间断下体负压暴露方式对下体负压耐力的影响

目的：探讨不同方式反复下体负压锻炼对下体负压耐力的影响,以期筛选最佳的负压锻炼方式。方法：27名男性健康受试者随机分成3组,分别进行－5.33kPa8min(A组）、6.67kPa4min（B组）、6.67kPa8min（C组）的下体负压锻炼后累积应激指数（CSI）、总耐受时间（DNP）较锻炼前显著提高,A、B组上述指标无显著变化,下体负压暴露时的心率较平静状态显著升高,收缩压显著降低,舒张压无显著变化。结论：经过－6.67kPa/d8min连续8d的间断下体负压可以显著提高下体负压耐力。     

下体负压对家兔血液动力学的影响

观察了家兔在-20、-40、-60mmHg下体负压下心输出量、心搏量、心率、血压以及心电图、脑电图、视网膜电图的变化。实验结果表明:心搏量与心输出量明显减少,在-60mmHg下作用10分钟两者可下降到负压前对照值的15％。心率大多数加快,以代偿心输出量的下降。如出现持续性心率过缓和心律不齐,标志代偿失调。收缩压、舒张压、平均动脉压、脉压均呈规律性下降。根据血压反应可将动物分为耐力良好、尚好、较差三种类型。心电图变化主要表现为冠脉供血不足,心肌缺氧特征,并伴有高尖状P波。脑电图出现缺氧性慢波、波幅降低。视网膜电图的b波波幅逐渐下降,持续期缩短,80％以上有b负波,这些变化可能与脑部及视网膜供血不足有关。     

立位加下身负压方法及其应用

航天员长期失重飞行后返回地面时,无一例外出现立位耐力降低。为了选拨心血管调节功能良好的航天员,美苏多采用单纯立位和下身负压方法。但由于前者下肢血液潴留较少,后者不存在静水压差对颈动脉窦压力感受器刺激,均未取得满意效果。考虑到长期失重后立位时,回心血量下降及对压力感受器的刺激量都大于飞行前,我们采用了立位加下身负压方法(简称负-立方法)模拟航天员返回地面后站立时心血管系统遇到的刺激量。经过几年实践,证明此     

四周尾部悬吊致大鼠立位耐力不良

目的:观察中期(4周)尾部悬吊大鼠在立位应激下的心血管反应。方法:采用本实验室改进的尾部悬吊方法,利用头高位倾斜和下体负压模拟立位应激,通过股动脉插管和心电图记录检测大鼠血压和心率改变。结果:与对照组相比,4周尾部悬吊(SUS)大鼠体重下降及后肢承重骨骼肌萎缩;其静息血压和心率与对照组(CON)相比无明显差别(P0.05);在两组大鼠中,头高位倾斜和下体负压均可导致血压降低和心率加快,但SUS大鼠平均动脉压下降幅度与CON大鼠相比显著增大(P0.05),而两组的心率增快幅度并无明显差别(P0.05)。结论:4周尾部悬吊大鼠在立位应激下维持血压稳定的能力减弱,可用于中期失重/模拟失重后立位耐力不良机理的研究。     

不同吸痰负压对重型颅脑损伤患者的效果比较

探讨3种不同的吸痰负压对重型颅脑损伤患者的影响,以寻找重型颅脑损伤患者最佳的吸痰负压。选取某三甲医院的ICU重症颅脑损伤患者46例,当患者出现吸痰指征时,分别以3种不同吸痰负压(-75 mmHg,-150 mmHg,-300 mmHg)对患者行密闭式吸痰,在吸痰前2 min、吸痰后5 min以及吸痰后10 min时记录患者的氧动力学和血流动力学变化,同时记录患者的吸痰时间间隔和效果。吸痰负压为-150 mmHg和-300 mmHg的吸痰效果和吸痰间隔时间要优于-75 mmHg的吸痰负压(p0.05),且吸痰负压为-150 mmHg时,吸痰的间隔时间最长(78.3±29.8)min;不同吸痰负压组不同时间点的氧分压,二氧化碳分压、收缩压、舒张压和平均动脉压差异有统计学意义(p0.01),且当吸痰负压是-150 mmHg时、吸痰后5 min和10 min时氧分压相对于吸痰前有明显的改善(p=0.00),当吸痰负压为-300 mmHg时,吸痰后5 min相较于吸痰前收缩压、舒张压和平均动脉压都明显提高,具有统计学意义(p=0.00)。-150 mmHg的吸痰负压是安全和有效的适合重型颅脑损伤患者的吸痰负压。     

坐位下体负压舱的研制

下体负压试验是10多年来推广使用的一种新试验方法,它可人为地定量改变正常血容量和血液的分布,目前已在航空医学中广泛应用。下体负压已被作为:评定心血管除适应作用的方法和促进恢复由于失重后引起的生理功能变化,生理学研究引起模拟出血的方     

VAC 技术治疗兔耳缺血性创面的实验研究

目的:观察间歇和持续负压下缺血创面不同处理与愈合的关系。方法:实验前1天,用脱毛剂(Nair,美国)对兔耳背脱毛。动物用1%戊巴比妥钠耳缘静脉注射麻醉(30 mg/kg体重),固定于手术台。75%乙醇消毒双侧耳背皮肤。距耳根3-3.5cm处分离、结扎兔耳中央神经血管束。在耳背中部形成直径2.5cm全层皮肤缺损创面(保留软骨膜)[1]。止血后置动物于特制木盒内。42只大白兔共84个创面,随机分为-50mmHg-75mmHg和-100mmHg 3大组,分别施以间歇负压(运行2分钟,停1分钟)和持续负压组。实验分别运用-50mmHg,-75mmHg,-100mmHg三个不同负压值进行连续、间歇治疗兔耳缺血性创面,观察伤后1,3,7,10,14,20d创面愈合情况,取伤后7d组织标本进行Western blot、HE染色,观察VEGF(vascular endothelial growth factor)的表达及创面上皮的再生和肉芽组织生长情况[1]。以及各时间点细胞凋亡的检测。结果:-50mmHg(纱布+海绵)间歇负压引流技术治疗兔耳缺血性创面的愈合最快,-75mmHg治疗组次之,-100mmHg治疗组创面愈合最慢。在同一时间点上,-50mmHg治疗组与-75mmHg,-100mmHg治疗组和空白对照组之间相比,能够更快地促进创面VEGF的表达和肉芽组织的再生,毛细血管增多。封闭负压治疗能够降低创面组织细胞的凋亡的发生。结论:(1)封闭负压治疗能够促进缺血创面的肉芽组织再生及VEGF的表达,减少创面组织细胞的凋亡的发生;(2)-50mmHg间歇封闭负压治疗效果最好。     

飞行(学)员ACE基因的多态性

血管紧张素转化酶 (ACE)第 16内含子的插入 缺失多态性与运动员耐力水平有关 .为了解这一多态性与飞行员飞行耐力的关系 ,对不同阶段飞行人员ACE第 16内含子基因型进行了分析和比较 .结果显示 ,ACEDD基因型百分率在招飞体检应征人员为 12 5 %、基础飞行学院学员 (未飞 )为 11 5 %、飞行学院初教机飞行学员为 10 0 %、歼击机飞行员为 3 0 % .歼击机飞行员组D等位基因频率及DD基因型明显低于其他 3组 (P <0 0 1) ,而后 3组之间无明显差异 (P >0 0 5 ) .进而观察到 ,飞行员体能测试成绩优者 ,无DD基因型 .提示 ,飞行员体能表现与ACE第 16内含子的插入 缺失多态性有关 ,具有I等位基因者 ,体能较好 ,飞行耐力也较好 .     

下体负压的生理学效应及其应用

下体负压实验是近十多年来发展的一项新实验技术,是研究血液动力学的一种无创伤性生理学方法。目前它不仅已成为航天医学中评价心血管功能的标准方法,而且在航空医学、临床医学和基础医学研究中也日益引起人们的广泛兴趣。本文就这项技术的方法学、生理学效应及应用作了介绍,着重讨论了在下体负压下循环系统功能的变化,并对实验方法及应用前景作了简要的概述。     

立位加下身负压耐力与 Gz耐力的关系

用立位75°加-5.333KPa下身负压试验(负-立),检查18名18-25岁健康青年男性,同时作人体离心机 Gz耐力检查。结果发现负-立试验中心血管反应特点与 Gz耐力相一致。不同状态下心血管反应的各个参数输入计算机,进行多元逐步回归处理,筛选出对 Gz贡献率大的13项指标。主要有反映血管调节能力的平均动脉压,脉压和外阻血管阻力,反映心脏调节的SV、CO、SV/HR和HR的动态变化斜率等。作者认为负-立试验时,心血管功能优劣主要由外周血管阻力调节作用和心率的反应决定。负-立试验中心血管反应与 Gz耐力之间存在高度的相关性。根据这种考虑,得到一个回归式: YGz=2.13 2.11×10~(-4)Rb 1.66×10~(-3)SV/HR 0.13tr=0.8473,P<0.001。式中YGz=预测 Gz耐力;Rb=负-立试验中外周血管阻力变化斜率;SV/HR=负-立试验中SV/HR的增长值,t=负-立试验的耐受时间。经用另外10人验证,估测值与实测值的相关系数为0.813,P<0.01。     

Hemodynamic and neuroendocrine predictors of lower body negative pressure (LBNP) intolerance in healthy young men.

Exposure to LBNP results in body fluid shift to lower extremities similarly as under influence of orthostatic stress. In susceptible persons it leads to syncope. For better understanding why certain individuals are more susceptible to orthostatic challenges it seemed necessary to collect more data on hemodynamic and neuroendocrine adjustments occurring before onset of presyncopal symptoms Accordingly, in this study heart rate (HR), blood pressure (BP), stroke volume (SV), cardiac output (CO), hematocrit, plasma catecholamines, adrenomedullin, ACTH and plasma renin activity (PRA) were measured in 24 healthy men during graded LBNP (-15, -30 and -50 mmHg). Thirteen subjects completed the test (HT group) whereas 11 had presyncope signs or symptoms at -30 mmHg or at the beginning of -50 mmHg (LT group). Comparison of these groups showed that LT subjects had lower baseline total peripheral resistance and higher plasma adrenomedullin. During LBNP plasma catecholamine and PRA increases were even greater in LT than in HT group while plasma adrenomedullin elevations were similar in both groups. Plasma ACTH increased only in LT group following presyncope symptoms. Low tolerant group showed more rapid decline of SV and CO than HT subjects from the beginning of LBNP. It is suggested that measurements of SV at the level of LBNP which did not evoke any adverse symptoms may be of predictive value for lower orthostatic tolerance.     

Effect of 6-week endurance training on hemodynamic and neurohormonal responses to lower body negative pressure (LBNP) in healthy young men.

Endurance training is considered as a factor impairing orthostatic tolerance although an improvement and lack of effect have been also reported. The mechanisms of the changes and their relation to initial tolerance of orthostasis are not clear. In the present study, effect of moderate running training on hemodynamic and neurohormonal changes during LBNP, a laboratory test simulating orthostasis, was investigated in subjects with high (HT) and low (LT) tolerance of LBNP. Twenty four male, healthy subjects were submitted to graded LBNP (-15, -30 and -50 mmHg) before and after training. During each test heart rate (HR), stroke volume (SV) and blood pressure, plasma catecholamines, ACTH, adrenomedullin, atrial natriuretic peptide, and renin activity were determined. Basing on initial test, 13 subjects who withstood LBNP at -50 mmHg for 10 min were allocated into HT group and 11 subjects who earlier showed presyncopal symptoms to LT group. Training improved LBNP tolerance in six LT subjects. This was associated with attenuated rate of HR increase and SV decline (before training, at -30 mmHg deltaHR was 21 +/- 4 beats/min and deltaSV - -36+/- 8 ml while after training the respective values were 8 +/- 4 beats/min and -11+/- 6 ml). No differences in hemodynamic response were found in HT subjects and those from LT group whose LBNP tolerance was unchanged. In neither group training affected neurohormonal changes except inhibition of plasma ACTH rise in subjects with improvement of LBNP tolerance. It is concluded that some subjects with low orthostatic tolerance may benefit from moderate training due to improvement of cardiac function regulation.     

Modulation of control of muscle sympathetic nerve activity during orthostatic stress in humans

We tested the hypothesis that orthostatic stress would modulate the arterial baroreflex (ABR)-mediated beat-by-beat control of muscle sympathetic nerve activity (MSNA) in humans. In 12 healthy subjects, ABR control of MSNA (burst incidence, burst strength, and total activity) was evaluated by analysis of the relation between beat-by-beat spontaneous variations in diastolic blood pressure (DAP) and MSNA during supine rest (CON) and at two levels of lower body negative pressure (LBNP: -15 and -35 mmHg). At -15 mmHg LBNP, the relation between burst incidence (bursts per 100 heartbeats) and DAP showed an upward shift from that observed during CON, but the further shift seen at -35 mmHg LBNP was only marginal. The relation between burst strength and DAP was shifted upward at -15 mmHg LBNP (vs. CON) and further shifted upward at -35 mmHg LBNP. At -15 mmHg LBNP, the relation between total activity and DAP was shifted upward from that obtained during CON and further shifted upward at -35 mmHg LBNP. These results suggest that ABR control of MSNA is modulated during orthostatic stress and that the modulation is different between a mild (nonhypotensive) and a moderate (hypotensive) level of orthostatic stress.     

Intrapericardial denervation: radial artery blood flow and heart rate responses to LBNP

Eight rhesus monkeys were used to study responses of radial artery blood flow velocity (RABFV) and heart rate (HR) to low (0 to -20 mmHg) and high (0 to -60 mmHg) ramp exposures during supine lower body negative pressure (LBNP). These levels were chosen to separate peripheral vascular responses associated with stimulation of low- and high-pressure baroreceptors. Four monkeys had efferent and afferent cardiac denervation by use of the Randall procedure with pharmacological (phenylephrine and atropine) verification. Animals were studied 3 wk after surgery to avoid reinnervation. Findings were compared with those of four identically treated intact animals. Denervated animals showed no change in RABFV or HR during low-level LBNP; however, HR increased significantly (P less than 0.05) when LBNP reached -50 mmHg and blood flow velocity also fell (P less than 0.05) starting at -30 mmHg pressure. In contrast, intact animals showed steady decreases in RABFV during both high- and low-pressure protocols, with HR showing a 6-beat/min increase (P less than 0.05) starting at -20 mmHg pressure. As with denervated animals, intact animals showed a more pronounced increase in HR after reaching a level of -60 mmHg suction. Cardiac output (electromagnetic flowmeter, ascending aorta) fell significantly in both groups starting at -30 mmHg pressure. Left ventricular pressure (Konigsberg pressure cell) in three intact animals showed a progressive fall in systolic pressure starting at -10 mmHg suction, which became significant at -55 mmHg pressure. These results demonstrate that cardiac denervation by use of the Randall technique significantly affects RABFV and HR responses to LBNP in rhesus monkeys. The lack of RABFV change during LBNP in denervated animals suggests that these changes coupled with HR response can be used as an effective method to verify the completeness of denervation of low-pressure baroreceptors in animals that have undergone intrapericardial denervation.     

Low LBNP tolerance in men is associated with attenuated activation of the renin-angiotensin system

Plasma vasoactive hormone concentrations [epinephrine (p(Epi)), norepinephrine (p(NE)), ANG II (p(ANG II)), vasopressin (p(VP)), endothelin-1 (p(ET-1))] and plasma renin activity (p(RA)) were measured periodically and compared during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the renin-angiotensin system, the latter being one of the most powerful vasoconstrictors in the body, is of major importance for LBNP tolerance. Healthy men on a controlled diet (2,822 cal/day, 2 mmol. kg(-1). day(-1) Na(+)) were exposed to 30 min of LBNP from -15 to -50 mmHg. LBNP was uneventful for seven men [25 +/- 2 yr, high-tolerance (HiTol) group], but eight men (26 +/- 3 yr) reached presyncope after 11 +/- 1 min [P < 0.001, low-tolerance (LoTol) group]. Mean arterial pressure (MAP) did not change measurably, but central venous pressure and left atrial diameter decreased similarly in both groups (5-6 mmHg, by approximately 30%, P < 0.05). Control (0 mmHg LBNP) hormone concentrations were similar between groups, however, p(RA) differed between them (LoTol 0.6 +/- 0.1, HiTol 1.2 +/- 0.1 ng ANG I. ml(-1). h(-1), P < 0.05). LBNP increased (P < 0. 05) p(RA) and p(ANG II), respectively, more in the HiTol group (9.9 +/- 2.2 ng ANG I. ml(-1). h(-1) and 58 +/- 12 pg/ml) than in LoTol subjects (4.3 +/- 0.9 ng ANG I. ml(-1). h(-1) and 28 +/- 6 pg/ml). In contrast, the increase in p(VP) was higher (P < 0.05) in the LoTol than in the HiTol group. The increases (P < 0.05) for p(NE) were nonsignificant between groups, and p(ET-1) remained unchanged. Thus there may be a causal relationship between attenuated activation of p(RA) and p(ANG II) and presyncope, with p(VP) being a possible cofactor. Measurement of resting p(RA) may be of predictive value for those with lower hypotensive tolerance.     

Relative role of low- and high pressure reflexes on sympathetic activity in humans during simulated gravitational stress

In order to determine the relative role of low- and high-pressure reflexes, respectively, on forearm sympathetic nerve activity (fSNA), 10 normal male subjects underwent a 4-step (5 min each) graded lower body negative pressure (LBNP) from -10 to -50 mmHg. Central venous pressure (CVP) and stroke volume gradually decreased (p<0.05), and arterial pulse pressure (PP) abruptly decreased at LBNP of -50 mmHg. Mean arterial pressure (MAP) remained unchanged. Forearm venous plasma norepinephrine concentration (fvNE) increased significantly at LBNP of -35 mmHg (p<0.05) and with a further sharp increase during LBNP of -50 mmHg (p<0.05). High degrees of intra-individual correlations were observed between changes in Log [fvNE] and CVP (r-values from -0.78 to -0.96, p<0.01). We conclude that low-pressure reflexes are the major determinants of fSNA during non-hypotensive gravitational stress (MAP and PP unchanged). When the gravitational stress is more pronounced, a decrease in PP further augments fSNA through inhibition of high-pressure arterial baroreflexes.     

Hysteresis in response to descending and ascending lower-body negative pressure

We have investigated the pattern of fluid redistribution and cardiovascular responses during graduated orthostatic stress. Twelve men, age 30-39 yr, underwent a 25-min lower-body negative pressure (LBNP) test protocol that involved sequential stages of LBNP at -8 mmHg (1 min), -16 mmHg (1 min), -30 mmHg (3 min), -40 mmHg (5 min), -50 mmHg (5 min), -40 mmHg (5 min), -30 mmHg (3 min), -16 mmHg (1 min), and -8 mmHg (1 min). Data were recorded at the end of each stage. For many measured variables values during the descending phase of LBNP (-8 to -40 mmHg) were significantly different from values during the ascending phase of (-40 to -8 mmHg). These differences appear to be due to a component of fluid translocation that occurs during LBNP and cannot be reversed within the duration of the procedure. We hypothesize that this slowly reversed component is sequestration of fluid in the interstitial and lymphatic compartments. In contrast, venous pooling is a rapidly reversible component of fluid movement during LBNP. A scheme describing fluid and cardiovascular responses to LBNP based on these data and the data of other investigators is presented.     

WISE-2005: tibial and gastrocnemius vein and calf tissue response to LBNP after a 60-day bed rest with and without countermeasures.

The objective of this study was to quantify by echography the changes in the intramuscular [gastrocnemius (Gast)] and nonintramuscular [posterior tibial (Tib)] calf veins cross-sectional area (CSA) and the superficial tissue thickness (STth) in response to lower body negative pressure (LBNP) after 60-day head-down bed rest (HDBR). Twenty-four healthy women (25-40 yr) were divided into three groups: control (Con), treadmill-LBNP and flywheel (Ex-Lb), nutrition (Nut; protein supplement). All underwent a LBNP (0 and -45 mmHg) before and on day 55 of HDBR. Subjects were identified as finisher (F) or nonfinisher (NF) of a 10-min tilt test after 60 days of HDBR. There were no differences in resting CSA of the Tib and Gast veins on HDBR day 55 compared with pre-HDBR for the Ex-Lb, Con and Nut, or the F groups; however, for NF both the Tib and Gast vein CSA at rest were significantly smaller after HDBR. At -45 mmHg LBNP, Tib and Gast CSAs were not significantly different from before HDBR in all groups (Ex-Lb, Con, Nut, F, NF). However, percent change in CSA of both veins from rest to -45 mmHg LBNP was significantly greater in the Con and Nut groups compared with Ex-Lb, and also NF compared with F. Similarly, the percent increase in STth on going from rest to -45 mmHg was higher after HDBR in the Con and Nut groups compared with Ex-Lb, as well as NF compared with F. These results showed that the Ex-Lb countermeasure minimized the bed rest effect on leg vein capacitance (CSA percent change) and STth increase during LBNP, whereas Nut had no effect and that higher leg vein and superficial tissue capacitance were associated with reduced orthostatic tolerance.     

Comparing cardiovascular responses during exercise between head-down tilt pedaling with lower body negative pressure and upright cycling in man

If lower body negative pressure (LBNP) loaded on exercise in weightlessness environment is able to derive a comparable cardiovascular responses to these in the ground, it should be identified as an optimal LBNP for exercise in space. To investigate the LBNP, 7 young subjects were exercised 4 work rates stepping up every 50 watts from 50 watts to 200 watts every 5 minutes in the upright position or 6 degree head down tilt position with each LBNP of 20, 40, 60, 80, and 100 mmHg. Oxygen uptake during tilt exercise with over 60 mmHg LBNP was not different from it in upright exercise. Heart rate and systolic arterial pressure responses to exercise were very similar between tilt exercise with 60 mmHg LBNP and upright exercise. In conclusion, the optimal LBNP loaded on exercise in space should be around 60 mmHg.     

Aging and the skin blood flow response to the unloading of baroreceptors during heat and cold stress.

Control of skin blood flow (SkBF) is on the efferent arm of both thermoregulatory and nonthermoregulatory reflexes. To what extent aging may affect the SkBF response when these two reflex systems interact is unknown. To determine the response of aged skin to the unloading of baroreceptors in thermoneutral, cold stress, and heat stress conditions, sequential bouts of nonhypotensive lower body negative pressure (LBNP) were applied at -10, -20, and -30 mmHg in 14 young (18-25 yr) and 14 older (63-78 yr) men. SkBF was measured by laser-Doppler velocimetry (averaged over 2 forearm sites), and data are expressed as percentage of maximal cutaneous vascular conductance (%CVC(max)). Total forearm blood flow was measured by venous occlusion plethysmography, and forearm vascular conductance (FVC) was calculated as the ratio of forearm blood flow to mean arterial pressure. In young men, all three intensities of LBNP in thermoneutrality decreased FVC significantly (P < 0.05), but FVC at -10 mmHg did not change in the older men. There were no significant LBNP effects on %CVC(max). Application of LBNP during cold stress did not significantly change %CVC(max) or FVC in either age group. During heat stress, -10 to -30 mmHg of LBNP decreased FVC significantly (P < 0.05) in both age groups, but these decreases were attenuated in the older men (P < 0.05). %CVC(max) decreased at -30 mmHg in the younger men only. These results suggest that older men have an attenuated skin vasoconstrictor response to the unloading of baroreceptors in heat stress conditions. Furthermore, the forearm vasoconstriction elicited by LBNP in older men reflects that of underlying tissue (i.e., muscle) rather than that of skin, whereas -30 mmHg LBNP also decreases SkBF in young hyperthermic men.