Inspiratory CO2 increases orthostatic tolerance during repeated tilt.

INTRODUCTION: The partial pressure of end tidal CO2 (PetCO2) is known to decrease with head-up tilt. Decreases in arterial CO2 reduce cerebral blood flow (CBF) and may increase the incidence of presyncope. We measured cerebral and central cardiovascular responses to repeated tilt where: 1) PetCO2 was allowed to change with tilt (eucapnic): and 2) PetCO2 was clamped at supine levels (isocapnic). METHODS: In eight healthy subjects breath-by-breath measurements were made of ventilation (VE) and PetCO2 along with beat-by-beat measurements of blood pressure (BP), heart rate (HR) and middle cerebral artery mean flow velocities (MFV). Following 30-min in the supine position, a series of six 10-min 90 degrees head-up tilts were performed, with 30-s of supine between each. Presyncopal subjects were returned immediately to the supine position. RESULTS: Statistical comparisons were made between the supine, and the first and last minute of the first tilt. BP, HR responses were not different between the eu- and isocapnic conditions; however, by the end of the first tilt VE was significantly higher than supine. MFV and BP at brain level decreased and HR increased from supine to tilt. MFV was higher in the isocapnic compared with the eucapnic condition but decreased from the beginning to the end of the first tilt in both conditions (i.e., tilt #1: eucap. 49.4 to 46.7; isocap. 65.0 to 59.6 cm s(-1); p < 0.05) while the BP remained constant. Five subjects were presyncopal in the study. With isocapnic tilt, presyncopal time was not reduced but was extended in four of the five subjects (2.2, 5.5, 6.3 and 31 min) yet at presyncope the values for MFV, BP and HR were the same in both conditions. CONCLUSIONS: Inspiratory CO2 contributed to increased MFV at the beginning of tilt and increased orthostatic tolerance.     

下体负压对男女飞行学员心血管调节功能的影响

观察男女飞行学员在下体负压条件下各项生理指标的变化差异，男女两组受试者分别下体负压裤，在－50mmHg负压下持续暴露8min。在下体负压（LBNP）作用时，同步记录心电图、心率、血压、脑血流量、负压暴露时间。结果显示，在LBNP作用下，随着负压暴露时间的增加，所有受试者均出现心率增快，收缩压降低、脑血流量下降。研究表明，下体负压所产生的生理学效应在男女飞行学员间相似。     

Gender differences in tolerance to lower body negative pressure

BACKGROUND: Previous studies suggest that women have lower tolerance than men do to lower body negative pressure (LBNP). The mechanism(s) responsible has not been determined. HYPOTHESES: Women would be less tolerant to presyncopal LBNP than men as determined by several indices of LBNP tolerance. Additionally, men and women, regardless of LBNP tolerance, would have similar cardiovascular responses to LBNP as presyncope was reached. METHODS: The subjects were 18 men and 18 women (average age 25) of similar fitness levels who volunteered for the study. A step-wise LBNP protocol to presyncope was employed. HR, stroke volume (SV), cardiac output (Q), BP, and systemic vascular resistance (SVR) were measured before and throughout the LBNP stress. Data from women were compared with those from all men, and to men with similar and higher LBNP tolerance. RESULTS: Women had significantly less LBNP tolerance than men regardless of index used: 30% less by duration of LBNP, 21% less by maximal LBNP tolerated, 44% less by a cumulative stress index, and 27% less by a linear tolerance index. Cardiovascular responses to LBNP were similar for women and men as presyncope was approached, whether the men were low-tolerant (LT) or high-tolerant (HT). In the 2 min pre-presyncope, HR increased by 80 +/- 6% in women, 72 +/- 7% in LT men and 96 +/- 14% in HT men; Q decreased by 47 +/- 3% in women, 52 +/- 6% in LT men and 55 +/- 2% in HT men. Similar comparisons occurred for the decline in BP and the rise in SVR. CONCLUSION: Women have lower LBNP tolerance than do men, although there is considerable gender overlap in tolerances. The cardiovascular response to LBNP is similar regardless of gender or tolerance level as presyncope is approached. Understanding the gender differences in LBNP tolerance may lie in determining how the LBNP stress is translated into a "trigger" for cardiovascular decompensation.     

Moderate sodium restriction does not alter lower body negative pressure tolerance.

HYPOTHESIS: Space travel with exposure to microgravity leads to a significant reduction in orthostatic tolerance on return to Earth, for which countermeasures are only partially successful. The purpose of this study was to examine the effect of moderate dietary sodium restriction on tolerance to LBNP. METHODS: Eight healthy men, age 25.1+/-1.3 yr, volunteered for the study. Subjects were exposed to presyncopal LBNP after consuming their "typical" diet (C) for 5 d and after consuming a sodium restricted (SR) diet for 5 d. Diet sequence was randomized and adherence was verified by 24-h urine collection on the 4th and 5th days of each diet. RESULTS: All subjects reached presyncope during the LBNP, regardless of diet. Urinary sodium excretion was 3390+/-950 mg on the C diet and 1174+/-560 mg on the SR diet. Urinary potassium was not different between the diets. Cumulative stress index scores were 655+/-460 (mm Hg x min) on the C diet and 639+/-388 (mm Hg x min) during SR. Cardiac volumes, BP and total peripheral resistance were not different at any stage of the LBNP between the diets, nor were catecholamines. Plasma renin activity, determined by radioimmunoassay, was significantly higher during SR at rest, and during all stages of LBNP in comparison with the control diet. CONCLUSION: Moderate dietary sodium restriction is not detrimental to orthostatic tolerance.     

Leg vascular responsiveness during acute orthostasis following simulated weightlessness

Ten men (35-49 years old) underwent lower body negative pressure (LBNP) exposures before and after 10 d of continuous 6 degrees head-down bedrest in order to predict the effect of weightlessness on the responsiveness of leg vasculature to an orthostatic stress. Heart rate (HR), mean arterial blood pressure (MAP), and impedance rheographic indices of arterial pulse volume (APV) of the legs were measured during rest and at 1 min of -30 mm Hg LBNP. Bedrest-induced deconditioning was manifested by decreases (p less than 0.05) in plasma volume (17%), peak oxygen uptake (16%), and LBNP tolerance (17%). Resting HR was unchanged after bedrest, but HR was higher (p less than 0.05) at 1 min of -30 mm Hg LBNP after, compared with before, bedrest. Responses of MAP to -30 mm Hg LBNP were not altered by bedrest. Resting APV was decreased (p less than 0.05) by simulated weightlessness. However, APV was reduced (p less than 0.05) from rest to 1 min -30 mm Hg LBNP by the same relative magnitude before and after bedrest (-21.4 +/- 3.4% and -20.5 +/- 2.7%, respectively). We conclude that peripheral arterial vasoconstriction, as indicated by reductions in APV during LBNP, was not affected by bedrest. These results suggest that there was no apparent alteration in responsiveness of the leg vasculature following simulated weightlessness. Therefore, it appears unlikely that control mechanisms of peripheral resistance contribute significantly to reduced orthostatic tolerance following spaceflight.     

Lower-body negative-pressure exercise and bed-rest-mediated orthostatic intolerance

PURPOSE: Supine, moderate exercise is ineffective in maintaining orthostatic tolerance after bed rest (BR). Our purpose was to test the hypothesis that adding an orthostatic stress during exercise would maintain orthostatic function after BR. METHODS: Seven healthy men completed duplicate 15-d 6 degrees head-down tilt BR using a crossover design. During one BR, subjects did not exercise (CON). During another BR, subjects exercised for 40 min.d(-1) on a supine treadmill against 50-60 mm Hg LBNP (EX). Exercise training consisted of an interval exercise protocol of 2- to 3-min intervals alternating between 41 and 65% (.)VO(2max). Before and after BR, an LBNP tolerance test was performed in which the LBNP chamber was decompressed in 10-mm Hg stages every 3 min until presyncope. RESULTS: LBNP tolerance, as assessed by the cumulative stress index (CSI) decreased after BR in both the CON (830 +/- 144, pre-BR vs 524 +/- 56 mm Hg.min, post-BR) and the EX (949 +/- 118 pre-BR vs 560 +/- 44 mm Hg.min, post-BR) conditions. However, subtolerance (0 to -50 mm Hg LBNP) heart rates were lower and systolic blood pressures were better maintained after BR in the EX condition compared with CON. CONCLUSION: Moderate exercise performed against LBNP simulating an upright 1-g environment failed to protect orthostatic tolerance after 15 d of BR.     

Hypovolemic intolerance to lower body negative pressure in female runners.

PURPOSE: An attenuated baroreflex response and orthostatic intolerance have been reported in endurance-trained male athletes; however, it is still unknown whether this occurs also in females. The purpose of the present study was to examine whether endurance exercise-trained women had a predisposition to orthostatic compromise, and if so, what causative factor(s) may induce orthostatic intolerance. METHODS: We studied cardiovascular and hormonal responses to graded lower body negative pressure (LBNP) (0 to -60 mm Hg) in 26 middle-distance female runners (18.6 +/- 0.1 yr) as the exercise-trained (ET) subjects and 23 age-matched untrained (UT) control subjects. On the basis of the occurrence of syncope episodes during LBNP, ET and UT subjects were further allocated to two groups; ET with presyncope (ET+syncope) and without presyncope (ET-syncope) and UT with presyncope (UT+syncope) and without presyncope (UT-syncope). RESULTS: Occurrence of presyncope episodes during LBNP was higher in ET (65.4%, P < 0.05) than that for UT (34.8%). Leg compliance was higher (P < 0.05) in ET than in UT. LBNP reduced stroke volume (SV) more (P < 0.05), increased heart rate (HR) higher (P < 0.05), and increased forearm vascular resistance (FVR) more in ET+syncope as compared with the other groups. Response of vasoactive hormones to LBNP was higher in ET+syncope (P < 0.05) than that of the other groups except for norepinephrine (NE); high in both ET+syncope and UT+syncope. The relationship between SV and NE, an index of sympathetic neuronal response, had no training-related changes during LBNP. CONCLUSION: We conclude that exercise-trained females have a high incidence of orthostatic intolerance during LBNP, with a greater reduction of SV independent of changes in baroreflex and neurohumoral function. A lower incidence of LBNP intolerance in UT may be accounted for by a lower reduction of SV during LBNP. An increase in leg compliance in the exercise-trained females may play an important role in inducing pronounced reduction of SV and hence the intolerance to LBNP.     

血容量减少对立位应激反应影响的仿真研究

目的 研究不同程度的血容量减少对心血管系统立位应激反应的影响,探讨血容量降低在航天失重后心血管失调和立位耐力降低机理中的意义。方法 在仿真下体负压（LBNP）暴露时心血管系统反应模型的血液重新分配子模型中引入血容量减少因素,仿真血容量减少0－25％后LBNP时心率（HR）和血压BP变化,结果 血容量减少低于总血量的5％条件下,心血管系统可以通过压力反射调节作用维持LBNP时政党的HR和BP;血容量减少超过约15％,在安静仰卧位时,HR和BP正常,但LBNP时BP迅速降低,系统可失去稳定性。结论 血容量减少将导致心血管系统对立位应激反应的改变。     

头低位暴露后直立位下体负压作用的耐力变化和心血管反应

目的观察头低位后直立位下体负压暴露的耐力和心血管反应。方法8名被试者在下体负压倾斜床上进行“直立位-倒立位30s-直立位联合下体负压(-60mmHg)致晕厥前症状”的模拟推拉效应试验及单纯直立位 下体负压(-60mmHg)致晕厥前症状的对照试验,用阻抗法测量了试验过程中心血管功能指标的变化。结果在模拟推拉效应试验中,8名被试者出现晕厥前症状的平均耐受时间为4.5±2.4min,显著低于对照试验时的8.4±2.1min(P<0.01)。在倒立位,被试者HR较直立位基础值降低,SV和CO较直立位基础值升高,均有显著性意义。和基础值相比,直立位下体负压时HR增加的百分比显著低于对照试验(P<0.05),而直立位下体负压时SV和CO降低的百分比均显著高于对照试验时SV和CO降低的百分比(P<0.05)。在直立位下体负压暴露时,对照试验的PP和基础值比较显著降低(P<0.05),TPR比基础值显著增加(P<0.05)。结论倒立位后,再进行直立位下体负压作用,出现晕厥前症状的平均耐受时间缩短,心血管反应降低。     

下体负压对抗21d头低位卧床后立位耐力不良的研究

目的观察ＬＢＮＰ对２１ｄＨＤＴ－６°卧床模拟失重所致立位耐力不良的对抗效果。方法１２名健康男性青年志愿者,进行２１ｄＨＤＴ－６°卧床实验。随机分为对照组和下体负压组,每组６人。与对照组不同,下体负压组在最后一周,每天进行１ｈ、－４．０ｋＰａ的下体负压锻炼。结果卧床前,１２名受试者顺利通过７５°、２０ｍｉｎ立位耐力检查。卧床第１０ｄ立位耐力检查时,对照组有５人、ＬＢＮＰ组有４人出现晕厥前或晕厥症状,两组平均耐受时间均低于卧床前（Ｐ＜０．０５）;第２１ｄ时,对照组有５人未通过,平均耐受时间较卧床前显著降低（Ｐ＜０．０５）;而ＬＢＮＰ组有１人未通过,平均耐受时间显著高于对照组（Ｐ＜０．０５）。结论２１ｄ头低位卧床后立位耐力显著降低。下体负压能够有效对抗头低位卧床导致的立位耐力降低。     

Radix astragali and orthostatic response: a double-masked crossover study

AIM: Recent results from animal experiments have shown that radix astragali (RA), a traditional Chinese herbal tonic, alleviates muscle atrophy under simulated weightlessness conditions, rendering RA a candidate for human use as a countermeasure against muscular atrophy. Possible cardiovascular side effects have not yet been investigated. We analyzed the effects of RA on the orthostatic stability of healthy men. METHODS: There were 10 test subjects who were assigned to a double-blinded, randomized crossover design using RA or placebo (PL) for 14 d each, respectively. Test runs were separated by a 14-d 'washout' interval. At the beginning and the end of every 14-d test run, graded orthostatic stress (GOS) consisting of head-up tilt (HUT) combined with lower body negative pressure (LBNP) was used to achieve a presyncopal endpoint. Orthostatic effects on cardiac and vascular function were continuously monitored. RESULTS: There were no significant differences between the RA vs. PL groups: mean arterial blood pressure dropped by 13 vs. 17%, pulse pressure 46 vs. 35%, heart rate increased 108 vs. 117%, and stroke volume index decreased 54 vs. 49% from supine control to presyncope. Neither did RA influence standing time compared to PL (18 +/- 7 vs. 17 +/- 6 min), nor did progression from the first to the fourth trial (15 +/- 6 to 18 +/- 7 min). CONCLUSION: RA does not influence resting cardiovascular variables and orthostatic capacity in humans. It can be expected that human studies of RA's musculo-skeletal countermeasure potential will not be compromised by any cardiovascular side effects at the dosage employed in this study.     

下体负压旋转床模拟航空推拉效应对心血管功能的影响

目的探讨下体负压旋转床模拟航空推拉效应的效果 ,观察推拉动作对心血管功能的影响。方法 8名被试者在下体负压旋转床上进行“直立位 (HUT ,+1Gz) -倒立位 -直立位 +下体负压 (LBNP ,- 5 0mmHg) 1 0min”的模拟推拉效应试验及单纯直立位 +下体负压 (- 5 0mmHg) 1 0min的对照试验 ,用阻抗法测量了试验过程中心率 (HR)、血压 (BP)、基础阻抗 (Z0 )、每搏心输出量 (SV)、心输出量 (CO)及总外周阻力 (TPR)等心血管功能指标的变化。结果在模拟推拉效应试验中 ,有 3名被试者没有完成直立位 +LB NP作用 1 0min的试验 ,出现晕厥前症状 ,8名被试者平均耐受时间为 8.99± 1 .47min。而对照试验时 ,被试者均完成了 1 0min的直立 +LBNP试验。模拟推拉效应试验时 ,在倒立位 ,被试者HR、Z0 较直立位对照值降低 ,SV和CO较直立位对照值升高 ,均有显著性意义 ;直立位 +LBNP过程中 ,HR、Z0 、TPR较对照和倒立位值显著增高 ,SV和CO较对照和倒立位值显著降低 ,SBP在HUT即刻较对照值显著性增高 ,在HUT +LBNP过程中显著性降低。在对照试验时 ,上述指标呈现出相同的变化 ,但增高或降低的百分比 (% )低于模拟推拉效应试验 (HR除外 )。结论倒立位后 ,再直立 +LBNP作用 ,心血管功能下降程度大于单纯直立 +LBNP作用 ,下体负压旋转床     

下体负压作用下脑氧饱和度的变化

The purpose of this study was to observe and analyse the changes of regional cerebral oxygen saturation (SrO2) under lower body negative pressure (LBNP). 12 healthy young subjects were tested in an LBNP chamber in sitting position. Incremental negative pressure was used and end points of test were onset of presyncopal symptoms or completion of the 15min test. The results were: (1) SrO2 showed a significant decrease under LBNP; (2) The magnitude of decrease of SaO2 showed significant differences among subjects with different reactions at the termination of LBNP; (3) Under LBNP the arterial oxygen saturation (SrO2) kept constant. The changes of SrO2 correlated strongly with the percentage changes of superaorbitalis arterial blood flow (r = 0.59-0.86, P < 0.05 or 0.01). It was suggested that the changes of SrO2 were related to the decrease of cerebral blood flow under LBNP. It was possible to use SrO2 to detect presyncopal and syncopal symptoms. So the monitoring of SrO2 could be used in studies of G-LOC.     

Model of depressed myocardium shows orthostatic intolerance with or without reduced blood volume

INTRODUCTION: The development of orthostatic hypotension (OH) is complex and multi-factorial. Previous simulation work indicates that myocardial contractility depression (MCD) may increase OH when there is a total blood volume decrease. This paper hypothesized that MCD increased OH in both humans with and without decrease in blood volume. METHODS: A model, which was previously used to reproduce cardiovascular response to lower body negative pressure (LBNP), hypovolemia, and MCD, was modified by incorporating the physiologic mechanism of plasma filtration into the interstitium during LBNP. The model was evaluated by human experimental results. Using the model, HR and BP response to LBNP were simulated at conditions of 10%, 20%, and 30% MCD. Additionally, HR and BP response to LBNP were simulated at conditions of 10% and 20% MCD with a 12% decrease in blood volume. RESULTS: Simulation results indicate that the increments of HR and decrements of systolic BP (SBP) and mean arterial pressure (MAP) rise with the increases of MCD. Specifically, simulation results indicate that about 30% MCD would cause OH (HR: 117 bpm; SBP: 92 mmHg; MAP: 78 mmHg). It also indicates that about 20% MCD would cause OH (HR: 134 bpm, SBP: 84 mmHg, MAP: 73 mmHg) with a 12% decrease in total blood volume. CONCLUSION: It is suggested that MCD increases OH whether or not there is a total blood decrease, and further suggested that MCD induced by both spaceflight and heart disease may increase OH.     

21天头低位(-6°)卧床前后下体负压和头高位倾斜暴露时的心血管反应

目的探讨２１天头低位（ＨＤＴ）卧床对人体立位应激下心血管反应的影响,以及比较下体负压（ＬＢＮＰ）和头高位倾斜（ＨＵＴ）两种立位应激下心血管反应的差异。方法６名受试者在２１天ＨＤＴ前、后分别进行ＬＢＮＰ（－４．００ｋＰａ／３ｍｉｎ、－６．６７ｋＰａ／３ｍｉｎ及－９．３３ｋＰａ／３ｍｉｎ）和ＨＵＴ试验（３０°／３ｍｉｎ、４５°／３ｍｉｎ、６０°／３ｍｉｎ及７５°／３ｍｉｎ）,以比较两种检测方法的血压（ＢＰ）和心率（ＨＲ）的变化情况。结果与ＬＢＮＰ（或ＨＵＴ）前相比：①ＬＢＮＰ（ＨＵＴ）时ＨＲ显著增加（Ｐ＜０．０１）,ＳＢＰ显著降低（Ｐ＜０．０５）;卧床后相应的变化量增加。②ＬＢＮＰ时ＤＢＰ降低（卧床后达显著,Ｐ＜０．０５）;而ＨＵＴ时ＤＢＰ增加（卧床后达显著,Ｐ＜０．０５）。③ＬＢＮＰ时ＭＡＰ均显著降低（Ｐ＜０．０５）;而ＨＵＴ时在卧床前无变化（Ｐ＞０．０５）,在卧床后显著增加（Ｐ＜０．０５）。结论ＬＢＮＰ和ＨＵＴ引起的ＣＶＳ反应并不相同。笔者认为,ＨＵＴ更能促进心血管系统对立位应激的调节作用。     

Cardiovascular response to lower body negative pressure (LBNP) following endurance training

Eleven sedentary male volunteers were assigned to either an exercise (E) group (n = 6; endurance exercise for 12 weeks) or a control (C) group (n = 5; no exercise). After training, E significantly increased (p less than 0.01) their VO2max (pretraining: 37.0 +/- 2.3; posttraining: 44.6 +/- 2.5), whereas C showed no significant change. Heart rate (HR), arterial blood pressure (BP) and forearm blood flow (FBF) were measured both pre- and posttraining at rest and during 2 levels of LBNP: -10 mm Hg and -40 mm Hg. Both C and E had similar decreases in systolic BP and similar increases in HR and diastolic BP during LBNP when comparing the pre- and posttraining periods. In both groups, FBF significantly decreased during -40 mm Hg of LBNP in the pretraining period. However, after training, E had a significantly attenuated (p less than 0.05) decrease in FBF at -40 mm Hg (pretraining: -45.0 +/- 3.7%; posttraining: -29.8 +/- 3.1%). In C, there was no difference in the response of FBF to -40 mm Hg of LBNP comparing pretraining and posttraining. These findings indicate that endurance exercise training decreases the forearm vasoconstrictor response to high levels of LBNP.     

坐位下体负压下人体大脑中动脉血流速度及血氧饱和度的改变

目的探讨坐位下体负压对人体大脑中动脉血流速度、心率和血氧饱和度的影响。方法 15名健康青年男性在坐位下体负压 - 4.0 0kPa、 - 6.67kPa条件下 ,分别测试负压前、下体负压暴露 0 .5、1、2、3、4、5min和卸压后 1、3、5min的大脑中动脉血流速度、心率和血氧饱和度。结果在 - 4.0kPa下体负压作用 4、5min时 ,脑血流速度减慢 (P <0 .0 5 ) ;负压作用 3、4、5min时心率增快 (P <0 .0 5 ) ;血氧饱和度无明显改变。在 - 6.67kPa下体负压作用 2、3min时 ,脑血流速度减慢 (P <0 .0 5 ) ,在 4min和 5min时显著减慢 (P <0 .0 1) ,卸压后 1min尚未恢复 (P <0 .0 5 ) ,随后恢复至对照水平 ;负压作用后各时间点心率均显著增快 (P <0 .0 1) ;血氧饱和度在负压暴露 5min时显著下降 (P <0 .0 5 )。结论坐位下体负压造成血液在下肢淤积 ,大脑中动脉血流速度减慢 ,引起大脑血供减少 ,为空中晕厥和立位耐力不良的医学鉴定提供了人体实验依据     

提踵动作对下体负压耐力的影响

目的验证提踵动作对提高下体负压耐力的有效性,并探讨其可能的作用机制。方法健康男性志愿者10名,在下体负压(LBNP)条件下分别随机进行2次头高位倾斜检查(HUT)测定其下体负压耐力。一次为志愿者的基础下体负压耐力(对照组),另外一次要求志愿者在LBNP条件下做提踵动作,直至耐力终点(提踵组)。结果提踵组下体负压耐受时间(DNP)和累计应激指数(CSI)均显著增加(P<0.05)。在下体负压过程中,提踵组平均动脉压呈升高趋势,心率增加呈降低趋势,每搏量增加,且均在-40 mmHg及-50 mmHg时达到显著水平(P<0.05)。结论提踵动作可以提高下体负压耐力,可望作为航天员在长期太空飞行后引起立位耐力不良时的应对措施,也可作为血管迷走性晕厥患者的预防措施和治疗手段。     

21d头低位卧床期间第一周和最后一周下体负压锻炼对立位耐力和心功能的影响

目的观察在 2 1d头低位卧床的第一周和最后一周进行下体负压锻炼对立位耐力和心功能的影响。方法 1 2名健康男性志愿者 ,随机分为对照组和LBNP组 ,每组 6人 ,均参加 - 6°头低位倾斜卧床实验。对照组在卧床期间不做任何处理 ,LBNP组在卧床第一周和最后一周 ,每天进行 1h、- 30mmHg的下体负压锻炼。卧床前和卧床第 1 0、2 1天在倾斜床上进行 3次立位耐力检查 ,卧床期间测量心脏泵血和收缩功能等指标。结果卧床前两组 1 2名被试者均顺利通过立位耐力检查。卧床第 1 0和 2 1天 ,对照组所有被试者均不能通过立位耐力检查 ,而下体负压组仅有 1人未通过 ,卧床第 2 1天下体负压组( 1 9.7± 0 .9min)平均耐受时间较对照组 ( 1 5 .0± 3.2min)显著延长 (P <0 .0 5 )。对照组每搏输出量(SV)及心输出量 (CO)在卧床第 3、1 0天较卧床前显著降低 (P <0 .0 5 ) ,而LBNP组SV及CO在卧床期间均无显著性变化 ;两组的射血前期 (PEP) /左室射血时间 (LVET)在卧床第 3、1 4天均显著升高 (P <0 .0 5 )。两组间比较 ,LBNP组PEP/LVET在卧床第 3天较对照组显著降低 (P <0 .0 5 ) ,LVET在卧床第 3、7和 1 4天较对照组显著升高 (P <0 .0 5 )。结论 2 1d头低位卧床可引起立位耐力、心脏泵血和收缩功能显著降低 ;在 2 1d头低位卧床的     

Effect of lower body negative pressure against orthostatic intolerance induced by 21 days head-down tilt bed rest

BACKGROUND: Exposure to actual or simulated weightlessness is known to induce orthostatic intolerance in humans. Many different methods have been suggested to counteract orthostatic hypotension. The repetitive or prolonged application of lower body negative pressure (LBNP) has shown beneficial effects to counter orthostatic intolerance, but devoting so much time to countermeasures is not compatible with space mission objectives or costs. The purpose of the present study was to assess the effects of brief LBNP sessions against orthostatic intolerance during a 21-d head-down tilt (HDT) bed rest. METHODS: There were 12 healthy male volunteers who were exposed to -6 degrees HDT bed rest for 21 d. Six subjects received -30 mm Hg LBNP sessions for 1 h x d(-1) from day 15 to day 21 of the HDT, and six others served as control. Orthostatic tolerance was assessed by means of standard tilt test. RESULTS: Before HDT, all the subjects in the two groups completed the tilt tests. After 21 d of HDT, five subjects of the control group and one subject of the LBNP group could not complete the tilt test due to presyncopal or syncopal symptoms. The mean upright time in the control group 13.0 +/- 4.0 min) was significantly shorter (p < 0.05) than that in the LBNP group (19.0 +/- 2.2 min). Body weight decreased significantly in the control group during HDT, while increasing significantly on day 21 of HDT in the LBNP group. Urine volume increased on days 15-21 of HDT in the control group, but remained unchanged throughout HDT in the LBNP group. A significant decrease in cardiac output and cardiac index, and a significant increase in total peripheral resistance, pre-ejection period, plasma renin activity, aldosterone, and prostaglandin 12 were observed during HDT in both groups. There were no significant differences in these parameters between the two groups. CONCLUSIONS: Brief daily LBNP sessions were effective in preventing orthostatic intolerance induced by 21 d HDT bed rest. However, it did not improve cardiac pump and systolic functions and did not preserve volume regulating hormones.