| Background and ObjectivesLowlanders usually suffered acute mountain sickness(AMS)when they are in the acute exposure to high altitude,which mostly affects the psychological mood,physical activity,productive capability and even threatens lives.It has been reported that hypoxia-induced fluid retention and change of hemodynamic trigger AMS.Besides,the renin-angiotensin-aldosterone System(RAAS)also plays an important role in maintaining the circulatory stability and body fluid equilibrium.However,how the RAAS changes during acute high-altitude exposure remains unclear,and the studies involved the correlation between RAAS and AMS are insufficient.Furthermore,whether the changes in hemodynamics,including an increase of heart rate(HR),cardiac output(CO),and cerebral blood flow(CBF)affect AMS after acute high-altitude exposure is yet at issue.Most of previous studies employed a hypoxic chamber to simulate high-altitude environment,and even the high-altitude field studies were conducted with small samples sizes,hence there were a few limitations.Based on our clinical database,this present research conducted a retrospective cohort analysis on the changes of the related markers of the RAAS and hemodynamics before and after high-altitude exposure.We aimed to explore the influence of RAAS and hemodynamics on AMS during acute high-altitude exposure.Methods:This is a retrospective study based on the clinical database.Normally-distributed continuous data were expressed as the mean±standard deviation.Comparisons between groups of normal distribution were performed with the independent-samples t-test.A paired-samples t-test was employed to compare self-matching data.The median(interquartile range)was used to represent the data that did not meet the criteria for a normal distribution.Comparisons between groups and self-matching data of abnormal distribution were made with Mann-Whitney and Wilcoxon signed-rank tests,respectively.A chi-square test was employed to compare categorical variables between groups.Univariate and adjusted logistic regression analysis were employed to evluate the correlation between the change of RAAS and hemodynamics with AMS during high-altitude exposure.Results:1.According to the inclusion and exclusion criteria,we analyzed 69 subjects.The data indicated that acute high-altitude exposure significantly raised the concentration of Ang II [768.29(696.77,872.13)pg/ml vs.543.80(427.57,794.56)pg/ml,P<0.001] and Ang(1-7)[79.64(57.31,97.25)pg/ml vs 49.99(40.78,68.96),P<0.001] in the circulating.On the contrary,the level of aldosterone at high altitude reduced [87.41(64.62,98.61)pg/ml vs.109.78(70.41,124.43)pg/ml,P=0.019] related to that at sea level.There is hardly any difference in renin(P>0.05)and ACE(P>0.05).2.We divided the subjects into the AMS(+)group and the AMS(-)group according to LLS questionnaire survey.We found that the AMS(+)group's plasma ACE concentration at sea level [1.63(1.36,2.19)ng/ml vs.1.38(0.81,2.17)ng/ml,P=0.045] and Ang II concentration [631.37(493.22,865.29)pg/ml vs.468.80(401.81,663.18)pg/ml,P=0.007] were markedly higher than the AMS(-)group's.After the acute exposure to high altitude,we noticed that the AMS(+)group's Ang II concentration [807.97(710.30,888.84)ng/ml vs.723.90(639.91,830.55)ng/ml,P=0.025] still markedly higher than the AMS(-)group's.There was no notable difference in the ACE concentration between the two groups.The concentration of plasma rennin,aldosterone,and Ang(1-7)witnessed no obvious changes(P>0.05).3.In adjusted logistic regression analysis,we found that the plasma concentration of ACE [OR:3.506,95%CI:1.267-9.703,P=0.016] and Ang II [OR:1.004,95%CI:1.001-1.007,P=0.025] were the independent risk factors for AMS.Part 2:1.Based on the inclusion and exclusion criteria,we recruited and analyzed 79 subjects.After acute high-altitude exposure,there was a significant rose in the HR,SV,LVEF in the circulating(P<0.05)and the blood flow velocity of cerebral circulation.However,there was a clear drop in PI and RI(P<0.05).Vasoconstriction factor ET-1 increased(P<0.05)while vasorelaxation factors NO,PGE2 and 5-HT drop(P<0.05).2.We divided the subjects into the AMS(+)group and the AMS(-)group according to LLS questionnaire survey.We found that the AMS(+)group's LVEDD at sea level was markedly higher than the AMS(-)group's(47.11±2.90 mm vs.45.51±2.17 mm,P=0.008).After the acute exposure to high altitude,the AMS(+)group's SAS and FSAS were markedly higher than the AMS(-)group's(P=0.001),and the blood flow velocity in the posterior circulation(basilar artery)was markedly higher than AMS(-)group's [(70.30±15.71)cm/s vs.(63.06±11.81)cm/s,P=0.026].3.In univariate and adjusted logistic regression analysis,we found that the LVEDD(OR:1.293,95% CI: 1.058~1.581,P=0.012)could independently predict the attack of AMS,and the Vs_BA after the acute high-altitude exposure(OR: 1.055,95% CI: 1.005-1.107,P=0.030),respectively.RAD(OR: 0.731,95% CI: 0.543-0.984,P=0.039)was also significantly related to AMS.Conclusions:1.Acute high-altitude exposure significantly raised plasma ACE and Ang II in comparison to those at sea level.The concentration of aldosterone dropped remarkably,while the concentration of renin and Ang(1-7)have no obvious changes.2.After the acute high-altitude exposure,the HR,SV,LVEF in the systemic circulation and the blood flow velocity of cerebral circulation significantly increased.The vasoconstriction factor ET-1 increased(P<0.05)while vasorelaxation factors NO,PGE2 and 5-HT decreased.3.The increase of the plasma concentration of ACE,Ang II and LVEDD at sea level were the independent risk factors for AMS after the acute high-altitude exposure.The increase of DBP and the blood flow velocity in the posterior circulation at high altitude were significantly related to AMS after the acute high-altitude exposure.4.The present study reveals that the occurrence of AMS is related to the dysfunction of RAAS and the increase of hemodynamics after the acute high-altitude exposure,yet,the mechanisms are uncovered which warrant further basic studies. |
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