过程；其余4组均在模拟5000 m海拔条件下进行。实验期间通过PowerLab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5000 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，iNOS）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iNOS，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5000 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。目的：為瞭全麵地反映急進高原過程中機體的一些真實改變，本實驗通過動態鑑測清醒和痳醉2種不同狀態下大鼠血流動力學指標，旨在探討清醒和痳醉狀態大鼠在急性缺氧時血流動力學的差異，併以此進一步探討其可能的機製。方法：實驗將SD大鼠隨機分為痳醉組、清醒組、5000 m痳醉對照（ A-5000-control）組、5000 m痳醉氨基胍（ A-5000-AG）組、5000 m清醒對照（ C-5000-control）組和5000 m清醒氨基胍（ C-5000-AG）組。痳醉組和清醒組大鼠在低壓氧艙從2260 m開始，以2 m／s模擬急進高原5000 m過程；其餘4組均在模擬5000 m海拔條件下進行。實驗期間通過PowerLab生理記錄儀實時、動態地鑑測整箇過程中大鼠的繫統動脈壓（ 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明顯高于痳醉組，但MAP明顯低于痳醉組。隨著海拔的逐漸升高，清醒組和痳醉組大鼠均齣現平均動脈壓（ mean arterial pressure，MAP）降低，且清醒組大鼠降低更為顯著。另外，在5000 m時，清醒組大鼠HR明顯降低，而整箇過程中2組大鼠的BR均無明顯改變。靜脈註射誘導型一氧化氮閤酶（ inducible nitric oxide synthase，iNOS）抑製劑氨基胍後，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。該現象可能的機製為：急性缺氧早期機體啟動自我保護機製，活化iNOS，大量產生併釋放NO，使血管舒張，可調節肺通氣、引起血壓下降；達到海拔5000 m左右甚至更早時，機體可能齣現失代償，使心率減慢，引起血壓進一步降低。由于受痳醉藥物戊巴比妥鈉的影響，痳醉狀態的大鼠血壓下降齣現得較為遲緩，而清醒大鼠對急進高原性低氧反應迅速，能夠更真實全麵地反映急進高原過程中低氧引起的血流動力學改變。
목적：위료전면지반영급진고원과정중궤체적일사진실개변，본실험통과동태감측청성화마취2충불동상태하대서혈류동역학지표，지재탐토청성화마취상태대서재급성결양시혈류동역학적차이，병이차진일보탐토기가능적궤제。방법：실험장SD대서수궤분위마취조、청성조、5000 m마취대조（ A-5000-control）조、5000 m마취안기고（ A-5000-AG）조、5000 m청성대조（ C-5000-control）조화5000 m청성안기고（ C-5000-AG）조。마취조화청성조대서재저압양창종2260 m개시，이2 m／s모의급진고원5000 m과정；기여4조균재모의5000 m해발조건하진행。실험기간통과PowerLab생리기록의실시、동태지감측정개과정중대서적계통동맥압（ system arterial pressure， Psa）、중심정맥압（ central venous pressure， CVP）、심솔（ heart rate， HR）화호흡빈솔（ breathing rate， BR）。결과：청성조대서적HR화BR명현고우마취조，단MAP명현저우마취조。수착해발적축점승고，청성조화마취조대서균출현평균동맥압（ mean arterial pressure，MAP）강저，차청성조대서강저경위현저。령외，재5000 m시，청성조대서HR명현강저，이정개과정중2조대서적BR균무명현개변。정맥주사유도형일양화담합매（ inducible nitric oxide synthase，iNOS）억제제안기고후，C-5000-AG조화A-5000-AG조대서동맥혈압균명현승고，이HR화BR미견명현변화。결론：재급진고원과정중，혈압화심솔회명현하강，이호흡빈솔변화불대。해현상가능적궤제위：급성결양조기궤체계동자아보호궤제，활화iNOS，대양산생병석방NO，사혈관서장，가조절폐통기、인기혈압하강；체도해발5000 m좌우심지경조시，궤체가능출현실대상，사심솔감만，인기혈압진일보강저。유우수마취약물무파비타납적영향，마취상태적대서혈압하강출현득교위지완，이청성대서대급진고원성저양반응신속，능구경진실전면지반영급진고원과정중저양인기적혈류동역학개변。
AIM:This study continuously monitors the hemodynamic changes in conscious and anesthetic rats during rapid ascent to high altitude to investigate whether there is difference between the 2 conditions and discuss the rela-ted underlying mechanism.METHODS: Sprague-Dawley rats were randomly divided into conscious group, anesthetic group, anesthetic-5000-control ( A-5000-control) group, anesthetic-5000-aminoguanidine ( A-5000-AG) group, conscious-5000-control ( C-5000-control ) group and conscious-5000-aminoguanidine ( C-5000-AG ) group.The rats in anesthetic group and conscious group were kept in a hypobaric chamber, in which the simulated altitude was increased from 2 260 m to 5 000 m at 2 m/s, and the rats in other 4 groups were at 5 000 m.The system arterial pressure ( Psa) , central venous pressure ( CVP) , heart rate ( HR) and breathing rate ( BR) were directly and continuously displayed and digitally recorded by a high-performance data acquisition (PowerLab 16/35, AD Instruments) at 200 Hz.RESULTS: The HR and BR in the conscious rats were higher and MAP was lower than those in the anesthetic rats obviously.A significant decrease in mean arterial pressure ( MAP) in conscious and anesthetic groups was observed following the increase in the altitude levels, and the net decrease in MAP in conscious group was significantly greater.Additionally, HR in the conscious rats was sig-nificantly lower at 5 000 m than that of the initial level.The rats in C-5000-AG group and A-5000-AG group showed a sig-nificant increase in the arterial pressure after the intravenous injection of AG, a selective inhibitor of inducible nitric oxide synthase ( iNOS) , and no marked change of HR and BR was found.CONCLUSION: Blood pressure and HR decrease during rapid ascent to high altitude, while the change of BR is not obvious.The mechanisms of self-safety would be trig-gered in the early stage of hypoxia, which activates iNOS and then leads to a larger number of nitric oxide.Plentiful NO di-astolizes the vessels to improve the ventilation-perfusion mismatch and lower the blood pressure.When the altitude arise to 5 000 m, even more earlier, a decompensatory stage may occur in the body, leading to decreased HR and blood pressure further more than those in the anesthetic rats.Due to the effects of pentobarbital sodium, the depression of blood pressure requires a lag period and the net decrease in MAP is less than that in the conscious rats.Therefore, hemodynamic changes during rapid ascent to high altitude in conscious rats are more comprehensive and authentic.