Inspiratory impedance effects on hemodynamic responses to orthostasis in normal subjects

BACKGROUND: Breathing through an impedance threshold device (ITD) might prove effective as a countermeasure against post-spaceflight orthostatic hypotension since it increased blood pressure (BP) and cardiac output in supine human subjects. OBJECTIVE: We tested the hypothesis that spontaneous breathing through an ITD would attenuate the reduction in stroke volume and BP during orthostasis in human subjects. METHODS: There were 19 volunteers (10 men, 9 women) who completed two 80 degrees head-up tilt (HUT) protocols with (active) and without (sham control) an ITD set to open at -7 cm H2O pressure. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR) were measured non-invasively during transition from supine to HUT. RESULTS: HUT caused significant elevation in HR and reductions in SV, CO, TPR, and MAP. Hemodynamic effects of HUT were similar for sham and active ITD. Further analysis revealed a subset (n = 11) of subjects who demonstrated a > 20% decrease in SV during HUT with the sham ITD. In this subset of subjects, the ITD attenuated (p = 0.004) the %deltaSV (-22.5 +/- 3.0%) during HUT compared with the sham ITD (%deltaSV = -37.4 +/- 2.6%). There was no statistical effect of ITD use in the subgroup who demonstrated < 20% reduction in SV (-16.6 +/- 0.4%). CONCLUSIONS: Use of an ITD may provide significant protection against orthostatic compromise in individuals with greater than 20% reductions in SV, such as astronauts returning from space.     

Acute cardiovascular adaptation to 10 consecutive episodes of head-up tilt

BACKGROUND: The cardiovascular system is highly adaptable to sustained +Gz acceleration. Little is known as to whether the cardiovascular system can adapt to acute, repetitive +Gz exposures. This study tested the hypothesis that the cardiovascular system would adapt to repeated orthostatic challenges in a single session. METHODS: Over a 70-min period, 14 subjects were exposed to 10 +75 degrees head-up tilts (HUT). Each tilt involved a 5-min supine period followed by a 2-min HUT. Heart rate (HR), systolic BP (SBP), diastolic BP (DBP), mean arterial pressure (MAP), total peripheral resistance (TPR), stroke volume (SV), and cardiac output (CO) were determined non-invasively. Cardiovascular responses to HUT10 for the final 30 s of the supine period and the first 30 s of the tilt period were compared with those of HUT1. Integrated cardiac baroreflex sensitivity (BRS) was assessed using the Valsalva maneuver. RESULTS: MAP and DBP increased in both supine (MAP p = 0.009, DBP p = 0.002) and tilt periods (MAP p = 0.003, DBP p = 0.009) for HUT10 compared with HUT1. TPR increased during the tilt period only (p = 0.001) during HUT10 compared with HUT1. CO and SV were decreased during the supine period at HUT10 relative to HUT1; however, there were no differences in the tilt period at HUT10 for either CO or SV. There was no change in the response of BRS, HR, or SBP from HUT1 to HUT10. CONCLUSIONS: This study indicates that 10 repetitive HUTs can elicit changes in the cardiovascular responses to orthostasis, reflected by an increased vascular resistance.     

Cardiovascular regulation response to hypoxia during stepwise decreases from 21% to 15% inhaled oxygen

INTRODUCTION: The classical view states that hypoxia beyond an oxygen concentration of about 17% induces tachycardia. However, few studies have investigated the dose-dependent effects of acute normobaric hypoxia on autonomic nervous regulation of the cardiovascular system. Therefore, we evaluated the effects of stepwise hypoxia on cardiovascular neural regulation and postulated that acute normobaric hypoxia causes vagal withdrawal and sympathetic activation from 17% 02. METHODS: There were 18 healthy men who were exposed to acute stepwise normobaric hypoxia (21%, 19%, 17%, 15% 02). Spectral analysis of the RR interval and BP variability were used. RESULTS: BP was not altered. Heart rate significantly increased at 15% (21%, 59 +/- 2; 15%, 62 +/- 2 bpm). The low-frequency power of systolic BP variability (an index of vasomotor sympathetic nerve activity) significantly increased at 15% (21%, 6.1 +/- 1.3; 15%, 9.9 +/- 1.3 mmHg2). The low-frequency power of the RR interval variability significantly increased from 17% (21%, 1036 +/- 233; 17%, 1892 +/- 409; 15%, 1966 +/- 362 ms2), However, the high-frequency power of RR interval variability (an index of cardiac parasympathetic nerve activity) did not change. Associated with these changes, the ratio of low- to high-frequency power of RR interval variability as an index of relative cardiac autonomic balance significantly shifted toward sympathetic dominance (21%, 1.5 +/- 0.3; 15%, 2.2 +/- 0.3). All indices of cardiac baroreflex function (transfer function and sequence gains) were unchanged. DISCUSSION: These results suggest that acute exposure to normobaric mild hypoxia (O2 > or = 15%) induces increases in sympathetic vasomotor activity and cardiac sympathetic dominance resulting in an increased heart rate. However, 15% O2 hypoxia might not induce changes in static BP, vagal activity, or spontaneous arterial-cardiac baroreflex function.     

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。     

The effect of caffeine on the cardiovascular responses to head-up tilt

BACKGROUND: Both caffeine and orthostasis have known cardiovascular effects. The possible interaction between these factors remains unknown. This study aimed to determine the effect of caffeine consumption on cardiovascular responses to head-up tilt. METHODS: Sixteen subjects underwent three +75 degree head-up tilts: i) control, ii) acute, after a dose of 5 mg x kg(-1) body mass of caffeine or placebo, and iii) chronic, following 7 d of caffeine or placebo consumption at a daily dose of 5 mg x kg(-1) body mass. Heart rate (HR), systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP) were measured using a Portapres BP monitor. RESULTS: The overall pattern of heart rate (HR) response in both caffeine and placebo groups showed a significant increase in HR after tilting for each tilt. Acute caffeine consumption significantly decreased resting HR (p < 0.05). After chronic consumption, resting HR was no longer significantly different. In the control condition, the overall pattern of response to tilt for SBP, DBP, and MAP showed no significant differences in either group. An acute dose of caffeine caused a significant fall (p < 0.05) in all BP variables in response to tilt. This effect was also seen after chronic caffeine consumption in SBP and MAP, but not in DBP. CONCLUSIONS: The results of this study indicate that both acute and chronic consumption of caffeine can lead to impaired cardiovascular function after exposure to an orthostatic challenge. This impaired function, reflected in a decreased resting HR and an inability to maintain MAP, is potentially due to impaired baroreflex function.     

Does endurance training affect orthostatic responses in healthy elderly men?

PURPOSE: To investigate the effects and time course of endurance training on the regulation of heart rate (HR), arterial pressure (AP), norepinephrine (NE), and plasma volume (PV) during orthostatic stress in healthy elderly men. METHODS: Thirty-one healthy men (65--75 yr) were randomly allocated into endurance training (N = 20, EX) and control (N = 11, CON) groups. The EX group cycled 3 d x wk(-1) for 30 min at 70% VO(2peak) for 12 wk x VO(2peak) was determined on an electronically braked cycle ergometer, before training and after 4, 8, and 12 wk of endurance training. The immediate (initial 30 s), early steady-state (1 min), and prolonged (5, 10, 15 min) beat-by-beat HR and AP responses during 90 degrees head-up tilt (HUT) were measured at least 3 d after each VO(2peak) test. Spontaneous baroreflex slopes were determined by application of linear regression to sequences of at least three cardiac cycles in which systolic blood pressure (SBP) and R-R interval changed in the same direction. Venous blood was collected during 90 degrees HUT and analyzed for changes in plasma NE concentrations, as well as hematocrit and hemoglobin to determine changes in PV. RESULTS: Endurance training significantly (P < 0.01) increased VO(2peak) (mL x kg(-1) x min(-1)) in EX by 10 +/- 2%. The immediate, early steady-state, and prolonged HR and AP responses and spontaneous baroreflex slopes during 90 degrees HUT were not significantly different (P > 0.05) between EX and CON groups before or after 4, 8, or 12 wk of endurance training. No significant differences (P > 0.05) were observed between EX and CON groups for peak changes in PV during orthostasis before (-15.0 +/- 1.4% vs -11.9 +/- 1.3%) or after 4 (-12.2 +/- 1.0% vs -12.7 +/- 1.4%), 8 (-13.7 +/- 1.2% vs -12.4 +/- 0.7%), and 12 wk (-10.8 +/- 1.6% vs -10.6 +/- 0.6%) of endurance training, suggesting a similar stimulus presented by 90 degrees HUT in both groups. Peak changes in NE concentrations during HUT were similar (P > 0.05) between EX and CON groups before (119 +/- 23 pg x mL(-1) vs 191 +/- 36 pg x mL(-1)) and after 4 (139 +/- 29 pg x mL(-1) vs 146 +/- 25 pg x mL(-1)), 8 (114 +/- 32 pg x mL(-1) vs 182 +/- 41 pg x mL(-1)), and 12 wk (143 +/- 35 pg x mL(-1) vs 206 +/- 42 pg.mL-1) of endurance training. CONCLUSIONS: These data indicate that in healthy elderly men, improvements in VO(2peak) can occur without compromising the regulation of HR, AP, NE, and PV during orthostatic stress.     

Baroreflex control of heart rate during heating in subjects with low orthostatic tolerance

BACKGROUND: Heat stress induces a reduction of orthostatic tolerance. The cardiovascular responses, including the cardiac baroreflex response to heat stress, were examined to test the hypothesis that subjects with orthostatically low tolerance demonstrate an impaired baroreflex control of heart rate (HR) during heat stress. METHODS: There were 44 healthy young volunteers who underwent whole body heat stress produced by a hot-water-perfused suit during supine rest for 45 min and 75 degrees head-up tilt (HUT) for 6 min. Esophageal temperature, HR, arterial pressure, and skin blood flow in the forearm and palm were measured continuously throughout the experiment. The sensitivity of the arterial baroreflex control of HR was calculated from the spontaneous changes in beat-to-beat arterial pressure and HR. RESULTS: The HUT was uneventful for 22 volunteers (higher tolerance group), but 22 volunteers (lower tolerance group) reached presyncope after 195 +/- 19 s. Esophageal temperature, HR, arterial pressure, and skin blood flow changed similarly in the two groups during heating. In the preheating condition, the sensitivity of the baroreflex control of HR did not differ significantly between the two groups. Heating did not alter the sensitivity of baroreflex control of HR in the higher tolerance group, but decreased it significantly in the lower tolerance group. Heating increased the number of heartbeats used for analysis of the baroreflex sensitivity in the higher tolerance group, but did not change it in the lower tolerance group. CONCLUSIONS: These results suggest that the impairment of vagal baroreflex control of HR during heat exposure aggravates the orthostatic intolerance in heat-stressed humans.     

Cardiovascular responses to head-up tilt after an endurance exercise program

The cardiovascular responses to 10 min of orthostasis were assessed before and after an aerobic exercise program. Five men and five women (18-25 years old) exercised for 7 weeks, four times per week, for 50 min per session at 70% of maximal heart rate (HR). Before and after the exercise program, maximal aerobic power (VO2max) was determined, and HR, systolic (SBP), diastolic (DBP), and pulse (PP) blood pressures were measured each minute during 5 min of supine rest, 10 min of foot-supported 70 degree head-up tilt (HUT), and 5 min of supine rest. Orthostatic tolerance was not determined. Calf compliance was measured in five of the subjects before and after the program as the change in leg volume at occluding pressures of 20, 40, 60, 80, and 100 mm Hg. Following the program, VO2max increased by 8.7% (p = 0.012), while decreases were noted in resting HR (9.4%, p = 0.041), SBP (5.0%, p less than 0.0005), and DBP (14.2%, p less than 0.0005). Despite a greater HR increase during HUT (7.1 beat.min-1, p = 0.034), SBP decreased by 3.4 mm Hg during HUT after the exercise program (p = 0.008). No differences were noted in the changes in DBP, MAP, or PP upon tilting (p greater than 0.05). After the program, the amount of fluid pooled in the calf at high occluding pressures (80 and 100 mm Hg) increased by 0.96 +/- 0.24 and 1.10 +/- 0.33 ml.100 ml tissue-1 (X +/- S.E.M., p = 0.017 and p = 0.028, respectively). We suggest that control of blood pressure during 10 min of orthostasis may be altered by endurance exercise training.     

倾斜床模拟推拉动作下心率和血压变化

目的建立倾斜床模拟推拉动作模型 ,并观察其引发的心血管反应性特点。方法以 1 0名健康歼击机飞行员为被试者 ,随机进行 3次 90°立位 (HUT)和 90°倒立位 (HDT)体位转换试验 ,HUT 1min→HDT 1 0s→HUT 1min ,第 2、3次体位转换时HDT的持续时间分别为 1 5s和 2 0s。床体旋转速度为45°/s。间隔 4s监测一次血压 ,连续记录心电图。结果在HDT期间 ,各时间心率和血压较基础HUT明显下降。随后HUT时 ,除 1 1～ 1 5s血压外 ,其余各时间心率和血压较基础HUT明显下降。结论采用倾斜床可以模拟推拉动作所引起的心血管的反应 ,故其可作为推拉动作的模型     

反复体位改变训练对人体立位耐力的影响

目的验证反复体位改变训练提高人体立位耐力的有效性 ,并探讨其机理。方法 6名被试者经受了为期 1 1d共 9次的反复体位改变训练。在训练前和训练后利用头高位倾斜检查立位耐力。结果训练后 ,被试者在立位耐力检查中的反应得到改善 ,表现为与训练前相比立位中不良症状明显减轻 (症状得分 4.5 0± 1 .0 5vs .2 .83± 1 .60 ,P <0 .0 5 ) ,心率的增量明显降低 [( 2 9.3± 4.3)bpmvs .( 1 3.5± 7.5 )bpm ,P <0 .0 1 ],平均动脉压的增量明显增加 [( 4 .8± 4.4)mmHgvs.( 9.0± 3.0 )mmHg ,P <0 .0 5 ],心血管反应指数明显减小 ( 34.42± 5 .0 0vs.2 2 .33± 8.2 7,P <0 .0 1 )。结论反复体位改变训练可提高人体立位耐力。该训练有望在飞行员 ,特别是航天员训练中得到应用     

Health risk for athletes at moderate altitude and normobaric hypoxia

Altitudes at which athletes compete or train do usually not exceed 2000-2500 m. At these moderate altitudes acute mountain sickness (AMS) is mild, transient and affects at the most 25% of a tourist population at risk. Unpublished data included in this review paper demonstrate that more intense physical activity associated with high-altitude training or mountaineering does not increase prevalence or severity of AMS at these altitudes. These conclusions can also be extended to the use of normobaric hypoxia, as data in this paper suggest that the severity of AMS is not significantly different between hypobaric and normobaric hypoxia at the same ambient pO(2). Furthermore, high-altitude cerebral or pulmonary oedema do not occur at these altitudes and intermittent exposure to considerably higher altitudes (4000-6000 m) used by athletes for hypoxic training are too short to cause acute high-altitude illnesses. Even moderate altitude between 2000 and 3000 m can, however, exacerbate cardiovascular or pulmonary disease or lead to a first manifestation of undiagnosed illness in older people that may belong to the accompanying staff of athletes. Moderate altitudes may also lead to splenic infarctions in healthy athletes with sickle cell trait.     

Squat-stand test response following 10 consecutive episodes of head-up tilt

INTRODUCTION: The cardiovascular system is adaptable to multiple exposures to gravity over several days, and to repeated exposures in a single day. This study aimed to investigate if the cardiovascular adaptation observed following 10 +75 degrees head-up tilts (HUT) would improve the responses to the squat-stand test (SST). METHODS: There were 16 subjects who were randomly allocated into either a tilting group that underwent 10 +75 degrees HUTs in 70 min (Tilting) or a control group that underwent 70 min of rest (Control). Before and after HUT or rest, subjects performed a SST (SST1 and SST2, respectively). Heart rate (HR), BP [systolic (SBP), diastolic (DBP), mean (MAP)], total peripheral resistance (TPR), stroke volume (SV), and cardiac output (CO) were determined during both SSTs. The final 30 s of squat and the first 30 s of stand (divided into three 10-s blocks termed Stand10, Stand20, and Stand30) were compared between SST1 and SST2. RESULTS: In the Tilting condition, during the squat phase of SST2, the following were significantly elevated: SBP (131 +/- 9 to 140 +/- 7.2 mmHg) and MAP (94 +/- 8.7 to 105 +/- 10.2 mmHg); DBP (76 +/- 9.4 to 87 +/- 11.9 mmHg); TPR (1197 +/- 524.6 to 229 +/- 610.5 dyn x s(-1) x cm(-5)) and HR were significantly decreased (78 +/- 6.9 to 73 +/- 7.5 bpm) compared with SST1. At Stand10, DBP and MAP were significantly increased (59 +/- 9.5 to 69 +/- 15.7 mmHg and 74 +/- 8.9 to 84 +/- 14.7 mmHg, respectively); at Stand20, SBP was increased (121 +/- 17 to 128 +/- 22 mmHg); and at Stand30 the following were increased: DBP (64 +/- 8.8 to 75 +/- 16.1 mmHg); SBP (127 +/- 9.2 to 139 +/- 15.8 mmHg); and MAP (79 +/- 8 to 90 +/- 14.9 mmHg). There were no differences observed between SST1 and SST2 in the Control group. DISCUSSION: Cardiovascular responses to the SST can be improved with 10 consecutive +75 degrees HUTs. This is predominantly due to an increase in DBP, indicative of a change in vascular resistance.     

Cardiovascular and humoral readjustment after different levels of head-up tilt in humans

PURPOSE: To get a more complete picture of cardiovascular regulation after postural changes, this investigation directly monitored volume-related, hemodynamic, and endocrine variables during and after 30 min of passive head-up tilt (HUT) of various degrees. It was hypothesized that the return of variables to pre-tilt control level is of system-specific duration and different from what is found after lower body negative pressure (LBNP). DESIGN: We tested 7 persons on 5 different days using, in random order, no (HUT0) or different intensity (12 degrees , 30 degrees , 53 degrees , and 70 degrees ) of passive orthostasis (HUT12, HUT30, HUT53, HUT70). Data were collected before (supine), during, and after (supine) HUT and compared with synchronous data from HUT0. RESULTS: There was graded alteration with the sine of tilt angle for all hormones and directly volume-related variables. The effects of HUT70 were of the same magnitude as previously documented by others. After HUT, hemodynamic variables and catecholamines returned to control levels most rapidly. Heart rate depression, as observed in a companion LBNP study in the same subjects, did not occur. Vasopressin, PRA, plasma volume and Z0 returned to nominal values more slowly. Plasma aldosterone was still elevated 50 min after reassuming supine posture. CONCLUSION: Besides specific dose-responses within hemodynamic, volume-dependent, and hormonal variables after orthostatic loading of different degree, the return to control levels after HUT occurs with distinctly different time-courses, which are not identical with those seen after LBNP-simulated orthostasis.     

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.     

Circulatory responses to orthostasis during alpha1-adrenergic receptor blockade at high altitude.

BACKGROUND: Increased blood level of norepinephrine, a primary alpha-adrenergic agonist, is associated with high-altitude exposure, and may help regulate key physiological functions (e.g., blood pressure). We hypothesized that blocking alpha1-adrenergic receptors would impair circulatory compensation for an orthostatic challenge to a greater extent at altitude than at sea level. METHODS: Sixteen healthy women (23 +/- 2 yr) were randomly assigned to receive either 2 mg prazosin (n = 8) or placebo (n = 8) t.i.d. (double-blind design) for 12 d at sea level and during the first 12 d of altitude residence (4300 m). Passive 60 degrees upright tilt was performed at sea level (10 d of treatment), and after 3 and 10 d at altitude. Mean arterial BP (MABP, via auscultation) and heart rate (HR, via ECG) were measured every min during 10 min each of supine rest and tilt. RESULTS: For the prazosin group compared with the placebo group: 1.) Supine and tilt MABP were consistently lower (p < 0.05) at sea level; 2.) MABP did not differ (p > 0.05) for either day at altitude; 3.) HR was similar for both positions at sea level and altitude; and 4.) MABP was consistently less only at sea level and HR was consistently greater only at altitude (both p < 0.05) in response to tilt. CONCLUSIONS: alpha1-adrenergic blockade altered MABP and HR responses to tilt at sea level and altitude, but circulatory responses to orthostasis were well maintained in both environments. At altitude, BP during tilt was sufficiently maintained by a compensatory increase in heart rate, likely mediated by parasympathetic withdrawal.     

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.     

Effects of sildenafil on exercise capacity in hypoxic normal subjects

The phosphodiesterase-5 inhibitor sildenafil has been reported to improve hypoxic exercise capacity, but the mechanisms accounting for this observation remain incompletely understood. Sixteen healthy subjects were included in a randomized, double-blind, placebo-controlled, cross-over study on the effects of 50-mg sildenafil on echocardiographic indexes of the pulmonary circulation and on cardiopulmonary cycle exercise in normoxia, in acute normobaric hypoxia (fraction of inspired O2, 0.1), and then again after 2 weeks of acclimatization at 5000 m on Mount Chimborazo (Ecuador). In normoxia, sildenafil had no effect on maximum VO2 or O2 saturation. In acute hypoxia, sildenafil increased maximum VO2 from 27 +/- 5 to 32 +/- 6 mL/min/kg and O2 saturation from 62% +/- 6% to 68% +/- 9%. In chronic hypoxia, sildenafil did not affect maximum VO2 or O2 saturation. Resting mean pulmonary artery pressure increased from 16 +/- 3 mmHg in normoxia to 28 +/- 5 mmHg in normobaric hypoxia and 32 +/- 6 mmHg in hypobaric hypoxia. Sildenafil decreased pulmonary vascular resistance by 30% to 50% in these different conditions. We conclude that sildenafil increases exercise capacity in acute normobaric hypoxia and that this is explained by improved arterial oxygenation, rather than by a decrease in right ventricular afterload.     

Decrement in postural control during mild hypobaric hypoxia

The effects of mild hypoxia on the postural control system of 39 naive subjects were examined by measuring the postural sway with a Kistler force platform, at ground level and at one of four simulated altitudes: 1,521 m (5,000 ft), 2,438 m (8,000 ft), 3,048 m (10,000 ft), or 3,658 m (12,000 ft). The total sway increased above the ground level controls for the 1,521 m, 2,438 m, and 3,048 m exposures (p less than or equal to 0.005) as did the sway at the lowest measurable frequency (p less than or equal to 0.002), but no change in sway was seen in those subjects exposed to 3,658 m as compared to ground level values. Significant interaction between altitude and exposure was observed at p less than or equal to 0.04, reflecting the definite effect at the lower altitudes and the lack of an effect at the higher altitude. The multiple comparison test indicated no difference between the responses at 1,524 m, 2,438 m, and 3,048 m. Both arterial oxygen saturation, SaO2, and the end-tidal oxygen partial pressure, PetO2, decreased in relation to the test altitudes with a statistically significant interaction between altitude and PetO2 (p less than or equal to 0.02), and SaO2 (p less than or equal to 0.005). There was no significant interaction between altitude and end-tidal carbon dioxide partial pressure (p = 0.4853). The postural control mechanisms, as an intergrative functional unit, are very sensitive to acute mild hypoxia. Arguments are advanced to indicate that intervention of compensatory mechanisms at higher altitudes may explain the recovery of postural stability at 3,658 m.     

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。     

Effects of repeated Valsalva maneuver straining on cardiac and vasoconstrictive baroreflex responses

INTRODUCTION: We hypothesized that repeated respiratory straining maneuvers (repeated SM) designed to elevate arterial BPs (arterial baroreceptor loading) would acutely increase baroreflex responses. METHODS: We tested this hypothesis by measuring cardiac baroreflex responses to carotid baroreceptor stimulation (neck pressures), and changes in heart rate and diastolic BP after reductions in BP induced by a 15-s Valsalva maneuver in 10 female and 10 male subjects at 1, 3, 6, and 24 h after performing repeated SM. Baroreflex responses were also measured in each subject at 1, 3, 6, and 24 h at the same time on a separate day without repeated SM (control) in a randomized, counter-balanced cross-over experimental design. RESULTS: There was no statistical difference in carotid-cardiac and peripheral vascular baroreflex responses measured across time following repeated SM compared with the control condition. Integrated cardiac baroreflex response (deltaHR/ deltaSBP) measured during performance of a Valsalva maneuver was increased by approximately 50% to 1.1 +/- 0.2 bpm x mm Hg(-1) at 1 h and 1.0 +/- 0.1 bpm x mm Hg(-1) at 3 h following repeated SM compared with the control condition (0.7 +/- 0.1 bpm x mm Hg(-1) at both 1 and 3 h, respectively). However, integrated cardiac baroreflex response after repeated SM returned to control levels at 6 and 24 h after training. These responses did not differ between men and women. CONCLUSIONS: Our results are consistent with the notion that arterial baroreceptor loading induced by repeated SM increased aortic, but not carotid, cardiac baroreflex responses for as long as 3 h after repeated SM. We conclude that repeated SM increases cardiac baroreflex responsiveness which may provide patients, astronauts, and high-performance aircraft pilots with protection from development of orthostatic hypotension.