下体负压对抗失重／模拟失重后立位耐力降低的研究进展

下体负压对抗失重／模拟失重后立位耐力降低的研究进展姚永杰吴兴裕在航天或头低位倾斜模拟失重时，如缺乏必要的对抗措施，通常要发生立位耐力不良，表现为：休息时心率较飞行或卧床前增快、体位性低血压、同等负荷下最大和次大氧耗量减少。在立位应激时，航天员可发生心...     

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。     

失重或模拟失重对人体交感肾上腺活动的影响

失重或模拟失重对人体交感肾上腺活动的影响杨玉华高淳航天时航天员的体液头向转移，使机体产生一系列的生理、生化变化。心血管功能失调是航天员返回地面时超重耐力和立位耐力下降的主要原因。因此失重对心血管系统的影响、失重时心血管系统的适应性变化过程，一直是航天...     

模拟失重对心血管功能与心肌超微结构的影响

模拟失重对心血管功能与心肌超微结构的影响张立藩（西安第四军医大学７１００３２）航天失重可引起航天员心血管功能失调（Ｃａｒｄｉｏｖａｓｃｕｌａｒｄｅｃｏｎｄｉｔｉｏｎｉｎｇ）变化，表现为运动能力与立位耐力的降低等。其发生机理目前仍不甚了解。飞行后的超声...     

失重或模拟失重时下肢顺应性变化研究的进展

失重或模拟失重引起下肢顺应性的增加，使立位时有较多的血液潴留在下肢，回流至右心房的血液减少，从而促使心输出量和动脉血压的下降，因而其变化是失重或模拟失重后立位耐力下降的主要机理之一，其研究对于深入理解立位耐力的下降机理和发展对抗方法具有一定意义，本文对失重或模拟失重时下肢顺应性的变化，测量方法，变化机理和防护方法等方面进行了论述。     

失重／模拟失重对心肌结构与功能的影响

自开展载人航天活动以来,已发现在失重环境停留可引起航天员运动能力及立位耐力下降.后者主要表现为:在失重条件下受到下体负压作用时,或返回地面IG条件下取直立体位时,航天员感到心慌、头晕,甚至出现晕厥,其体征则为心率过分增快,维持正常动脉血压的能力明显减弱;一般需数日至数周始能恢复.目前,将此类症状与体征称为“心血管脱适应(cardiovascular deconditioning)”,或者称为心血管机能障碍(cardiovascular dysfunct-ion).虽经几十年研究,对这种心血管机能障碍的机理仍然不甚清楚,特别是关于长期失重所致的心血管机能障碍的机理则了解更少.虽然为期一年的载人航天已经实现,但所用对抗措施并不理想,亦不能完全克服心血管机能障碍所带来的各种问题.为保证未来长时间航天活动,也急需发展新的对抗措施.     

加压套带对抗头低位卧床模拟失重生理影响的作用

为研究四肢加压套带在对抗失重对心血管系统影响中的作用，１２名受试者随机分为对照组和套带组，进行了１０ｄ头低位卧床实验。卧床中套带组四肢使用持续加压套带１２ｈ／ｄ，对照组涂任何对措施，卧床前后检测立位耐力。结果显示：卧床前１人全部通过立位耐力试验；卧床后，套带组６人中通过５人，对照组６人仅通过１人；提示：套带加压能有效阻止头低位卧床模拟失重产生的立位耐力下降。     

模拟失重4周大鼠心血管功能失调及血流动力学改变

目的　探讨模拟失重 4周大鼠心血管调节功能和血流动力学指标变化。　方法　选体重 2 5 0～ 2 90 g的雄性大鼠2 0只随机分为悬吊组和对照组各 10只。采用尾部悬吊模拟失重大鼠模型 ,以倾斜 (HDT)和下体负压 (L BNP)实验及左心室插管方法检测立位耐力及血流动力学结果。　结果　模拟失重 4周大鼠在 30°、 40°及 6 0°倾斜作用下 ,其平均动脉压的下降幅度远大于对照大鼠 (P<0 .0 5 ) ;在 - 30°、-45°以及 - 6 0°HDT时 ,其平均动脉压的上升幅度有大于对照组的趋势 ,但差别均未达显著程度。在 L BNP作用下 ,模拟失重 4周大鼠平…     

中药复方对模拟失重兔血流变特性及循环系统的调节作用

目的研究中药复方对模拟失重兔血流变及循环系统的调节作用,为防护失重对心血管功能的不良影响提供依据。方法用兔头低位(-20°)倾斜9d模拟失重,观察中药复方对兔血液流变学、血脂指标及立位耐力的影响。结果兔模拟失重后红细胞压积减少,红细胞变形能力明显下降,纤维蛋白原含量有增加趋势;胆固醇和低密度脂蛋白明显增加,甘油三脂有轻度增高趋势。中药复方对血液流变学指标改善不明显,但有降低甘油三脂的趋势,对胆固醇的增加也有抑制的趋势。在负压-立位实验过程中,对照组兔模拟失重后立位耐受时间减少,中止实验前出现了ST段下移、T波倒置及心律紊乱等明显的心肌缺血性改变;而中药组兔心率平稳,心电图缺血性改变不明显,立位耐受时间增加。结论中药复方对模拟失重兔的立位耐力降低具有显著的防护作用,同时还能改善血脂代谢,从整体上对机体各系统进行调节,提高了机体适应外界不良环境、抵御不良刺激的能力。     

心肌收缩功能降低对下体负压效应影响的仿真研究

目的：研究不同程度心肌收缩功能降低对心血管系统立位应激反应的影响，探讨心肌收缩功能改变在航天失重心后心血管失调和立位耐力降低机理中的意义。方法：以我们原有仿真血量减少后下体负压（LBNP）暴露时心血管系统反应的模型为基础，对其心脏工作子模型中最大弹性系数（maximum elastance)乘以一个反映心肌收缩功能改变的系数。然后逐渐降低收缩功能改变系，仿真血容量减少12％后，心肌收缩功能降低0－305后LBNP时心率（HR）、血压（BP）和心输出量（CO）的变化。结果：心肌收缩功能降低将使LBNP时，HR加快，BP降低和CO减小。结论：心肌收缩功能降低导致心血管系统对立位应激的调节能力降低。     

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。     

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.     

Effect of a central redistribution of fluid volume on response to lower-body negative pressure

We studied cardiovascular responses to lower-body negative pressure (LBNP) following 1 hour (h) of 6 degrees head-down tilt to determine whether a redistribution of blood volume toward the central circulation modifies the subsequent response to orthostatic stress. Responses of 12 men, ages 30-39 years, were evaluated by electrocardiography, impedance cardiography, sphygmomanometry, and measurement of calf circumference. During the LBNP that followed head-down tilt--as compared with control LBNP (no preceding head-down tilt)--subjects had smaller stroke volume and cardiac output, greater total peripheral resistance, and less calf enlargement. These differences reflect differences in the variables immediately preceding LBNP. Magnitudes of the responses from pre-LBNP to each pressure stage of the LBNP procedure did not differ between protocols. Mean and diastolic arterial pressures were slightly elevated after LBNP-control, but they fell slightly during LBNP post-tilt. These cardiovascular responses to simulated gravitational stress following head-down tilt may reflect the manner in which adaptation to microgravity affects subsequent responses to orthostatic stress on return to Earth.     

Peripheral effector mechanism hypothesis of postflight cardiovascular dysfunction

Studies on the mechanisms of cardiovascular dysfunction after space-flight are important to illustrate the cardiovascular effect of microgravity and develop appropriate multi-system countermeasures for future long-duration spaceflights. Over the past 10 yr, we have systematically studied the adaptational changes in structure and function of both the heart and vessels, using the tail-suspension rat model to simulate microgravity effects. Our results indicate that simulated microgravity induced atrophic changes and reduced contractility of the heart muscle, and upward- and downward-regulation in structure, function, and innervation state of vessels in the brain and hind body of the rat. In addition, more recent advances in relevant ground-based and space-flight studies from different laboratories have also been reviewed. Based on these studies, it has been speculated that, in addition to hypovolemia, the microgravity-induced adaptational changes in the structure and function of the two main effectors of the cardiovascular system, i.e., the arterial smooth muscle and the cardiac muscle, might be among the most important mechanisms responsible for postflight cardiovascular dysfunction and orthostatic intolerance. In this paper we will review the available evidence with comments.     

Cardiovascular adaptation during simulated microgravity: lower body negative pressure to counter orthostatic hypotension

The cardiovascular function is one of the main functions disturbed by microgravity. It is particularly affected by the astronaut's return to Earth, where one of the symptoms of the cardiovascular adaptation syndrome is orthostatic hypotension; the clinical consequence can be presyncopal state or a syncope. Lower body negative pressure (LBNP) is intended to stimulate the venous system of the lower limbs. Studies performed in the U.S. have shown that LBNP constitutes an efficient countermeasure, but this approach is impractical because 4 to 6 h/d of application are required. Five volunteers took part in two recent antiorthostatic bed rest experiments for 30 days. In the first experiment, three subjects were submitted to several sessions of LBNP per day and two others were controls; in the second, the LBNP group of the first experiment became control and vice versa. Two orthostatic investigations were performed: 5 d before bed rest; and at the end of the 30-d bed rest period. The results showed that: 1) when the subjects were controls, a high orthostatic hypotension post bed rest with three syncopes and one presyncopal state during the first minutes of the tilt test appeared; 2) when the subjects were submitted to LBNP sessions, no orthostatic hypotension was noted. These two experiments proved the beneficial effects of the LBNP as a countermeasure against orthostatic hypotension.     

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.     

航天中的心血管问题

人体的心血管系统具有向全身各组织、器官输送营养物质、排泄代谢产物、参与体液和电解质的调节、维持体内环境稳定的作用,并具有防御和保护功能。心血管系统是维持人体进行正常生理功能的重要系统,它的功能改变必然引起体内其它生理系统功能的紊乱。载人航天实践证明,轨道飞行中的微重力对心血管系统有明显的影响,可引起心血管功能失调。因而,微重力对心血管系统的影响及其防护措施的研究已成为航天医学研究中的一个重要课题。     

前庭系统适应性变化对心血管调节和立位耐力的影响

空间飞行初期人体感受到的空间适应综合征,主要由前庭传入的改变和体液头向分布引起,这种适应性的逆向变化同样发生在人体由微重力返回正常1G重力时,造成航天员返回后出现步态不稳及立位耐力下降。动物模型的证据和人体实验的部分数据表明,前庭系统通过自主神经系统影响心血管调节,其中耳石感受器的传入起着重要作用。由于心血管调节异常引起的立位耐力下降是载人航天的重要医学问题。在心血管功能和立位耐力下降过程中前庭系统功能变化有重要影响。     

Orthostatic response in rats after hindlimb unloading: effect of transcranial electrical stimulation

INTRODUCTION: Orthostatic hypotension is a commonly observed phenomenon after exposure to microgravity and in various forms of autonomic failure. It has been suggested that insufficient activation of supraspinal structures responsible for descending sympathetic drive could play a significant role in this disorder. We examined the effect of transcranial electrical stimulation (TES) of autonomic nuclei within the brain on the orthostatic hypotension induced by exposure to simulated microgravity using a hindlimb unloading model. METHODS: There were 20 male Wistar rats that were suspended by their tail with the angle of elevation between the cage floor and the rat's body approximately 40 degrees. There were 11 age-matched Wistar rats used as cage controls. Orthostatic stability was examined by using an orthostatic challenge test (450 head-up test for a period of 3 min). In 10 rats from the tail-suspended group, the orthostatic challenge test was applied during TES. RESULTS: In the rats exposed to simulated microgravity (tail suspension), the orthostatic challenge test caused a significant decrease in mean arterial blood pressure by 18.4 +/- 2.2%. TES attenuated this microgravity-induced orthostatic hypotension to 9.5 +/- 1.8% (P < 0.05), which was similar to the observed response to an orthostatic challenge in the control group (6.9 +/- 1.1%). DISCUSSION: Results of this study suggest that TES significantly reduces the changes in blood pressure during an orthostatic challenge test in animals exposed to simulated microgravity. Our observations support the notion that a reduction in descending sympathoexcitatory input from supraspinal structures could contribute to orthostatic hypotension and intolerance observed in astronauts following their return from spaceflight.