中国青年男性急性高原暴露后急性高原病危险因素分析:高原野外现场的队列研究
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摘要
目的探讨急性高原暴露后发生急性高原病(AMS)的危险因素及其预测因子。方法该研究为队列研究,共纳入83位受试者,从成都乘飞机空运至拉萨。根据AMS评分(LLS AMS scores 2018)将受试者是否发生AMS分成AMS(+)组(n=44)和AMS(–)组(n=35)。所有受试者在平原和高原均接受相关检测:通过病例报告表(CRF)进行人口学资料、AMS相关症状、焦虑评分(SAS)、疲劳评分(FSAS)的采集,同时检测心率、血压及血氧饱和度;心脏超声及脑血流检测;采集受试者静脉血,进行血管舒缩因子的ELISA检测,并进行自身前后对照分析。对AMS(+)组与AMS(–)组各指标进行比较,并通过logistic回归分析筛选AMS的独立危险因素。结果失访4人,最后纳入分析人群共79人。急性高原暴露后,SAS、FSAS、心率明显增加(P<0.05),而血氧饱和度明显降低(P<0.05);受试者体循环和脑循环血流速度明显增加(P<0.05);内皮素-1、缓激肽升高(P<0.05),而一氧化氮、前列腺素E、五羟色胺下降(P<0.05)。此外,在平原时AMS(+)组左室舒张末期内径(LVEDD)明显高于AMS(–)组[(47.11±2.90)mm vs.(45.51±2.17)mm,P=0.008];在高原暴露后,AMS(+)组SAS、FSAS明显高于AMS(–)组(P=0.001),且基底动脉收缩期血流速度明显高于AMS(–)组[(70.30±15.71)cm/svs.(63.06±11.81)cm/s,P=0.026]。回归分析发现,平原LVEDD可独立预测AMS的发生(OR=1.293,95%CI:1.058～1.581,P=0.012),而高原暴露后基底动脉收缩期血流速度(Vs_BA)(OR=1.055,95%CI:1.005～1.107,P=0.030)、右心房内径(RAD)(OR=0.731,95%CI:0.543～0.984,P=0.039)、SAS(OR=1.219,95%CI:1.027～1.447,P=0.023)、FSAS(OR=1.105,95%CI:1.016～1.201,P=0.019)评分与AMS明显相关。结论平原LVEDD对AMS具有预测价值,高原暴露后,循环血流动力学及焦虑、疲劳等心理状态可能参与了AMS的发生。
Objective To investigate the risk factors and predictive factors for acute mountain sickness(AMS) after acute exposure to high altitude. Methods Eighty-three subjects were airlifted from Chengdu(elevation 500 m) to Lhasa(elevation3700 m) in 2 hours, and divided into AMS(+) group and AMS(–) group according to the LLS AMS scores(2018). Subjects were tested both in plain(Chengdu) and plateau(Lhasa). With the case report form(CRF), the demographic data, AMS related symptoms, self-rating anxiety scale(SAS) and fatigue self-assessment scale(FSAS) were collected, meanwhile the heart rate, blood pressure and percutaneous oxygen saturation(SpO2) were detected. The cardiac ultrasound was performed, and the subjects' venous blood was collected to detect vasoconstriction and vasodilatation factors with ELISA. Logistic regression analysis was performed to screen the independent risk factors for AMS. Results As 4 subjects were lost, a total of 79 subjects were eventually included in present study. After acutely exposed to high altitude, the subjects' SAS, FSAS and HR aroused obviously(P<0.05), while the SpO2 decreased markedly(P<0.05). There was also a significant increase in systemic and cerebral hemodynamics(P<0.05). Plasma levels of endothelin-1 and bradykinin increased(P<0.05), while of nitric oxide, prostaglandin E and serotonin decreased(P<0.05).Furthermore, when the subjects were located in plain area, the left ventricular end-diastolic diameter(LVEDD) was obviously higher in AMS(+) group [(47.11±2.90)mm] than in AMS(–) group [(45.51±2.17)mm, P=0.008], while after acutely exposed to high altitude, the SAS and FSAS were markedly higher in AMS(+) group than in AMS(–) group(P=0.001), and the systolic blood flow velocity of basilar artery was also higher in AMS(+) group [(70.30±15.71)cm/s] than in AMS(–) group [(63.06±11.81)cm/s,P=0.026]. With regression analysis, it is shown that LVEDD could independently indicate the occurrence of AMS in the plain area(OR=1.293, 95%CI 1.058-1.581, P=0.012), and the systolic blood flow of basilar artery(OR=1.055, 95%CI 1.005-1.107, P=0.030),right atrium diameter(RAD, OR=0.731, 95%CI 0.543-0.984, P=0.039), SAS(OR=1.219, 95%CI 1.027-1.447, P=0.023) and FSAS(OR=1.105, 95%CI 1.016-1.201, P=0.019) were closely correlated with AMS after acutely exposed to high-altitude(P<0.05).Conclusions The baseline LVEDD has predictive value for AMS in plain area. After exposure to high altitude, the posterior cerebral circulation hemodynamics, anxiety and fatigue may trigger the occurrence of AMS.
Objective To investigate the risk factors and predictive factors for acute mountain sickness(AMS) after acute exposure to high altitude. Methods Eighty-three subjects were airlifted from Chengdu(elevation 500 m) to Lhasa(elevation3700 m) in 2 hours, and divided into AMS(+) group and AMS(–) group according to the LLS AMS scores(2018). Subjects were tested both in plain(Chengdu) and plateau(Lhasa). With the case report form(CRF), the demographic data, AMS related symptoms, self-rating anxiety scale(SAS) and fatigue self-assessment scale(FSAS) were collected, meanwhile the heart rate, blood pressure and percutaneous oxygen saturation(SpO2) were detected. The cardiac ultrasound was performed, and the subjects' venous blood was collected to detect vasoconstriction and vasodilatation factors with ELISA. Logistic regression analysis was performed to screen the independent risk factors for AMS. Results As 4 subjects were lost, a total of 79 subjects were eventually included in present study. After acutely exposed to high altitude, the subjects' SAS, FSAS and HR aroused obviously(P<0.05), while the SpO2 decreased markedly(P<0.05). There was also a significant increase in systemic and cerebral hemodynamics(P<0.05). Plasma levels of endothelin-1 and bradykinin increased(P<0.05), while of nitric oxide, prostaglandin E and serotonin decreased(P<0.05).Furthermore, when the subjects were located in plain area, the left ventricular end-diastolic diameter(LVEDD) was obviously higher in AMS(+) group [(47.11±2.90)mm] than in AMS(–) group [(45.51±2.17)mm, P=0.008], while after acutely exposed to high altitude, the SAS and FSAS were markedly higher in AMS(+) group than in AMS(–) group(P=0.001), and the systolic blood flow velocity of basilar artery was also higher in AMS(+) group [(70.30±15.71)cm/s] than in AMS(–) group [(63.06±11.81)cm/s,P=0.026]. With regression analysis, it is shown that LVEDD could independently indicate the occurrence of AMS in the plain area(OR=1.293, 95%CI 1.058-1.581, P=0.012), and the systolic blood flow of basilar artery(OR=1.055, 95%CI 1.005-1.107, P=0.030),right atrium diameter(RAD, OR=0.731, 95%CI 0.543-0.984, P=0.039), SAS(OR=1.219, 95%CI 1.027-1.447, P=0.023) and FSAS(OR=1.105, 95%CI 1.016-1.201, P=0.019) were closely correlated with AMS after acutely exposed to high-altitude(P<0.05).Conclusions The baseline LVEDD has predictive value for AMS in plain area. After exposure to high altitude, the posterior cerebral circulation hemodynamics, anxiety and fatigue may trigger the occurrence of AMS.
引文
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[19]Boos CJ,Woods DR,Varias A,et al.High altitude and acute mountain sickness and changes in circulating endothelin-1,interleukin-6,and interleukin-17a[J].High Alt Med Biol,2016,17(1):25-31.
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[22]Kourembanas S,Morita T,Liu Y,et al.Mechanisms by which oxygen regulates gene expression and cell-cell interaction in the vasculature[J].Kidney Int,1997,51(2):438-443.
[23]Wang TH.Physiology[M].9th ed.Beijing:People's Medical Publishing House,2018:89-96.[王庭槐.生理学[M].9版.北京:人民卫生出版社,2018:89-96.]
[24]Guo WY,Bian SZ,Zhang JH,e t al.Physiologi c a l and psychological factors associated with onset of high-altitude headache in Chinese men upon acute high-altitude exposure at3700m[J].Cephalalgia,2016,37(4):336-347.
[25]Bian S,Jin J,Zhang JH,et al.Principal component analysis and risk factors for acute mountain sickness upon acute exposure at3700m[J].PLoS One,2015,10(11):e142375.
[2]Yu Wu,Chi Zhang,Yu Chen,et al.Association between acute mountain sickness(AMS)and age:a meta-analysis[J].Mil Med Res,2018,5(1):14.
[3]Roach RC,Hackett PH,Oelz O,et al.The 2018 lake Louise acute mountain sickness score[J].High Alt Med Biol,2018,19(1):4-6.
[4]Yin SY,Lv YD,Niu WZ,et al.Scoring and criteria of acute altitude sickness[J].J High Alt Med,1993,3(2):1-3.[尹昭云,吕永达,牛文忠,等.急性高原反应分度及标准[J].高原医学杂志,1993,3(2):1-3.]
[5]Bian SZ,Jin J,Zhang JH,et al.Principal component analysis and risk factors for acute mountain sickness upon acute exposure at3700m[J].PLoS One,2015,10(11):e0142375.
[6]Zheng SJ,Qin J,Yu J,et al.Changes in heart rate,blood pressure and arterial oxygen saturation among healthy young men on4400 meters plateau after a month of acclimatization at 3600meters,and their relationship with acute mountain sickness[J].Mil Med,2013,37(5):325-328.[郑双锦,覃军,余洁,等.健康青年男性高原习服后进入更高海拔的心率、血压和血氧饱和度变化规律及与急性高原病的关系[J].军事医学,2013,37(5):325-328.]
[7]Kumar K,Sharma S,Vashishtha V,et al.Terminalia arjuna bark extract improves diuresis and attenuates acute hypobaric hypoxia induced cerebral vascular leakage[J].J Ethnopharmacol,2016,180:43-53.
[8]Li M,Zhang JH,Zhao GX,e t al.A speci f ic object i ve supplemental factor in evaluating acute mountain sickness:ΔHRin combination with SaO2[J].Mil Med Res,2015,2:26.
[9]Bian SZ,Jin J,Li QN,et al.Cerebral hemodynamic characteristics of acute mountain sickness upon acute high-altitude exposure at 3,700m in young Chinese men[J].Eur J Appl Physiol,2014,114(10):2193-2200.
[10]Bian SZ,Jin J,Li QN,et al.Hemodynamic characteristics of high-altitude headache following acute high altitude exposure at 3700m in young Chinese men[J].J Headache Pain,2015,16:527.
[11]Bian SZ,Zhang JH,Gao XB,et al.Risk factors for high-altitude headache upon acute high-altitude exposure at 3700m in young Chinese men:A cohort study[J].J Headache Pain,2013,14:35.
[12]Stewart DJ.Endothelin in cardiopulmonary disease:factor paracrine vs neurohumoral[J].Eur Heart J,1993,14(Suppl I):48-54.
[13]Davenport AP,Hyndman KA,Dhaun N,et al.Endothelin[J].Pharmacol Rev,2016,68(2):357-418.
[14]Busse R,Fleming I.Regulation of endothelium-derived vasoactive autacoid production by hemodynamic forces[J].Trends Pharmacol Sci,2003,24(1):24-29.
[15]Rubanyi GM.Endothelium-derived relaxing and contracting factors[J].J Cell Biochem,1991,46(1):27-36.
[16]Faraci FM,Heistad DD.Regulation of the cerebral circulation:role of endothelium and potassium channels[J].Physiol Rev,1998,78(1):53-97.
[17]Bartsch P,Gibbs JS.Effect of altitude on the heart and the lungs[J].Circulation,2007,116(19):2191-2202.
[18]Barker KR,Conroy AL,Hawkes M,et al.Biomarkers of hypoxia,endothelial and circulatory dysfunction among climbers in Nepal with AMS and HAPE:A prospective case-control study[J].JTravel Med,2016,23(3):taw005.
[19]Boos CJ,Woods DR,Varias A,et al.High altitude and acute mountain sickness and changes in circulating endothelin-1,interleukin-6,and interleukin-17a[J].High Alt Med Biol,2016,17(1):25-31.
[20]Iglesias D,Gómez Rosso L,Vainstein N,et al.Vascular reactivity and biomarkers of endothelial function in healthy subjects exposed to acute hypobaric hypoxia[J].Clin Biochem,2015,48(16-17):1059-1063.
[21]Phelan MW,Faller DV.Hypoxia decreases constitutive nitric oxide synthase transcript and protein in cultured endothelial cells[J].J Cell Physiol,1996,167(3):469-476.
[22]Kourembanas S,Morita T,Liu Y,et al.Mechanisms by which oxygen regulates gene expression and cell-cell interaction in the vasculature[J].Kidney Int,1997,51(2):438-443.
[23]Wang TH.Physiology[M].9th ed.Beijing:People's Medical Publishing House,2018:89-96.[王庭槐.生理学[M].9版.北京:人民卫生出版社,2018:89-96.]
[24]Guo WY,Bian SZ,Zhang JH,e t al.Physiologi c a l and psychological factors associated with onset of high-altitude headache in Chinese men upon acute high-altitude exposure at3700m[J].Cephalalgia,2016,37(4):336-347.
[25]Bian S,Jin J,Zhang JH,et al.Principal component analysis and risk factors for acute mountain sickness upon acute exposure at3700m[J].PLoS One,2015,10(11):e142375.