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All sourcesNASA NTRSDOE OSTI
NASA NTRS2004

An Earth-based Model of Microgravity Pulmonary Physiology

There are currently only two practical methods of achieving microgravity for experimentation: parabolic flight in an aircraft or space flight, both of which have limitations. As a result, there are many important aspects of pulmonary physiology that have not been investigated in microgravity. We propose to develop an earth-based animal model of microgravity by using liquid ventilation, which will allow us to fill the lungs with perfluorocarbon, and submersing the animal in water such that the density of the lungs is the same as the surrounding environment. By so doing, we will eliminate the effects of gravity on respiration. We will first validate the model by comparing measures of pulmonary mechanics, to previous space flight and parabolic flight measurements. After validating the model, we will investigate the impact of microgravity on aspects of lung physiology that have not been previously measured. These will include pulmonary blood flow distribution, ventillation distribution, pulmonary capillary wedge pressure, ventilation-perfusion matching and pleural pressures and flows. We expect that this earth-based model of microgravity will enhance our knowledge and understanding of lung physiology in space which will increase in importance as space flights increase in time and distance.

Hirschl, Ronald B.↗
NASA NTRS2004

An Earth-Based Model of Microgravity Pulmonary Physiology

There are currently only two practical methods of achieving micro G for experimentation: parabolic flight in an aircraft or space flight, both of which have limitations. As a result, there are many important aspects of pulmonary physiology that have not been investigated in micro G. We propose to develop an earth-based animal model of micro G by using liquid ventilation, which will allow us to fill the lungs with perfluorocarbon, and submersing the animal in water such that the density of the lungs is the same as the surrounding environment. By so doing, we will eliminate the effects of gravity on respiration. We will first validate the model by comparing measures of pulmonary physiology, including cardiac output, central venous pressures, lung volumes, and pulmonary mechanics, to previous space flight and parabolic flight measurements. After validating the model, we will investigate the impact of micro G on aspects of lung physiology that have not been previously measured. These will include pulmonary blood flow distribution, ventilation distribution, pulmonary capillary wedge pressure, ventilation-perfusion matching, and pleural pressures and flows. We expect that this earth-based model of micro G will enhance our knowledge and understanding of lung physiology in space which will increase in importance as space flights increase in time and distance.

Hirschl, Ronald B.↗
NASA NTRS1978

Continuous distributions of specific ventilation recovered from inert gas washout

A new technique is described for recovering continuous distributions of ventilation as a function of tidal ventilation/volume ratio from the nitrogen washout. The analysis yields a continuous distribution of ventilation as a function of tidal ventilation/volume ratio represented as fractional ventilations of 50 compartments plus dead space. The procedure was verified by recovering known distributions from data to which noise had been added. Using an apparatus to control the subject's tidal volume and FRC, mixed expired N2 data gave the following results: (a) the distributions of young, normal subjects were narrow and unimodal; (b) those of subjects over age 40 were broader with more poorly ventilated units; (c) patients with pulmonary disease of all descriptions showed enlarged dead space; (d) patients with cystic fibrosis showed multimodal distributions with the bulk of the ventilation going to overventilated units; and (e) patients with obstructive lung disease fell into several classes, three of which are illustrated.

Lewis, S. M.↗
NASA NTRS1977

Specialized physiological studies in support of manned space flight

Breath-by-breath measurements of pulmonary capillary O2 transfer and ventilation with a box-balloon spirometer and mass spectrometer were made on 3 subjects before, during and after 10 min of lower body negative pressure (LBNP) at -20, -40 and -60 Torr with arterial samples at -60 Torr. Deficits in blood O2 stores (O2B) were noted during LBNP with repayment of O2B during recovery being related to the intensity of LBNP stress. Concurrent calf volume, measured with a Hg strain gauge, decreased towards baseline well before the peak rise in pulmonary capillary O2 transfer after the release of LBNP which signified that O2B changes were related to blood volume shifts. The return of O2-depleted pooled blood to the central circulation during the first min. of recovery caused significant stress-related hyperpnea which peaked near 30 sec. and returned to near baseline after the first min. Three-compartment lung model analyses indicated an increase in the ventilated unperfused lung fraction from 0.09 to 0.17 with the effective compartment decreasing from 0.83 to 0.77. It appears that the 30% increase in ventilation equivalent was primarily the result of less effective lung perfusion during the LBNP.

Source record↗
NASA NTRS1992

Ventilation-perfusion matching during exercise

In normal subjects, exercise widens the alveolar-arterial PO2 difference (P[A-a]O2) despite a more uniform topographic distribution of ventilation-perfusion (VA/Q) ratios. While part of the increase in P(A-a)O2 (especially during heavy exercise) is due to diffusion limitation, a considerable amount is caused by an increase in VA/Q mismatch as detected by the multiple inert gas elimination technique. Why this occurs is unknown, but circumstantial evidence suggests it may be related to interstitial pulmonary edema rather than to factors dependent on ventilation, airway gas mixing, airway muscle tone, or pulmonary vascular tone. In patients with lung disease, the gas exchange consequences of exercise are variable. Thus, arterial PO2 may increase, remain the same, or fall. In general, patients with advanced chronic obstructive pulmonary disease (COPD) or interstitial fibrosis who exercise show a fall in PO2. This is usually not due to worsening VA/Q relationships but mostly to the well-known fall in mixed venous PO2, which itself results from a relatively smaller increase in cardiac output than VO2. However, in interstitial fibrosis (but not COPD), there is good evidence that a part of the fall in PO2 on exercise is caused by alveolar-capillary diffusion limitation of O2 transport; in COPD (but not interstitial fibrosis), a frequent additional contributing factor to the hypoxemia of exercise is an inadequate ventilatory response, such that minute ventilation does not rise as much as does CO2 production or O2 uptake, causing arterial PCO2 to increase and PO2 to fall.

Non-NASA Center↗
NASA NTRS1998

Contributions of tidal lung inflation to human R-R interval and arterial pressure fluctuations

We studied the effects of mechanical lung inflation on respiratory frequency R-R interval and arterial pressure fluctuations in nine healthy young adults undergoing elective orthopedic surgery. We conducted this research to define the contribution of pulmonary and thoracic stretch receptor input to respiratory sinus arrhythmia. We compared fast Fourier transform spectral power during three modes of ventilation: (1) spontaneous, frequency-controlled (0.25 Hz) breathing, (2) intermittent positive pressure ventilation (0.25 Hz, with a tidal volume of 8 ml/kg) and (3) high frequency jet ventilation (5.0 Hz, 2.5 kg/cm2), after sedation and vecuronium paralysis. Mean R-R intervals, arterial pressures and arterial blood gas levels were comparable during all three breathing conditions. Respiratory frequency systolic pressure spectral power was comparable during spontaneous breathing and conventional mechanical ventilation, but was significantly reduced during high frequency jet ventilation (P < 0.05). Respiratory frequency R-R interval spectral power (used as an index of respiratory sinus arrhythmia) declined dramatically with sedation and muscle paralysis (P < 0.05), but was greater during conventional mechanical, than high frequency jet ventilation (P < 0.05). These results suggest that although phasic inputs from pulmonary and thoracic stretch receptors make a statistically significant contribution to respiratory sinus arrhythmia, that contribution is small.

Clinical Trial↗
NASA NTRS1998

Redistribution of pulmonary blood flow during unilateral hypoxia in prone and supine dogs

We used fluorescent-labeled microspheres in pentobarbital-anesthetized dogs to study the effects of unilateral alveolar hypoxia on the pulmonary blood flow distribution. The left lung was ventilated with inspired O2 fraction of 1.0, 0.09, or 0.03 in random order; the right lung was ventilated with inspired O2 fraction of 1.0. The lungs were removed, cleared of blood, dried at total lung capacity, then cubed to obtain approximately 1,500 small pieces of lung ( approximately 1.7 cm3). The coefficient of variation of flow increased (P < 0.001) in the hypoxic lung but was unchanged in the hyperoxic lung. Most (70-80%) variance in flow in the hyperoxic lung was attributable to structure, in contrast to only 30-40% of the variance in flow in the hypoxic lung (P < 0.001). When adjusted for the change in total flow to each lung, 90-95% of the variance in the hyperoxic lung was attributable to structure compared with 70-80% in the hypoxic lung (P < 0.001). The hilar-to-peripheral gradient, adjusted for change in total flow, decreased in the hypoxic lung (P = 0.005) but did not change in the hyperoxic lung. We conclude that hypoxic vasoconstriction alters the regional distribution of flow in the hypoxic, but not in the hyperoxic, lung.

NASA Discipline Cardiopulmonary↗
NASA NTRS1989

Venous gas embolism - Time course of residual pulmonary intravascular bubbles

A study was carried out to determine the time course of residual pulmonary intravascular bubbles after embolization with known amounts of venous air, using an N2O challenge technique. Attention was also given to the length of time that the venous gas emboli remained as discrete bubbles in the lungs with 100 percent oxygen ventilation. The data indicate that venous gas emboli can remain in the pulmonary vasculature as discrete bubbles for periods lasting up to 43 + or - 10.8 min in dogs ventilated with oxygen and nitrogen. With 100 percent oxygen ventilation, these values are reduced significantly to 19 + or - 2.5 min.

Butler, B. D.↗
NASA NTRS1992

Ventilation-perfusion relationships in the lung during head-out water immersion

Mechanisms of altered pulmonary gas exchange during water immersion were studied in 12 normal males: 6 young (aged 20-29) and 6 older (aged 40-45). It is concluded that, in young subjects with closing volume (CV) less than expiratory reserve volume (ERV), gas exchange was enhanced during immersion, because normal ventilation-perfusion relations were preserved, and by mass balance, the ventilation/O2 uptake changes elevated arterial P(O2). In older males with CV greater than ERV and 52 percent of tidal volume below CV, immersion-induced airways closure during tidal breathing was associated with minimally increased shunt that did not significantly impair gas exchange. It is suggested that airways closure of this degree is of little importance to gas exchange.

Derion, Toniann↗
NASA NTRS2004

Investigations of Pulmonary Epithelial Cell Damage due to Air-Liquid Interfacial Stresses in a Microgravity Environment

Pulmonary airway closure is a potentially dangerous event that can occur in microgravity environments and may result in limited gas exchange for flight crew during long-term space flight. Repetitive airway collapse and reopening subjects the pulmonary epithelium to large, dynamic, and potentially injurious mechanical stresses. During ventilation at low lung volumes and pressures, airway instability leads to repetitive collapse and reopening. During reopening, air must progress through a collapsed airway, generating stresses on the airway walls, potentially damaging airway tissues. The normal lung can tolerate repetitive collapse and reopening. However, combined with insufficient or dysfunctional pulmonary surfactant, repetitive airway collapse and reopening produces severe lung injury. Particularly at risk is the pulmonary epithelium. As an important regulator of lung function and physiology, the degree of pulmonary epithelial damage influences the course and outcome of lung injury. In this paper we present experimental and computational studies to explore the hypothesis that the mechanical stresses associated with airway reopening inflict injury to the pulmonary epithelium.

Gaver, Donald P., III↗
NASA NTRS1991

Cardiopulmonary responses to acute hypoxia, head-down tilt and fluid loading in anesthetized dogs

Cardiopulmonary responses to acute hypoxia (HY), fluid loading by saline infusion (FL), and head-down tilt (HD) of mechanically ventilated anesthetized dogs were investigated by measuring thermodynamics and pulmonary gas exchange. It was found that HD decreased the total respiratory compliance both during HY and normoxia (NO) and that the reduction in compliance by FL was twice as large as by HD. Superimposing HD on HY doubled the increase in vascular resistance due to HY alone. In the systemic circulation, HD lowered the resistance to below NO levels. There was a significant positive correlation between the changes in blood volume and in pulmonary artery pressure for experimental transitions, suggesting that a shift in blood volume from systemic to pulmonary circulations and changes in the total blood volume may contribute substantially to these apparent changes in resistance.

Loeppky, J. A.↗
NASA NTRS1999

Influence of Gravity on Blood Volume and Flow Distribution

In our previous experiments during NASA Shuttle flights SLS 1 and 2 (9-15 days) and EUROMIR flights (30-90 days) we observed that pulmonary blood flow (cardiac output) was elevated initially, and surprisingly remained elevated for the duration of the flights. Stroke volume increased initially and then decreased, but was still above 1 Gz values. As venous return was constant, the changes in SV were secondary to modulation of heart rate. Mean blood pressure was at or slightly below 1 Gz levels in space, indicating a decrease in total peripheral resistance. It has been suggested that plasma volume is reduced in space, however cardiac output/venous return do not return to 1 Gz levels over the duration of flight. In spite of the increased cardiac output, central venous pressure was not elevated in space. These data suggest that there is a change in the basic relationship between cardiac output and central venous pressure, a persistent "hyperperfusion" and a re-distribution of blood flow and volume during space flight. Increased pulmonary blood flow has been reported to increase diffusing capacity in space, presumably due to the improved homogeneity of ventilation and perfusion. Other studies have suggested that ventilation may be independent of gravity, and perfusion may not be gravity- dependent. No data for the distribution of pulmonary blood volume were available for flight or simulated microgravity. Recent studies have suggested that the pulmonary vascular tree is influenced by sympathetic tone in a manner similar to that of the systemic system. This implies that the pulmonary circulation is dilated during microgravity and that the distribution of blood flow and volume may be influenced more by vascular control than by gravity. The cerebral circulation is influenced by sympathetic tone similarly to that of the systemic and pulmonary circulations; however its effects are modulated by cerebral autoregulation. Thus it is difficult to predict if cerebral perfusion is increased and if there is edema in space. Anecdotal evidence suggests there may be cerebral edema early in flight. Cerebral artery velocity has been shown to be elevated in simulated microgravity. The elevated cerebral artery velocity during simulated microgravity may reflect vasoconstriction of the arteries and not increased cerebral blood flow. The purpose of our investigations was to evaluate the effects of alterations in simulated gravity (+/-), resulting in changes in cardiac output (+/-), and on the blood flow and volume distribution in the lung and brain of human subjects. The first hypothesis of these studies was that blood flow and volume would be affected by gravity, but their distribution in the lung would be independent of gravity and due to vasoactivity changing vascular resistance in lung vessels. The vasodilitation of the lung vasculature (lower resistance) along with increased "compliance" of the heart could account for the absence of increased central venous pressure in microgravity. Secondly, we postulate that cerebral blood velocity is increased in microgravity due to large artery vasoconstriction, but that cerebral blood flow would be reduced due to autoregulation.

Pendergast, D.↗
NASA NTRS1975

Fluctuations in O2 stores and gas exchange with passive changes in posture

The purpose of the present study is to determine the effects of changes in posture on oxygen transfer at the mouth and pulmonary capillary membrane and to observe concomitant subtle changes in ventilation under specified assumptions. Breath-by-breath calculations are carried out with a box-balloon spirometer and mass spectrometer. Measurements are made before, during, and after passive tilt to 60 deg and on return to recumbency after 10 min erect. It is found that from supine to upright oxygen stores in the lung increases rapidly and oxygen stores in the blood drops slowly, creating a net deficit in oxygen transfer at the mouth of 130 ml in 10 min. Changes in oxygen stores in the blood result from shifts in blood volume and flow more than from changes in cardiac output. Refilling of oxygen stores in the blood is found to cause transient hypoxia with substantial hyperpnea.

Loeppky, J. A.↗
NASA NTRS2000

Regional ventilation-perfusion distribution is more uniform in the prone position

The arterial blood PO(2) is increased in the prone position in animals and humans because of an improvement in ventilation (VA) and perfusion (Q) matching. However, the mechanism of improved VA/Q is unknown. This experiment measured regional VA/Q heterogeneity and the correlation between VA and Q in supine and prone positions in pigs. Eight ketamine-diazepam-anesthetized, mechanically ventilated pigs were studied in supine and prone positions in random order. Regional VA and Q were measured using fluorescent-labeled aerosols and radioactive-labeled microspheres, respectively. The lungs were dried at total lung capacity and cubed into 603-967 small ( approximately 1.7-cm(3)) pieces. In the prone position the homogeneity of the ventilation distribution increased (P = 0.030) and the correlation between VA and Q increased (correlation coefficient = 0.72 +/- 0.08 and 0.82 +/- 0.06 in supine and prone positions, respectively, P = 0.03). The homogeneity of the VA/Q distribution increased in the prone position (P = 0.028). We conclude that the improvement in VA/Q matching in the prone position is secondary to increased homogeneity of the VA distribution and increased correlation of regional VA and Q.

NASA Program Biomedical Research and Countermeasur↗
NASA NTRS1983

Human respiration at rest in rapid compression and at high pressures and gas densities

The ventilation (V), end-tidal PCO2 (PACO2), and CO2 elimination rate were determined in men at rest breathing CO2-free gas over the pressure range 1-50 ATA and the gas density range 0.4-25 g/l, during slow and rapid compressions, at stable elevated ambient pressures and during slow decompressions. Progressive increase in pulmonary gas flow resistance due to elevation of ambient pressure and inspired gas density to the He-O2 equivalent of 5000 feet of seawater was found to produce a complex pattern of change in PACO2. It was found that as both ambient pressure and pulmonary gas flow resistance were progressively raised, PACO2 at first increased, went through a maximum, and then declined towards values near the 1 ATA level. It is concluded that this pattern of PACO2 change results from the interaction on ventilation of the increase in pulmonary resistance due to the elevation of gas density with the increase in respiratory drive postulated as due to generalized central nervous system excitation associated with exposure to high hydrostatic pressure. It is suggested that a similar interaction exists between increased gas flow resistance and the increase in respiratory drive related to nitrogen partial pressure and the resulting narcosis.

Gelfand, R.↗
NASA NTRS1998

Effects of posture on blood flow diversion by hypoxic pulmonary vasoconstriction in dogs

We used differential excretion of sulphur hexafluoride from the left and right lung to measure blood flow diversion by hypoxic pulmonary vasoconstriction (HPV) in the prone and supine positions in dogs (n = 9). Gas exchange was assessed using the multiple inert gas elimination technique. Blood flow diversion from the hypoxic (3% oxygen) left lung was mean 70.7 (SD 11.2)% in the supine compared with 57.0 (12.1)% in the prone position (P < 0.02). The supine position was associated with increased perfusion to low VA/Q regions (P < 0.05). The increased flow diversion with hypoxia in the supine position was associated with more ventilation to high VA/Q regions (P < 0.05). We conclude that flow diversion by hypoxic pulmonary vasoconstriction is greater in the supine position. This effect could contribute to the variable response in gas exchange with positioning in patients with ARDS.

Non-NASA Center↗
NASA NTRS1997

Ventilation during simulated altitude, normobaric hypoxia and normoxic hypobaria

To investigate the possible effect of hypobaria on ventilation (VE) at high altitude, we exposed nine men to three conditions for 10 h in a chamber on separate occasions at least 1 week apart. These three conditions were: altitude (PB = 432, FIO2 = 0.207), normobaric hypoxia (PB = 614, FIO2 = 0.142) and normoxic hypobaria (PB = 434, FIO2 = 0.296). In addition, post-test measurements were made 2 h after returning to ambient conditions at normobaric normoxia (PB = 636, FIO2 = 0.204). In the first hour of exposure VE was increased similarly by altitude and normobaric hypoxia. The was 38% above post-test values and end-tidal CO2 (PET(CO2) was lower by 4 mmHg. After 3, 6 and 9 h, the average VE in normobaric hypoxia was 26% higher than at altitude (p < 0.01), resulting primarily from a decline in VE at altitude. The difference between altitude and normobaric hypoxia was greatest at 3 h (+ 39%). In spite of the higher VE during normobaric hypoxia, the PET(CO2) was higher than at altitude. Changes in VE and PET(CO2) in normoxic hypobaria were minimal relative to normobaric normoxia post-test measurements. One possible explanation for the lower VE at altitude is that CO2 elimination is relatively less at altitude because of a reduction in inspired gas density compared to normobaric hypoxia; this may reduce the work of breathing or alveolar deadspace. The greater VE during the first hour at altitude, relative to subsequent measurements, may be related to the appearance of microbubbles in the pulmonary circulation acting to transiently worsen matching. Results indicate that hypobaria per se effects ventilation under altitude conditions.

NASA Discipline Environmental Health↗