Partitioning of pulmonary resistance in calves

Nine right apical lobes of healthy Friesian calves and 10 right apical lobes of double-muscled calves of Belgian White and Blue (BWB) breed were suspended in an airtight box, inflated at a constant transpulmonary pressure (Ptp), and subjected to quasi-sinusoidal pressure changes (amplitude: 0.5 kPa) at a frequency of 30 cycles/min. Lobar resistance (RL) was partitioned at six different lung volumes into three components: central airway resistance (Rc), small airway resistance (Rp), and tissue resistance (Rt). Pressure in small airways (2-3 mm ID) was measured with a retrograde catheter. Alveolar pressure was sampled in capsules glued onto the punctured pleural surface. RL was minimal at values of Ptp comprised between 0.5 and 0.7 kPa and increased at higher and lower values of Ptp. At a Ptp of 0.5 kPa, Rc, Rp, and Rt represented 30, 15, and 55% of RL, respectively, in Friesian calves and 25, 25, and 50% in BWB calves. Rp increased markedly at low lung volumes. Rt was responsible for the increase of RL at high Ptp. Rc tended to decrease at high Ptp. The significantly higher values of Rp in BWB calves (P less than 0.05) might explain the sensitivity of this breed to severe bronchopneumonia.     

Partitioning of pulmonary resistance during constriction in the dog: effects of volume history

We assessed the relative changes in airways and lung tissue with bronchoconstriction, and the changes in each during and following a deep inhalation (DI). We partitioned pulmonary resistance (RL) into airway (Raw) and tissue (Vtis) components using alveolar capsules in 10 anesthetized, paralyzed, and open-chested dogs ventilated sinusoidally with 350-ml breaths at 1 Hz. We made measurements before and during bronchoconstriction induced by vagal stimulation or inhalation of histamine or prostaglandin F2 alpha (PGF2 alpha), each of which decreased dynamic compliance by approximately 40%. With histamine and PGF2 alpha the rise in RL was predominantly due to Vtis. With vagal stimulation there was a relatively greater increase in Raw than Vtis. At higher lung volumes, Vtis increases offset falls in Raw, producing higher RL at these volumes before and during constriction with PGF2 alpha and histamine. During constriction with vagal stimulation, the fall in Raw with inflation overrode the rise in Vtis, resulting in a lower RL at the higher compared with the lower lung volume. The changes seen after a DI in the control and constricted states were due to alterations in tissue properties, both viscous and elastic. However, the relative hysteresis of the airways and parenchyma were equal, since Raw, our index of airway size, was unchanged after a DI.     

Partitioning of pulmonary resistance in dogs: effect of tidal volume and frequency

To determine the sensitivity of pulmonary resistance (RL) to changes in breathing frequency and tidal volume, we measured RL in intact anesthetized dogs over a range of breathing frequencies and tidal volumes centering around those encountered during quiet breathing. To investigate mechanisms responsible for changes in RL, the relative contribution of airway resistance (Raw) and tissue resistance (Rti) to RL at similar breathing frequencies and tidal volumes was studied in six excised, exsanguinated canine left lungs. Lung volume was sinusoidally varied, with tidal volumes of 10, 20, and 40% of vital capacity. Pressures were measured at three alveolar sites (PA) with alveolar capsules and at the airway opening (Pao). Measurements were made during oscillation at five frequencies between 5 and 45 min-1 at each tidal volume. Resistances were calculated by assuming a linear equation of motion and submitting lung volume, flow, Pao, and PA to a multiple linear regression. RL decreased with increasing frequency and decreased with increasing tidal volume in both isolated and intact lungs. In isolated lungs, Rti decreased with increasing frequency but was independent of tidal volume. Raw was independent of frequency but decreased with tidal volume. The contribution of Rti to RL ranged from 93 +/- 4% (SD) with low frequency and large tidal volume to 41 +/- 24% at high frequency and small tidal volume. We conclude that the RL is highly dependent on breathing frequency and less dependent on tidal volume during conditions similar to quiet breathing and that these findings are explained by changes in the relative contributions of Raw and Rti to RL.     

Partitioning of airway and respiratory tissue mechanical impedances by body plethysmography

Peslin, R., and C. Duvivier. Partitioning of airway andrespiratory tissue mechanical impedances by body plethysmography. J. Appl. Physiol. 84(2): 553-561, 1998.We have tested the feasibility of separating the airway (Zaw)and tissue (Zti) components of total respiratory input impedance(Zrs,in) in healthy subjects by measuring alveolar gas compression bybody plethysmography (Vpl) during pressure oscillations at the airwayopening. The forced oscillation setup was placed inside a bodyplethysmograph, and the subjects rebreathedBTPS gas. Zrs,in and the relationship between Vpl and airway flow (Hpl) were measured from 4 to 29 Hz. Zawand Zti were computed from Zrs,in and Hpl by using the monoalveolar T-network model and alveolar gas compliance derived from thoracic gasvolume. The data were in good agreement with previous observations: airway and tissue resistance exhibited some positive and negative frequency dependences, respectively; airway reactance was consistent with an inertance of 0.015 ± 0.003 hPa · s² · l¹and tissue reactance with an elastance of 36 ± 8 hPa/l. The changes seen with varying lung volume, during elastic loading of the chest andduring bronchoconstriction, were mostly in agreement with the expectedeffects. The data, as well as computer simulation, suggest that thepartitioning is unaffected by mechanical inhomogeneity and onlymoderately affected by airway wall shunting.

     

Effects of unilateral nasal occlusion on ventilation and pulmonary resistance in infants

There is evidence implying an active role of airway epithelium in the modulation of bronchomotor tone. To study this phenomenon, we designed an in vitro system allowing pharmacological stimulation of either the inside or outside of the airway lumen. Rat tracheas were excised, cannulated, and their inside and outside perfused independently with Krebs solution. Two hooks were inserted through opposite sides of the tracheal wall, the lower one was attached to a fixed point, while the upper one was connected to a force transducer. Isometric contractions of the tracheal muscle were elicited by carbachol solution perfused in single and cumulative concentrations. In one-half of the preparations the epithelium was mechanically removed. Stimulation of the inside or outside of the trachea produced equal maximal tracheal muscle tension [1.55 +/- 0.14 and 1.2 +/- 0.09 (SE) g in and out, respectively]. The time course of tension development was longer when carbachol was administered inside the trachea: an effect that was abolished when the epithelium was removed. In addition, removal of the epithelium was found 1) to increase the maximal tension irrespective of the route of carbachol perfusion and 2) to increase the sensitivity of the preparation to carbachol stimulation.     

Radionuclide plethysmography for noninvasive evaluation of peripheral arterial blood flow

We validated a noninvasive radionuclide plethysmography technique to evaluate peripheral arterial blood flow during reactive hyperemia. This method, based on the measurement of blood volume variations during repetitive venous occlusions, was compared with strain-gauge venous impedance plethysmography. The technique uses 99mTc-labeled autologous red blood cells scintigraphy to determine the rate of change of forearm scintigraphic counts during venous occlusion. Thirteen subjects were simultaneously evaluated with radionuclide and impedance plethysmography. Six baseline flow measurements were performed to evaluate the reproducibility of each method. Twenty-seven serial measurements were then made to evaluate flow variation during forearm reactive hyperemia. After 30 min of recovery, resting forearm blood flows were again evaluated. Impedance and radionuclide methods showed excellent reproducibility with intraclass correlation coefficients of 0.96 and 0.93, respectively. There was also good correlation of flows between both methods during reactive hyperemia (r = 0.87). Resting flows at 30 min after reactive hyperemia were slightly lower than at baseline with both methods. We conclude that radionuclide plethysmography could be used for the noninvasive evaluation of forearm blood flow and its dynamic variations during reactive hyperemia.     

Airway resistance due to alveolar gas compression measured by barometric plethysmography in mice.

We developed a method for measuring airway resistance (R(aw)) in mice that does not require a measurement of airway flow. An analysis of R(aw) induced by alveolar gas compression showed the following relationship for an animal breathing spontaneously in a closed box: R(aw) = A(bt)V(b)/[V(t) (V(e) + 0.5V(t))]. Here A(bt) is the area under the box pressure-time curve during inspiration or expiration, V(b) is box volume, V(t) is tidal volume, and V(e) is functional residual capacity (FRC). In anesthetized and conscious unrestrained mice, from experiments with both room temperature box air and body temperature humidified box air, the contributions of gas compression to the box pressure amplitude were 15 and 31% of those due to the temperature-humidity difference between box and alveolar gas. We corrected the measured A(bt) and V(t) for temperature-humidity and gas compression effects, respectively, using a sinusoidal analysis. In anesthetized mice, R(aw) averaged 4.3 cmH(2)O.ml(-1).s, fourfold greater than pulmonary resistance measured by conventional methods. In conscious mice with an assumed FRC equal to that measured in the anesthetized mice, the corrected R(aw) at room temperature averaged 1.9 cmH(2)O.ml(-1).s. In both conscious mice and anesthetized mice, exposure to aerosolized methacholine with room temperature box air significantly increased R(aw) by around eightfold. Here we assumed that in the conscious mice both V(t) and FRC remained constant. In both conscious and anesthetized mice, body temperature humidified box air reduced the methacholine-induced increase in R(aw) observed at room temperature. The method using the increase in A(bt) with bronchoconstriction provides a conservative estimate for the increase in R(aw) in conscious mice.     

Partitioning of inhaled ventilation between the nasal and oral routes during sleep in normal subjects.

The oral and nasal contributions to inhaled ventilation were simultaneously quantified during sleep in 10 healthy subjects (5 men, 5 women) aged 43 +/- 5 yr, with normal nasal resistance (mean 2.0 +/- 0.3 cmH(2)O. l(-1). s(-1)) by use of a divided oral and nasal mask. Minute ventilation awake (5.9 +/- 0.3 l/min) was higher than that during sleep (5.2 +/- 0.3 l/min; P < 0.0001), but there was no significant difference in minute ventilation between different sleep stages (P = 0.44): stage 2 5.3 +/- 0.3, slow-wave 5.2 +/- 0.2, and rapid-eye-movement sleep 5.2 +/- 0.2 l/min. The oral fraction of inhaled ventilation during wakefulness (7.6 +/- 4%) was not significantly different from that during sleep (4.3 +/- 2%; mean difference 3.3%, 95% confidence interval -2.1-8.8%, P = 0.19), and no significant difference (P = 0.14) in oral fraction was observed between different sleep stages: stage two 5.1 +/- 2.8, slow-wave 4.2 +/- 1.8, rapid-eye-movement 3.1 +/- 1.7%. Thus the inhaled oral fraction in normal subjects is small and does not change significantly with sleep stage.     

Alae nasi activation decreases nasal resistance during hyperoxic hypercapnia

It has beenproposed that decreases in nasal resistance (Rn) during hypercapnia areentirely due to vasoconstriction in the nasal cavity. We hypothesizedthat alae nasi (AN) muscle activity dilates the nasal vestibule andcontributes to the decrease in Rn during hypercapnia. Nine normalsubjects were studied during hyperoxic hypercapnia (HH). Rn andvestibular resistance (Rvest) for one nasal passage were measuredsimultaneously with the AN electromyogram before and after nasaldecongestion. HH decreased Rvest from 1.6 ± 0.6 to 0.8 ± 0.9 cmH₂O · l¹ · s(predecongestant) and from 1.3 ± 0.8 to 0.6 ± 0.7 cmH₂O · l¹ · s(postdecongestant; both P < 0.01).Nasal decongestant decreased Rn but not Rvest. Significant inverselinear relationships between Rvest and AN electromyogram weredemonstrated for all subjects. We conclude that in normal subjectsduring HH 1) decreases in Rvest arepredominantly due to increases in AN activity; and2) decreases in Rn are due to acombination of mucosal vasoconstriction and ANactivation.

     

Evaluation of airway resistance determined by whole-body plethysmography

Methods of estimation of the airway resistance by flow-pressure curve obtained in whole-body plethysmography are investigated. The analysis of the physical processes controlling the flow-limitation during expiration shows that these methods are useful only for healthy subjects for the estimation of the airway resistance. The way for estimation of the airway resistance by flow-pressure curve is proposed.