Transformation of Bacillus subtilis using the particle inflow gun and submicrometer particles obtained by the polyol process.
Explore the source record for details and available documents.
Bacillus subtilis↗
Biomedical subjects
A R Elliott
Publications and source records attributed to A R Elliott.
Helium and sulfur hexafluoride bolus washin in short-term microgravity.
We performed single-breath washout (SBW) tests in which He and sulfur hexafluoride (SF6) were inspired throughout the vital capacity inspirations or were inhaled as discrete boluses at different points in the inspiration. Tests were performed in normal gravity (1 G) and in up to 27 s of microgravity (microG) during parabolic flight. The phase III slope of the SBW could be accurately reconstructed from individual bolus tests when allowance for airways closure was made. Bolus tests showed that most of the SBW phase III slope results from events during inspiration at lung volumes below closing capacity and near total lung capacity, as does the SF6-He phase III slope difference. Similarly, the difference between 1 G and microG in phase III slopes for both gases was entirely accounted for by gravity-dependent events at high and low lung volumes. Phase IV height was always larger for SF6 than for He, suggesting at least some airway closure in close proximity to airways that remain open at residual volume. These results help explain previous studies in microG, which show large changes in gas mixing in vital capacity maneuvers but only small effects in tidal volume breaths.
Adult↗
Multiple-breath washin of helium and sulfur hexafluoride in sustained microgravity.
We performed multiple-breath washouts of N2 and simultaneous washins of He and SF6 with fixed tidal volume (approximately 1,250 ml) and preinspiratory lung volume (approximately the subject's functional residual capacity in the standing position) in four normal subjects (mean age 40 yr) standing and supine in normal gravity (1 G) and during exposure to sustained microgravity (microG). The primary objective was to examine the influence of diffusive processes on the residual, nongravitational ventilatory inhomogeneity in the lung in microG. We calculated several indexes of convective ventilatory inhomogeneity from each gas species. A normal degree of ventilatory inhomogeneity was seen in the standing position at 1 G that was largely unaltered in the supine position. When we compared the standing position in 1 G with microG, there were reductions in phase III slope in all gases, consistent with a reduction in convection-dependent inhomogeneity in the lung in microG, although considerable convective inhomogeneity persisted in microG. The reductions in the indexes of convection-dependent inhomogeneity were greater for He than for SF6, suggesting that the distances between remaining nonuniformly ventilated compartments in microG were short enough for diffusion of He to be an effective mechanism to reduce gas concentration differences between them.
Adult↗
Cardiogenic oscillation phase relationships during single-breath tests performed in microgravity.
We studied the phase relationships of the cardiogenic oscillations in the phase III portion of single-breath washouts (SBW) in normal gravity (1 G) and in sustained microgravity (microG). The SBW consisted of a vital capacity inspiration of 5% He-1.25% sulfurhexafluoride-balance O2, preceded at residual volume by a 150-ml Ar bolus. Pairs of gas signals, all of which still showed cardiogenic oscillations, were cross-correlated, and their phase difference was expressed as an angle. Phase relationships between inspired gases (e.g., He) and resident gas (n2) showed no change from 1 G (211 +/- 9 degrees) to microG (163 +/- 7 degrees). Ar bolus and He were unaltered between 1 G (173 +/- 15 degrees) and microG (211 +/- 25 degrees), showing that airway closure in microG remains in regions of high specific ventilation and suggesting that airway closure results from lung regions reaching low regional volume near residual volume. In contrast, CO2 reversed phase with He between 1 G (332 +/- 6 degrees) and microG (263 +/- 27 degrees), strongly suggesting that, in microG, areas of high ventilation are associated with high ventilation-perfusion ratio (VA/Q). This widening of the range of VA/Q in microG may explain previous measurements (G.K. Prisk, A.R. Elliott, H.J.B. Guy, J.M. Kosonen, and J.B. West J. Appl. Physiol. 79: 1290-1298, 1995) of an overall unaltered range of VA/Q in microG, despite more homogeneous distributions of both ventilation and perfusion.
Adult↗
Hypercapnic ventilatory response in humans before, during, and after 23 days of low level CO2 exposure.
Alterations in ventilation and the chemoreceptor response to CO2 during 23 d of 1.2% inspired CO2 were studied in four male subjects. Resting ventilation (VE), tidal volume (VT), respiratory frequency (fR), inspired and end tidal O2 and CO2 and the hypercapnic ventilatory response (HCVR) measured by CO2 rebreathing were measured once before entering the chamber, on days 2, 5, 11, and 22 of CO2 exposure, and one day after. Resting VE slightly increased (5%) on day 2 of exposure and significantly increased (22%) by day 5 followed by a progressive decrease to pre-chamber levels by day 22 and on the first day of recovery. Tidal volume and fR were not statistically different. During the exposure PetCO2 was significantly elevated with day 2 having the largest increase (19.6%). PetCO2 returned to normal within 24 h post exposure. The HCVR was characterized by the slope (SHCVR), intercept at zero ventilation (B), and the ventilation at a PCO2 = 60 mmHg (VE60). The SHCVR decreased (14%) on day 2, but was not significant; the SHCVR on the other exposure days were also not different. The SHCVR on the first recovery day significantly increased (37%). The HCVR B was shifted to the right on day 2 by 5.2 mmHg, then progressively returned to the pre-exposure position. On recovery the B significantly shifted 6.9 mmHg to the right of pre-exposure B. The VE60 decreased by approximately 32% and 16% on day 2 and 5, respectively, then returned within pre-exposure range for the remainder of the exposure and during recovery. During the early phase and one day after the exposure the HCVR was right shifted. One day after exposure chemoreceptor sensitivity to elevated CO2 was increased but, the B was right shifted resulting in a reduced HCVR below PCO2 of 60 mmHg and a greater HCVR above 60 mmHg.
Adaptation, Physiological↗
Pulmonary function in space.
The lung is exquisitely sensitive to gravity, and so it is of interest to know how its function is altered in the weightlessness of space. Studies on National Aeronautics and Space Administration (NASA) Spacelabs during the last 4 years have provided the first comprehensive data on the extensive changes in pulmonary function that occur in sustained microgravity. Measurements of pulmonary function were made on astronauts during space shuttle flights lasting 9 and 14 days and were compared with extensive ground-based measurements before and after the flights. Compared with preflight measurements, cardiac output increased by 18% during space flight, and stroke volume increased by 46%. Paradoxically, the increase in stroke volume occurred in the face of reductions in central venous pressure and circulating blood volume. Diffusing capacity increased by 28%, and the increase in the diffusing capacity of the alveolar membrane was unexpectedly large based on findings in normal gravity. The change in the alveolar membrane may reflect the effects of uniform filling of the pulmonary capillary bed. Distributions of blood flow and ventilation throughout the lung were more uniform in space, but some unevenness remained, indicating the importance of nongravitational factors. A surprising finding was that airway closing volume was approximately the same in microgravity and in normal gravity, emphasizing the importance of mechanical properties of the airways in determining whether they close. Residual volume was unexpectedly reduced by 18% in microgravity, possibly because of uniform alveolar expansion. The findings indicate that pulmonary function is greatly altered in microgravity, but none of the changes observed so far will apparently limit long-term space flight. In addition, the data help to clarify how gravity affects pulmonary function in the normal gravity environment on Earth.
Humans↗
Paradoxical helium and sulfur hexafluoride single-breath washouts in short-term vs. sustained microgravity.
During single-breath washouts in normal gravity (1 G), the phase III slope of sulfur hexafluoride (SF6) is steeper than that of helium (He). Two mechanisms can account for this: 1) the higher diffusivity of He enhances its homogeneous distribution; and 2) the lower diffusivity of SF6 results in a more peripheral location of the diffusion front, where airway asymmetry is larger. These mechanisms were thought to be gravity independent. However, we showed during the Spacelab Life Sciences-2 spaceflight that in sustained microgravity (microG) the SF6-to-He slope difference is abolished. We repeated the protocol during short periods (27 s) of microG (parabolic flights). The subjects performed a vital-capacity inspiration and expiration of a gas containing 5% He-1.25% SF6-balance O2. As in sustained microG, the phase III slopes of He and SF6 decreased. However, during short-term microG, the SF6-to-He slope difference increased from 0.17 +/- 0.03%/l in 1 G to 0.29 +/- 0.06%/l in microG, respectively. This is contrary to sustained microG, in which the SF6-to-He slope difference decreased from 0.25 +/- 0.03%/l in 1 G to -0.01 +/- 0.06%/l in microG. The increase in phase III slope difference in short-term microG was caused by a larger decrease of He phase III slope compared with that in sustained microG. This suggests that changes in peripheral gas mixing seen in sustained microG are mainly due to alterations in the diffusive-convective inhomogeneity of He that require > 27 s of microG to occur. Changes in pulmonary blood volume distribution or cardiogenic mixing may explain the differences between the results found in short-term and sustained microG.
Adult↗
Forced expirations and maximum expiratory flow-volume curves during sustained microgravity on SLS-1.
Gravity is known to influence the mechanical behavior of the lung and chest wall. However, the effect of sustained microgravity (microG) on forced expirations has not previously been reported. Tests were carried out by four subjects in both the standing and supine postures during each of seven preflight and four postflight data-collection sessions and four times during the 9 days of microG exposure on Spacelab Life Sciences-1. Compared with preflight standing values, peak expiratory flow rate (PEFR) was significantly reduced by 12.5% on flight day 2 (FD2), 11.6% on FD4, and 5.0% on FD5 but returned to standing values by FD9. The supine posture caused a 9% reduction in PEFR. Forced vital capacity and forced expired volume in 1 s were slightly reduced (approximately 3-4%) on FD2 but returned to preflight standing values on FD4 and FD5, and by FD9 both values were slightly but significantly greater than standing values. Forced vital capacity and forced expiratory volume in 1 s were both reduced in the supine posture (approximately 8-10%). Forced expiratory flows at 50% and between 25 and 75% of vital capacity did not change during microG but were reduced in the supine posture. Analysis of the maximum expiratory flow-volume curve showed that microG caused no consistent change in the curve configuration when individual in-flight days were compared with preflight standing curves, although two subjects did show a slight reduction in flows at low lung volumes from FD2 to FD9. The interpretation of the lack of change in curve configuration must be made cautiously because the lung volumes varied from day to day in flight. Therefore, the flows at absolute lung volumes in microG and preflight standing are not being compared. The supine curves showed a subtle but consistent reduction in flows at low lung volumes. The mechanism responsible for the reduction in PEFR is not clear. It could be due to a lack of physical stabilization when performing the maneuver in the absence of gravity or a transient reduction in respiratory muscle strength.
Adult↗
Ventilatory inhomogeneity determined from multiple-breath washouts during sustained microgravity on Spacelab SLS-1.
We used multiple-breath N2 washouts (MBNW) to study the inhomogeneity of ventilation in four normal humans (mean age 42.5 yr) before, during, and after 9 days of exposure to microgravity on Spacelab Life Sciences-1. Subjects performed 20-breath MBNW at tidal volumes of approximately 700 ml and 12-breath MBNW at tidal volumes of approximately 1,250 ml. Six indexes of ventilatory inhomogeneity were derived from data from 1) distribution of specific ventilation (SV) from mixed-expired and 2) end-tidal N2, 3) change of slope of N2 washout (semilog plot) with time, 4) change of slope of normalized phase III of successive breaths, 5) anatomic dead space, and 6) Bohr dead space. Significant ventilatory inhomogeneity was seen in the standing position at normal gravity (1 G). When we compared standing 1 G with microgravity, the distributions of SV became slightly narrower, but the difference was not significant. Also, there were no significant changes in the change of slope of the N2 washout, change of normalized phase III slopes, or the anatomic and Bohr dead spaces. By contrast, transition from the standing to supine position in 1 G resulted in significantly broader distributions of SV (P < 0.05) and significantly greater changes in the changes in slope of the N2 washouts (P < 0.001), indicating more ventilatory inhomogeneity in that posture. Thus these techniques can detect relatively small changes in ventilatory inhomogeneity. We conclude that the primary determinants of ventilatory inhomogeneity during tidal breathing in the upright posture are not gravitational in origin.
Adult↗
Pulmonary gas exchange and its determinants during sustained microgravity on Spacelabs SLS-1 and SLS-2.
We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological dead space (VDB) decreased in microG, and alveolar dead space (VDB-VDa) was significantly less in microG than in preflight standing (-30%) or supine (-15%), consistent with a more uniform topographic distribution of blood flow. The net result was that, although total ventilation fell, alveolar ventilation was unchanged in microG compared with standing in normal gravity (1 G). Expired vital capacity was increased (6%) compared with standing but only after the first few days of exposure to microG. There were no significant changes in O2 uptake, CO2 output, or end-tidal PO2 in microG compared with standing in 1 G. End-tidal PCO2 was unchanged on the 9-day flight but increased by 4.5 Torr on the 14-day flight where the PCO2 of the spacecraft atmosphere increased by 1-3 Torr. Cardiogenic oscillations in expired O2 and CO2 demonstrated the presence of residual ventilation-perfusion ratio (VA/Q) inequality. In addition, the change in intrabreath VA/Q during phase III of a long expiration was the same in microG as in preflight standing, indicating persisting VA/Q inequality and suggesting that during this portion of a prolonged exhalation the inequality in 1 G was not predominantly on a gravitationally induced topographic basis. However, the changes in PCO2 and VA/Q at the end of expiration after airway closure were consistent with a more uniform topographic distribution of gas exchange.
Adult↗
Morphine-isoflurane interaction in dogs, swine and rhesus monkeys.
In monkeys, dogs and swine (six each) we tested the reduction of the isoflurane MAC (minimal alveolar concentration) produced by 2 mg.kg-1 morphine intravenously (i.v.) and the concurrent effect on PCO2 with spontaneous ventilation. MAC fell to a minimum of 55% of control at 53 min in monkeys, 50% at 38 min in dogs and 13% at 33 min in swine. PaCO2 rose at constant MAC with morphine to 55-60 mmHg, but did not fall over the next several hours despite the decline of plasma morphine concentration, and the resulting needed rise in isoflurane concentration to keep the anaesthesia depth at 1 MAC. After isoflurane concentration had returned to pre-morphine control levels, naloxone immediately reduced PaCO2 to or below control level. Morphine pharmacokinetics in the three species studied conformed to a two-compartment model.
Anesthesia↗
Inhomogeneity of pulmonary ventilation during sustained microgravity as determined by single-breath washouts.
Gravity is known to cause inhomogeneity of ventilation. Nongravitational factors are also recognized, but their relative contribution is not understood. We therefore studied ventilatory inhomogeneity during sustained microgravity during the 9-day flight of Spacelab SLS-1. All seven crew members performed single-breath nitrogen washouts. They inspired a vital capacity breath of 100% oxygen with a bolus of argon at the start of inspiration, and the inspiratory and expiratory flow rates were controlled at 0.5 l/s. Control measurements in normal gravity (1 G) were made pre- and postflight in the standing and supine position. Compared with the standing 1-G measurements, there was a marked decrease in ventilatory inhomogeneity during microgravity, as evidenced by the significant reductions in cardiogenic oscillations, slope of phase III, and height of phase IV for nitrogen and argon. However, argon phase IV volume was not reduced, and considerable ventilatory inhomogeneity remained. For example, the heights of the cardiogenic oscillations during microgravity for nitrogen and argon were 44 and 24%, respectively, of their values at 1 G, whereas the slopes of phase III for nitrogen and argon were 78 and 29%, respectively, of those at 1 G. The presence of a phase IV in microgravity is strong evidence that airway closure still occurs in the absence of gravity. The results were qualitatively similar to those found previously during short periods of 0 G in parabolic flight.
Aged↗
Inhomogeneity of pulmonary perfusion during sustained microgravity on SLS-1.
We studied the effects of gravity on the inhomogeneity of pulmonary perfusion in humans by performing hyperventilation-breath-hold single-breath measurements before, during, and after 9 days of continuous exposure to microgravity during the Spacelab Life Sciences-1 (SLS-1) mission. In microgravity the indicators of inhomogeneity of perfusion, especially the size of cardiogenic oscillations in expired CO2 and the height of phase IV, were markedly reduced. Cardiogenic oscillations were reduced to approximately 60% of their preflight standing size, and the height of phase IV was between 0 and -8% (a terminal fall became a small terminal rise) of the preflight standing value. The terminal change in expired CO2 was nearly abolished in microgravity, indicating more uniformity of blood flow between lung units that close and those that remain open at the end of expiration. A possible explanation of this observation is the disappearance of gravity-dependent topographic inequality of blood flow. The residual cardiogenic oscillations in expired CO2 imply a persisting inhomogeneity of perfusion in the absence of gravity, probably in lung regions that are not within the same acinus.
Adult↗
Lung volumes during sustained microgravity on Spacelab SLS-1.
Gravity is known to influence the mechanical behavior of the lung and chest wall. However, the effect of sustained microgravity (mu G) on lung volumes has not been reported. Pulmonary function tests were performed by four subjects before, during, and after 9 days of mu G exposure. Ground measurements were made in standing and supine postures. Tests were performed using a bag-in-box-and-flowmeter system and a respiratory mass spectrometer. Measurements included functional residual capacity (FRC), expiratory reserve volume (ERV), residual volume (RV), inspiratory and expiratory vital capacities (IVC and EVC), and tidal volume (VT). Total lung capacity (TLC) was derived from the measured EVC and RV values. With preflight standing values as a comparison, FRC was significantly reduced by 15% (approximately 500 ml) in mu G and 32% in the supine posture. ERV was reduced by 10-20% in mu G and decreased by 64% in the supine posture. RV was significantly reduced by 18% (310 ml) in mu G but did not significantly change in the supine posture compared with standing. IVC and EVC were slightly reduced during the first 24 h of mu G but returned to 1-G standing values within 72 h of mu G exposure. IVC and EVC in the supine posture were significantly reduced by 12% compared with standing. During mu G, VT decreased by 15% (approximately 90 ml), but supine VT was unchanged compared with preflight standing values. TLC decreased by approximately 8% during mu G and in the supine posture compared with preflight standing. The reductions in FRC, ERV, and RV during mu G are probably due to the cranial shift of the diaphragm, an increase in intrathoracic blood volume, and more uniform alveolar expansion.
Adult↗
Pulmonary diffusing capacity, capillary blood volume, and cardiac output during sustained microgravity.
We measured pulmonary diffusing capacity (DL), diffusing capacity per unit lung volume, pulmonary capillary blood volume (Vc), membrane diffusing capacity (Dm), pulmonary capillary blood flow or cardiac output (Qc), and cardiac stroke volume (SV) in four subjects exposed to 9 days of microgravity (weightlessness, 0 G). The same subjects were studied standing and supine numerous times preflight and in the week immediately after return from space. DL in microgravity was elevated (28%) compared with preflight standing values and was higher than preflight supine because of the elevation of both Vc (28%) and Dm (27%). The elevation in Vc was comparable to that measured supine in 1 G, but the increase in Dm was in sharp contrast to the supine value (which was unchanged). We postulate that, in 0 G, pulmonary capillary blood is evenly distributed throughout the lung, providing for uniform capillary filling, leading to an increase in the surface area available for diffusion. By contrast, in the supine 1-G state, the capillaries are less evenly filled, and although a similar increase in blood volume is observed, the corresponding increase in surface area does not occur. DL and its subdivisions showed no adaptive changes from the first measurement 24 h after the start of 0 G to 8 days later. Similarly, there were no trends in the postflight data, suggesting that the principal mechanism of these changes was gravitational. The increase in Dm suggests that subclinical pulmonary edema did not result from exposure to 0 G. Qc was modestly increased (18%) inflight and decreased (9%) post-flight compared with preflight standing. Compared with preflight standing, SV was increased 46% inflight and decreased 14% in the 1st wk postflight. There were temporal changes in Qc and SV during 0 G, with the highest values recorded at the first measurement, 24 h into the flight. The lowest values of Qc and SV occurred on the day of return.
Adult↗
Influence of inhaled anesthetics on the pharmacokinetics and pharmacodynamics of morphine.
We determined the magnitude and duration of the effect of morphine (1.0 mg/kg intravenous bolus) on isoflurane and halothane minimum alveolar concentration (MAC) in six dogs anesthetized on two occasions in cross-over fashion. Plasma morphine concentration-time profiles and changes in PaCO2 were determined after morphine injection. After morphine injection, the end-tidal anesthetic dose was manipulated over the course of a 4-h observation period to account for the decline in plasma morphine concentration and to maintain an anesthetic level equivalent to 1.0 MAC isoflurane or halothane alone. Morphine decreased the MAC of halothane and isoflurane. The magnitude of MAC decrease was related to time after morphine injection and was similar for a given time with both halothane and isoflurane. For example, at 28.8 +/- 3.6 (mean +/- SE) and 34.8 +/- 6.3 min after morphine injection, the MAC for halothane and isoflurane were reduced by 35.7% +/- 4.5% and 39.3% +/- 3.4%, respectively. By 4 h after morphine injection, the MAC reduction for both anesthetics was less than 10% in most of the animals. Except for systemic clearance of morphine during halothane and isoflurane (40.1 +/- 6.1 and 53.7 +/- 5.6 mL.min-1.kg-1, respectively), there were no differences in disposition kinetics of free morphine associated with the two inhaled anesthetics. Morphine increased PaCO2 to a similar degree with both halothane (from 42.2 +/- 2.1 mm Hg to 55.6 +/- 2.3 mm Hg) and isoflurane (46.2 +/- 2.4 mm Hg to 55.3 +/- 2.1 mm Hg). Respiratory depression was abolished by noxious stimulation (tail clamp) and naloxone in all animals with both anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesia, Inhalation↗
Circulatory and respiratory responses of spontaneously breathing, laterally recumbent horses to 12 hours of halothane anesthesia.
Cardiovascular and respiratory changes that accompany markedly long periods (12 hours) of halothane anesthesia were characterized. Eight spontaneously breathing horses were studied while they were positioned in left lateral recumbency and anesthetized only with halothane in oxygen maintained at a constant end-tidal concentration of 1.06% (equivalent to 1.2 times the minimal alveolar concentration for horses). Results of circulatory and respiratory measurements during the first 5 hours of constant conditions were similar to those previously reported from this laboratory (ie, a time-related significant increase in systemic arterial blood pressure, cardiac output, stroke volume, left ventricular work, PCV, plasma total solids concentration, and little change in respiratory system function). Beyond 5 hours of anesthesia, arterial blood pressure did not further increase, but remained above baseline. Cardiac output continued to increase, because heart rate significantly (P < 0.05) increased. Peak inspiratory gas flow increased significantly (P < 0.05) in later stages of anesthesia. There was a significant decrease in inspiratory time beginning at 4 hours. Although PaO2 and PaCO2 did not significantly change during the 12 hours of study, PVO2 increased significantly (P < 0.05) and progressively with time, beginning 6 hours after the beginning of constant conditions. Metabolic acidosis increased with time (significantly [P < 0.05] starting at 9 hours), despite supplemental IV administered NaHCO3. Plasma concentrations of eicosanoids: 6-keto-prostaglandin F1 alpha (PGF1 alpha, a stable metabolite of PGI2), PGF2 alpha, PGE, and thromboxane (TxB2, a stable metabolite of TxA2) were measured in 5 of the 8 horses before and during anesthesia. Significant changes from preanesthetic values were not detected. Dynamic thoracic wall and lung compliances decreased with time.
Anesthesia, Inhalation↗
High lung volume increases stress failure in pulmonary capillaries.
We previously showed that when pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to test whether stress failure occurred more frequently at high than at low lung volumes for the same Ptm. Lungs of anesthetized rabbits were inflated to a transpulmonary pressure of 20 cmH2O, perfused with autologous blood at 32.5 or 2.5 cmH2O Ptm, and fixed by intravascular perfusion. Samples were examined by both transmission and scanning electron microscopy. The results were compared with those of a previous study in which the lung was inflated to a transpulmonary pressure of 5 cmH2O. There was a large increase in the frequency of stress failure of the capillary walls at the higher lung volume. For example, at 32.5 cmH2O Ptm, the number of endothelial breaks per millimeter cell lining was 7.1 +/- 2.2 at the high lung volume compared with 0.7 +/- 0.4 at the low lung volume. The corresponding values for epithelium were 8.5 +/- 1.6 and 0.9 +/- 0.6. Both differences were significant (P less than 0.05). At 52.5 cmH2O Ptm, the results for endothelium were 20.7 +/- 7.6 (high volume) and 7.1 +/- 2.1 (low volume), and the corresponding results for epithelium were 32.8 +/- 11.9 and 11.4 +/- 3.7. At 32.5 cmH2O Ptm, the thickness of the blood-gas barrier was greater at the higher lung volume, consistent with the development of more interstitial edema. Ballooning of the epithelium caused by accumulation of edema fluid between the epithelial cell and its basement membrane was seen at 32.5 and 52.5 cmH2O Ptm. At high lung volume, the breaks tended to be narrower and fewer were oriented perpendicular to the axis of the pulmonary capillaries than at low lung volumes. Transmission and scanning electron microscopy measurements agreed well. Our findings provide a physiological mechanism for other studies showing increased capillary permeability at high states of lung inflation.
Air Pressure↗