To characterize the intrathoracic thermal events that occur during breathing in humans, we developed a flexible probe (OD 1.4 mm) containing multiple thermistors evenly spaced over 30.2 cm, that could be inserted into the tracheobronchial tree with a fiberoptic bronchoscope. With this device we simultaneously recorded the airstream temperature at six points from the trachea to beyond the subsegmental bronchi in six normal subjects while they breathed ambient and frigid air at multiple levels of ventilation (VE). During quiet breathing of room air the average temperature ranged from 32.0 +/- 0.05 degrees C in the upper trachea to 35.5 +/- 0.3 degrees C in the subsegmental bronchi. As ventilation was increased, the temperature along the airways progressively decreased, and at a VE of 100+ 1/min the temperature at the above two sites fell to 29.2 +/- 0.5 and 33.9 +/- 0.8 degrees C, respectively. Interval points were intermediate between these extremes. With cold air, the changes were considerably more profound. During quiet breathing, local temperatures approximated those recorded in the maximum VE room-air trial, and at maximum VE, the temperatures in the proximal and distal airways were 20.5 +/- 0.6 and 31.6 +/- 1.2 degrees C, respectively. During expiration, the temperature along the airways progressively decreased as the air flowed from the periphery of the lung to the mouth: the more the cooling during inspiration, the lower the temperature during expiration. These data demonstrate that in the course of conditioning inspired air the intrathoracic and intrapulmonic airways undergo profound thermal changes that extend well into the periphery of the lung.
When large volumes of air are inhaled at rapid rates of ventilation, substantial segments of the tracheobronchial tree become involved in the conditioning process and the inspirate does not reach body conditions of temperature and humidity until it passes well into the peripheral bronchi. To determine if the manner in which ventilation is elevated is an important factor in producing this response, we measured the temperature of the airstream at six points in the tracheobronchial tree from the pharynx to the subsegmental bronchi during 5 min of exercise and voluntary hyperventilation in seven normal subjects while they inhaled frigid air. Minute ventilation and respiratory frequency were recorded at minute intervals and intrathoracic temperatures were measured continuously. With both forms of hyperpnea, airway temperature fell dramatically, and there were no significant differences between exercise and hyperventilation. These results demonstrate that the thermal events that occur within the lung during short, moderately intense degrees of exercise can be readily simulated by voluntary hyperventilation when ventilation and inspired air conditions are matched. Our data also indicate that this form of exercise does not result in an increase in airstream temperature and raise the possibility that the bronchial blood supply may be determined by the local thermal needs of the airways to recover heat and water independent of, at least moderate, increases in cardiac output.
The purpose of this study was to test the hypothesis that mediators and cells associated with bronchoconstriction or inflammation are locally synthesized and/or released in the airways of asthmatic subjects in response to isocapnic hyperpnea (ISH). Seven atopic, mildly asthmatic subjects were studied. Baseline measurements were reported previously and included forced expiratory volumes, flow rates, bronchoalveolar lavage (BAL), and methacholine reactivity. Approximately 1 yr later, spirometry and BAL were repeated, but BAL was performed immediately after ISH challenge. As indices of inflammation, BAL measurements were made of eosinophils, neutrophils, epithelial cells, leukotrienes B4, C4, D4, and E4, prostaglandins D2, E2, and F2 alpha, thromboxane B2, histamine, and total protein. Compared with baseline, ISH was associated with higher BAL concentrations of the following: leukotriene B4 (10 versus 121 pg/ml, p = 0.02), leukotrienes C4/D4/E4 (46 versus 251 pg/ml, p = 0.02), eosinophils (0.8 versus 2.2%, p = 0.04), and epithelial cells (2.1 versus 6.1%, p = 0.05). Trends toward significant increases were seen in BAL concentrations of neutrophils and prostaglandin D2. No statistically significant increases were found in BAL measurements of total protein, histamine, prostaglandins E2 or F2 alpha, thromboxane B2, lymphocytes, or macrophages. The magnitude of the response to ISH, as measured by change in FEV1, did not correlate with BAL levels of cells or mediators. This study indicates that ISH, even in mildly asthmatic subjects, is associated with airway increases in a spectrum of bronchoactive mediators and inflammatory cells, supporting the observations of others that antagonists of a single mediator are unlikely to have major clinical effectiveness in ISH or exercise-induced asthma.
We developed and tested a method, based on conduction heat transfer analysis, to infer airway mucosal temperatures from airstream temperature-time profiles during breath-hold maneuvers. The method assumes that radial conduction of heat from the mucosal wall to inspired air dominates heat exchange during a breath-hold maneuver and uses a simplified conservation of energy analysis to extrapolate wall temperatures from air temperature vs. time profiles. Validation studies were performed by simultaneously measuring air and wall temperatures by use of a retractable basket probe in the upper airways of human volunteers and intrathoracic airways of paralyzed intubated dogs during breath holding. In both protocols, a good correlation was demonstrated between directly measured wall temperatures and those calculated from adjacent airstream temperature vs. time profiles during a breath hold. We then calculated intrathoracic bronchial wall temperatures from breath-hold airstream temperature-time profiles recorded in normal human subjects after cold air hyperpnea at 30 and 80 l/min. The calculations show airway wall temperatures in the upper intrathoracic airways that are below core body temperature during hyperpnea of frigid air and upper thoracic airways that are cooler than more peripheral airways. The data suggest that the magnitude of local intrathoracic heat/water flux is not represented by heat/water loss measurements at the airway opening. Both the magnitude and locus of heat transport during cold gas hyperventilation vary with changes in inspired gas temperature and minute ventilation; both may be important determinants of airway responses.
We measured lung and chest wall compliance as well as rib cage and abdominal dimensions in the supine position in five acute C4-7 quadriplegics. Studies were performed serially from 1 to 12 months after injury. Results were compared with those of control groups of chronic (greater than 1 yr after injury) quadriplegics and normal volunteers. We found that lung compliance was lower in acute and chronic quadriplegics (0.129 +/- 0.023 and 0.176 +/- 0.043 L/mm Hg, respectively) than in normal subjects (0.278 +/- 0.086 L/mm Hg) and that these changes apparently occurred within 1 month of injury. Specific lung compliance appeared to be reduced to a lesser degree, suggesting that the changes in lung compliance were partly due to reduced lung volumes and partly to altered mechanical properties of the lung. During respiratory maneuvers, abdomen and rib cage dimensional changes demonstrated rib cage distortion. This distortion was less severe in chronic than in acute quadriplegics. The improvement in chest wall stability was likely due to increased strength of cervical accessory muscles of respiration and improved coupling of the various rib cage elements in chronic quadriplegics.
Previous studies suggest that abdominal binding may affect the interaction of the rib cage and the diaphragm over the tidal range of breathing in quadriplegia. To determine whether abdominal binding influences rib cage motion over the entire range of inspiratory capacity, we used spirometry and the helium-dilution technique to measure functional residual capacity (FRC), inspiratory capacity, and total lung capacity (TLC) in eight quadriplegic and five normal subjects in supine, tilted (37 degrees), and seated positions. Combined data in all three positions indicated that, with abdominal binding, FRC and TLC decreased in normal subjects [delta FRC = -0.33 + 0.151 (SD) P less than 0.01); delta TLC = -0.16 + 0.121, P less than 0.05]. In quadriplegia there was also a reduction in FRC with binding (delta FRC = -0.32 + 0.101, P less than 0.001). However, TLC increased in quadriplegia (delta TLC = 0.07 + 0.061, P less than 0.025). In an additional six quadriplegic and five normal subjects, we used magnetometers to define the influences of abdominal binding on rib cage dimensions and TLC. In quadriplegia, rib cage dimensions were increased at TLC with abdominal binding, whereas there was no change in normals. Our data suggest that this inspiratory effect of abdominal binding on augmenting rib cage volume in quadriplegia is greater than the effect of impeding diaphragm descent, and thus abdominal binding produces a net increase in TLC in quadriplegia.
We assessed the difference between isovolumic maximal expiratory flows (Vmax) using maneuvers begun at mid-lung volumes, so-called partial expiratory flow-volume curves (P), vs. those begun at full inflation, so-called maximal expiratory flow-volume curves (M), in 10 asthmatic subjects before and following obstruction induced by isocapnic hyperpnea with cold air and before and after bronchodilation with a beta-agonist or antimuscarinic agent. Volume history effects were quantitated as an M-to-P ratio of Vmax at 30% vital capacity (M/P V30). Although M/P V30 was variable among patients at base line, there was a uniform increase in M/P V30 during constriction and a consistent decrease below base line after dilation. Blunting of induced obstruction with beta-agonists also diminished the increase in M/P V30. Antimuscarinics, despite equivalent bronchodilation, failed to alter the degree of obstruction induced by cold air or the increase in M/P V30 seen during obstruction. The level of airway tone, as indicated by specific resistance, related directly to the M/P V30. We conclude that the response of the asthmatic lung to a deep inhalation is relatively predictable when acute changes in airway tone are produced.
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