No abstract

Although the airway conductance1 increases at larger lung volumes in normal subjects (1), it is reduced in patients with asthma or emphysema who are breathing with a large functional residual capacity (FRC) (2). We have therefore tried to assess the influence of other factors which might affect the airway conductance in both normal subjects and in patients with asthma, bronchitis and emphysema. These include the interrelationship of lung volume, lung elastic pressure and airway conductance, the effect of exercise, forced breathing and normal aging, and the composition of the respired gas and bronchomotor drugs. We investigated the balance of forces regulating the diameter of the airway lumen, i.e., the tone of the airway wall, directed inward, opposed by the traction of the lung tissues, directed outward. We studied whether, in normal subjects, this balance was altered by bronchmotor drugs or by a change in lung elastic pressure following chest strapping, and whether in patients with asthma, the airway conductance/lung volume relationship was altered after forced breathing or exercise. Patterns of disturbance leading to air trapping § Established Investigator of the American Heart Association.1 Airway conductance, the reciprocal of airway resistance, is defined as the rate of airflow at the mouth for unit pressure difference between alveolus and mouth. It was measured over the range of 0 to 0.5 L per second of inspiratory airflow.were studied in patients who had emphysema or bronchitis of toxic etiology. METHODSAirway resistance and thoracic gas volume were measured during panting2 using an upright body plethysmograph (2). The methods hinge on Boyle's law for compression of gases. Volume change owing to compression of gas inside the thorax is measured by -the equal and opposite small displacement of gas around the body. After appropriate calibrations, the intrathoracic gas volume changes found when rebreathing the air of the chamber through a heated flowmeter are converted mathematically to alveolar pressure changes, thence to airway resistance and airway conductance; or, when breathing against a closed shutter and manometer, to thoracic gas volume. In practice, these values are read directly from a precalibrated scale and protractor on the face of an oscilloscope, thus reducing labor. Esophageal pressure and mouth pressures were measured alternately using a capacitance manometer and Brush recorder. Lung elastic pressure (3) at each lung volume was measured as mean esophageal pressure, while panting (4). Chest constriction was accomplished by binding the subj ect's chest or abdomen, in the expiratory position, with adhesive tape or a long strip of rubber (4). Other tests of pulmonary function were performed according to generally accepted methods. All measurements were made with the subj ect in the sitting position. Lung volumes are expressed at BTPS. RESULTS ON HEALTHY SUBJECTSSpontaneous variation of airway resistance with time. The airway resistance of six healthy subjects was studied at 20 minute intervals o...

Publication costs assisted by Atomic Energy of Canada LimitedThe overall deuterium isotope separation factor between hydrogen and liquid water, a, has been measured directly for the first time between 280 and 370 K. The data are in good agreement with values of a calculated from literature data on the equilibrium constant for isotopic exchange between hydrogen and water vapor, Ki, and the liquid-vapor separation factor, • The temperature dependence of a over the range 273-473 K based upon these new experimental results and existing literature data is given by the equation In a = -0.2143 + (368.9/T) + (27 870/T2). Measurements on ay given in the literature have been surveyed and the results are summarized over the same temperature range by the equation In ay = 0.0592 -(80.3/T) + (25 490/T2).

Patients with chronic obstructive pulmonary disease (COPD) markedly increase their pulmonary artery wedge pressure on mild exercise even though they have no overt left heart disease and no increase in the esophageal pressure (as a reflection of mean intrathoracic pressure). We wondered if lung distension due to gas trapping during the hyperpnea of exercise might cause the wedge pressure to rise by increasing juxtacardiac pressures above esophageal pressures. If this were so, then (1) tachypnea alone, without exercise, should cause the FRC and intracardiac pressures to increase in patients with COPD, (2) there should be an increase in FRC associated with the rise in wedge pressure on exercise, and (3) these changes should not occur in patients without COPD. We studied 39 patients with COPD (Ppa = 21 +/- 6 mm Hg [mean +/- SD], FEV1 [% predicted] = 39 +/- 16) and 13 control patients with similar pulmonary artery pressures but no airflow obstruction (Ppa = 22 +/- 20 mm Hg, FEV1 [% predicted] = 110 +/- 24). In those with COPD, light exercise raised the FRC by 0.5 +/- 0.5 L. Tachypnea alone, at the rate present during exercise, raised the FRC by 0.6 +/- 0.4 L and there was a 10% increase in left lower lobe area on lateral chest X-ray. Wedge, right atrial, and pulmonary artery pressures rose together during tachypnea with and without exercise. By contrast, in the control patients without COPD, the right atrial pressure change on exercise did not reflect that of the left atrium in extent or direction.(ABSTRACT TRUNCATED AT 250 WORDS)

We investigated the dynamic history dependence of lung surface area-to-volume ratio (S/V) during tidal breathing in live rabbits with use of our recently developed technique of diffuse optical scattering. We also examined the effect of methacholine (continuous intravenous infusion, 1-10 micrograms.kg-1.min-1) on lung micromechanics with the same technique. Animals were anesthetized, tracheostomized, and mechanically ventilated, and the left lung was exposed through a thoracotomy. An optical fiber delivering light from a He-Ne laser was attached normal to the pleural surface, producing a circular light pattern on the pleural surface from diffusively scattered light within the parenchyma. The pattern of light intensities was measured using a CCD video camera connected to a computer. S/V during tidal breathing changed in a manner qualitatively consistent with geometric similarity. There was a small but significant hysteresis in S/V vs. volume, with S/V inspiration greater than S/V expiration at the same volume. However, during methacholine challenge, the sense of hysteresis reversed; S/V inspiration was less than S/V expiration at isovolume points. Moreover, S/V during methacholine challenge systematically decreased at all lung volumes compared with control. These findings suggest that 1) during normal tidal breathing, stress hysteresis in ductal tissue is larger than septal stress hysteresis (septal tissue plus surface tension) and 2) the effect of methacholine on tissue in the septa is greater than the corresponding effect in ductal tissue.