Elastic Recoil Pressure Research Articles

Temporal dynamics of pulmonary response to intravenous histamine in dogs: effects of dose and lung volume.

We measured tracheal pressure (Ptr) and tracheal flow (V) in open-chest anesthetized paralyzed dogs. The lungs were maintained at a fixed volume (initial positive end-expiratory pressure 0.5 kPa) for 80 s while small-amplitude oscillations in V at 1 and 6 Hz were applied simultaneously at the tracheal opening. A bolus of histamine was given intravenously at the start of the oscillation period. The time course of lung elastic recoil pressure (Pel) was obtained by passing a running average over Ptr to smooth out its oscillations. The oscillations themselves were separated into their 1- and 6-Hz components, as were those in V. By fitting models to the 1- and 6-Hz components of Ptr and V by recursive least squares, we obtained time courses of lung resistance at 6 Hz (RL6), dynamic lung elastance at 1 Hz (EL1), and the difference between dynamic lung resistance at 1 and 6 Hz (RL1-RL6). In four dogs we studied the effects of histamine doses of 0.05, 1.0, and 20 mg. We found that Pel increased quickly and plateaued, RL6 continued to increase throughout the oscillation period, and EL1 exhibited features of both Pel and RL6. Furthermore, the ratio of RL1-RL6 to EL1 was qualitatively similar in time course to Pel. We explain these varied time courses in terms of the development of regional ventilation inhomogeneity throughout the lung as the reaction to histamine develops. In four dogs we also studied the effects of reducing the initial positive end-expiratory pressure by 0.25 kPa and found that the changes in RL6, EL1, and RL1-RL6 were greatly magnified, presumably because of the reduced forces of parenchymal interdependence.

Growth of airways and air spaces in teenagers is related to sex but not to symptoms

To determine growth patterns of the lung and airways in adolescents, we analyzed maximal expiratory flow-volume curves, closing capacity, and residual volume. They were obtained every 6 mo for up to 7 yr in 430 boys and 125 girls (11-19 yr), of whom 143 boys and 36 girls were classified as symptomatic; symptoms were most often minor and limited to childhood. Development of flows vs. volumes was used to investigate growth of the airways relative to lung size. A model of isotropic growth of the airways and air spaces (J. Appl. Physiol. 65: 822-828, 1988) was modified for increasing elastic recoil pressure with growth. Growth of airways relative to volume occurred faster in teenage boys than in teenage girls and was compatible with isotropic growth in 92% of asymptomatic boys and in 44% of asymptomatic girls: dysanaptic growth in teenage girls seems to be a normal phenomenon and not a unique characteristic of symptomatic subjects. Subjects with respiratory symptoms in childhood and/or adolescence have lower flows for a given lung size and airway closure at a greater lung volume when they enter adulthood. However, no difference in patterns of lung growth was observed in association with the presence of respiratory symptoms.

Relationship of Resting Lung Mechanics and Exercise Pattern of Breathing in Patients With Chronic Obstructive Lung Disease

To investigate the influence of resting pulmonary mechanics on the pattern of breathing during exercise in chronic obstructive pulmonary disease (COPD), we studied 29 patients with moderate to severe COPD (FEV1 50 +/- 20 percent predicted), and 10 normal subjects. Lung mechanics were studied using esophageal balloon technique and body-box. Incremental exercise testing was performed to exhaustion. As minute ventilation (VE) increases, COPD patients with the highest pulmonary resistance (RI) or lowest elastic recoil pressure (PL), used a greater tidal volume/vital capacity ratio (VT/VC) than the COPD patients with more normal RL or lowest PL. To describe the breathing pattern during exercise, an exponential constant (K) describes the rates of increase in VT/VC ratio with increasing VE, calculated according to the equation VT = VC(1-e-KVE). The K values achieved by COPD patients were higher than in normal subjects. In addition, K value correlated negatively with the resting FEV1 and FVC of COPD patients. When COPD patients were grouped according to their K values, it was revealed that patients with high K values generated greater VT/VC ratio and also have the most abnormal resting lung mechanics. These results suggest that the exercise breathing pattern in COPD patients is significantly influenced by the degree of impairment of resting lung mechanics.

Does alveolar recruitment occur with positive end-expiratory pressure in adult respiratory distress syndrome patients?

We studied the effects of positive end-expiratory pressure (PEEP) (2 to 14 cm H 2O) on alveolar recruitment (Vrec), static respiratory compliance, and end-expiratory lung volume (EELV) in nine sedated, paralyzed, mechanically ventilated adult respiratory distress syndrome patients. Positive end-expiratory pressure was applied in increasing and decreasing steps of 2 cm H 2O. Flow, tidal volume, and airway pressure were measured. We used the rapid airway occlusion technique to determine static end-inspiratory elastic recoil pressure of the respiratory system (Pst, rs) and intrinsic PEEP (PEEPi). The changes in EELV were measured with respiratory inductive plethysmography. Alveolar recruitment was estimated as the difference in lung volume between PEEP and zero end-expiratory pressure (ZEEP) for the same end-inspiratory Pst,rs (20 cm H 2O). We found that (1) Vrec with PEEP up to 14 cm H 2O was in general rather small and was absent in two patients; (2) all patients exhibited PEEN at ZEEP (5.6 ± 1.0 cm H 2O) and little change in EELV and Vrec was achieved until the external PEEP exceeded PEEPi; (3) if end-inspiratory Pst, rs is high at ZEEP, there is little or no alveolar recruitment with PEEP; and (4) Vrec and EELV were slightly higher during stepwise deflation than stepwise inflation with PEEP, except at ZEEP where EELV did not change after inflation-deflation runs with PEEP.

Tissue and airway impedance of excised normal, senile, and emphysematous lungs.

We partitioned pulmonary resistance (RL) in excised normal, senile, and emphysematous human lungs at various distending pressures; peripheral resistance (Rp) was measured by means of retrograde catheters and lung tissue resistance (Rti) by means of pleural capsules. By subtracting Rp from RL and Rti from Rp, we obtained, respectively, central (Rcaw) and peripheral (Rpaw) airway resistance. We determined also lung volumes, the elastic recoil pressure-volume curve, and the forced expiratory volume in 1 s-to-vital capacity ratio (FEV1/VC). The functional data were related to morphometry: mean linear intercept (Lm), diameter (d), and density (n/cm2) of membranous bronchioles. In the three groups of lungs, Rti demonstrates a marked negative frequency dependence and increases with transplumonary pressure. In emphysematous lungs, the increase of RL is mainly due to an increase of Rpaw; in addition, Rcaw and Rti are higher than normal. In the group of senile lungs, airway resistances are within normal range, but Rti is slightly increased. FEV1/VC is related to Rpaw and elastic recoil pressure; Rpaw is related to d and n/cm2, and Rti is related to dynamic elastance and to Lm.

P-V characteristics in heart-pulsation affected and non-affected lung units: A model

Elastic recoil pressure, pleural pressure and pressure pulsation of the heart (P hrt) control the expired flow from a small lung unit. Variability in each trait may affect the expirate. The same (SDPV) or different (DDPV) regional distribution of P-V characteristics, regional effects of P hrt-affected (O) and non-affected units (N) and regional differences in pleural pressure, were incorporated into a computer model. Output acceptability was judged by the alveolar slope of the N 2 washout, cardiogenic oscillations (CO) and the phase shift between P hrt and CO. Can SDPV be in both O and N units? What causes CO and phase shift? With SDPV in O and N units, CO were negligibly small. The incorporation of the pleural pressure difference did not fulfill the three criteria, which were met when there was DDPV in the N and O units. We conclude that the distribution of P-V characteristics changes with the distance from a pulsating artery, and only DDPV, and not different time constants or pleural pressure difference, can explain CO.

The Effects of Positive End-expiratory Pressure on Respiratory Resistance in Patients with the Adult Respiratory Distress Syndrome and in Normal Anesthetized Subjects

We investigated the effects of positive end-expiratory pressure (PEEP) upon respiratory resistance during mechanical ventilation in 21 subjects anesthetized for surgery (normal subjects) and in 11 patients with the adult respiratory distress syndrome (ARDS). We measured tracheal pressure (Ptr) near the end of the endotracheal tube through a 1.5-mm ID catheter and airflow (V) at 0, 5, and 10 cm H2O PEEP (normal subjects) and at 0, 5, 10, 15, and 20 cm H2O PEEP (patients with ARDS). We computed respiratory system static elastance (Estrs), maximal (Rrsmax) and minimal (Rrsmin) inspiratory resistance by the end-inspiratory occlusion method during constant-flow inflation. Rrsmin represents the ohmic respiratory resistance, whereas Rrsmax is Rrsmin plus the additional respiratory impedance caused by the stress adaptation phenomena of the respiratory system tissues and to time constant inhomogeneities between lung units (pendelluft). The difference (Rrsmax - Rrsmin) has been termed DRrs. We also computed expiratory resistance (Rrsexp) at preselected volume (50% of expiration; Rrsexp50) and flow (0.3 L/s; Rrsexp0.3) using the equation: Rrsexp = (Pelrs(t) - Ptr(t]/Flow(t), where elastic recoil pressure (Pelrs) at time t was computed as:Estrs . V(t) + PEEP, in which V(t) is the volume above end-expiratory volume at time t. We found that (1) at PEEP 0, expiratory resistances (Rrsexp50: 7.38 +/- 1.92 versus 5.35 +/- 1.97 cm H2O.L-1.s) and DRrs (3.08 +/- 1.9 versus 1.66 +/- 0.77 cm H2O.L-1.s) were significantly higher in the ARDS group than in the normal group.(ABSTRACT TRUNCATED AT 250 WORDS)

Endotoxin and the mechanical properties of the canine peripheral circulation

To determine if alterations in venous vascular mechanics by endotoxin contribute to the hemodynamic disorder of septic shock, we studied eight dogs before and after the injection of 5 to 10 mg/kg of Escherichia coii endotoxin. We isolated the venous drainage of the peripheral (ie, superior plus inferior vena cava below the renal veins) and splanchnic vasculatures, and measured venous pressure (Pv) and flow (electromagnetic flow meter) in each region. Blood drained through vascular waterfalls that controlled the Pv of each region and then into a reservoir. A constant flow pump returned blood to the right atrium. By temporarily stopping all flows, we measured the elastic recoil pressures of each region. We changed regional volumes by changing Pv and integrating the transient changes of outflow. This allowed the calculation of compliance (Cv in mL/mm Hg/kg), venous resistance (Rv), venous time constant (τv in seconds), and fractional flow of each region. Endotoxin produced a large loss of reservoir volume but did not change the fractional flows. Peripheral Cv increased and Rv did not change, so that peripheral τv was 3.8 ± 1.0 before and 5.7 ± 2.7 (mean ± SD; P < .024) after endotoxin. The splanchnic compliance tended to decrease (0.776 ± 0.801 before and 0.487 ± 0.418 after; P = NS) and Rv did not change, so that splanchnic τv decreased from 14.6 ± 5.6 before to 10.8 ± 5.1 after endotoxin ( P < .024). In the intact animal, without a reservoir, the decrease in stressed volume would decrease cardiac output and the decrease in the splanchnic τv would increase cardiac output.

Extent of pulmonary emphysema in man and its relation to the loss of elastic recoil

1. We assessed lung density, determined by computerized tomography, as a measure of emphysema and related this to lung function and measurement of the elastic recoil of the lung in normal subjects and patients with chronic obstructive lung disease. 2. We found a significant correlation between measurements of elastic recoil pressure at 90% of total lung capacity and both the forced expiratory volume in 1 s (r = 0.80, P less than 0.001) and the transfer factor for carbon monoxide (r = 0.70, P less than 0.001). Measurements of elastic recoil of the lung also correlated with lung density as measured by computerized tomography scanning (P less than 0.001). 3. Multiple regression analysis demonstrated a correlation between the density of the lowest fifth percentile of the computerized tomography lung-density histogram, and both the natural logarithm of the shape parameter of the pressure-volume curve (P less than 0.01), and the transfer factor for carbon monoxide (P less than 0.01). However, the mean computerized tomography lung density correlated, in addition, with the elastic recoil pressure of the lungs at 90% of total lung capacity (P less than 0.001). 4. Since the elastic recoil pressure correlates with computerized tomography lung density, and hence with emphysema, and since elastic recoil pressure also correlates with the forced expiratory volume in 1 s, these results suggest that loss of elastic recoil is one determinant of airflow limitation in patients with chronic obstructive lung disease.

Vascular mechanics of venous drainage in dog hindlimbs

The time constant of venous drainage (tau v) of a vascular bed is an important determinant of the change in regional volume that will occur with a change in blood flow or venous pressure (Pv). Therefore, to measure tau v of the dog hindlimb, the vasculature was isolated and perfused with a pump. Inflow and outflow were measured with electromagnetic flow probes. Blood volume was changed (delta V) by changing flow (delta Q), and a double-occlusion procedure was used to obtain the venous elastic recoil pressure (Pel) from the plateau of Pv. Venous resistance (Rv), compliance (Cv), and tau v could then be calculated. Rv was 7.7 +/- 1.4 mmHg.ml-1.min.100 g-1 and Cv was 0.59 +/- 0.25 ml/mmHg, tau v calculated from the product of Rv and Cv was 4.20 +/- 1.58 s and from the ratio of delta V to delta Q was 4.95 +/- 1.53 s (P = NS) at a mean Pel of 17.6 +/- 3.7 mmHg. delta V was also produced by changing Pv; the average tau v (1.95 +/- 0.37 s), was shorter than that with changes in flow. Finally, a ramp increase in flow was used to calculate tau v from the time delay between inflow and outflow. tau v by this method was longer (6.06 +/- 1.70 s) and was probably influenced by the change in Pv. In conclusion, the hindlimb has a short tau v of venous drainage and would not be expected to store large volumes of blood even with large increases in blood flow.

Effect of forced expirations on mucus clearance in patients with chronic airflow obstruction: effect of lung recoil pressure.

Spontaneous mucus clearance and the effect of forced expirations and coughing on mucus clearance were investigated in eight patients with chronic airflow obstruction and low elastic recoil pressure (emphysema group: mean FEV1 45% predicted) and in seven patients with chronic airflow obstruction and normal elastic recoil pressure (chronic bronchitis group: mean FEV1 57% predicted). Mucus clearance was measured in a central and a peripheral lung region by a radioactive aerosol tracer technique. Spontaneous mucus clearance from the peripheral lung region was higher in the patients with emphysema than in those with chronic bronchitis. There was no difference in central mucus clearance between the two groups. Mucus clearance from the peripheral lung region increased significantly during forced expirations and coughing in the patients with chronic bronchitis but not in those with emphysema. It is concluded that in patients with chronic airflow obstruction and regular sputum production spontaneous peripheral mucus clearance is greater in those with decreased elastic recoil pressure. Physiotherapy that includes forced expirations and coughing can enhance mucus clearance in such patients when elastic recoil pressure is normal but is unlikely to be effective when elastic recoil pressure is decreased.

Effect of age on changes in flow rates and airway conductance after a deep breath

The effects of aging on changes in maximal expiratory flow rates and specific airway conductance after a deep breath were evaluated in 64 normal subjects. Flow rates (Vp) on partial expiratory flow-volume curves (PEFV), initiated from 60-70% of the vital capacity (VC), were compared with those (Vc) on maximal flow-volume curves (MEFV), initiated from total lung capacity (TLC), at a lung volume corresponding to 25% of VC on the MEFV curves. Specific airway conductance was measured before (sGaw) and after a deep inspiration (sGawDI). Bronchodilation after inspiration to TLC was inferred by Vp/Vc less than 1 and sGaw/sGawDI less than 1. The mean Vp was less than Vc. However, the ratio Vp/Vc increased significantly with age (r = 0.75, P less than 0.001). Specific conductance also increased after a deep inspiration (sGaw less than sGawDI). The ratio sGaw/sGawDIj increased slightly but significantly with age (r = 0.28, P less than 0.02). Measurement of lung elastic recoil pressures before and after a deep breath in a subgroup of patients (n = 14) suggested that the age-related increase in Vp/Vc was secondary to a decrement in the ability of a deep breath to decrease the upstream airway resistance. These findings suggest that even though changes in airway size after a deep breath as measured by sGaw/sGawDI have minimal age dependence, aging diminishes expiratory flow rates of MEFV curves relative to PEFV curves because of a decrease in the ability of a deep breath to increase the size of the peripheral airways.

Neonatal pulmonary oxygen toxicity in the rat and lung changes with aging

The aims of this study were to determine if neonatal hyperoxia exposure causes permanent lung damage and to define the relationship between neonatal lung oxygen toxicity and aging. Sprague-Dawley newborn rats (n = 85) breathed 100% oxygen (O2) or room air (RA) during the first 8 days of life, and then RA. At 2 and 22 months of age we assessed right ventricular (RV) systolic pressure (RVSP), RV weight, saline and air pressure-volume curves, volume density of lung parenchyma and nonparenchyma, parenchymal air space (PAS), mean linear intercept (Lm), number of small arteries/mm2 and the extent of their medial muscularization. Aging in RA did not affect the RVSP, RV weight, the number of small arteries/mm2, or their muscularization. The maximal lung volume/g of dry lung and the elastic recoil pressure between 40 and 90% maximal lung volume decreased. The volume density of lung parenchyma increased but the fraction of the lung parenchyma that was PAS decreased and that of the alveolar septa and Lm increased. The O2-treated rats at 60 days of age had increased RVSP and RV weights with a decrease in the small arteries/mm2. The lung parenchymal volume density and PAS increased and the density of alveolar septa decreased. The Lm increased and the alveoli/mm2 and elastic recoil pressure decreased. The lung damage seen in the O2-treated rats at 60 days persisted and in addition underwent the changes seen in the aging controls. However, the extent of muscularization of the arteries decreased. We conclude that neonatal hyperoxia causes permanent functional and structural changes of the lung but these do not interact with aging; that is, the effects of O2 toxicity and aging are additive but not synergistic.

Reexamination of the Elastic Properties of Emphysematous Lungs

We calculated specific lung elastance (Es,L) as the change of lung elastic recoil pressure (Pel,L) required to produce a given fractional change in lung volume (delta VL/VL,0) as a function of transpulmonary pressure (PL) from published data in normal lungs, and in patients with chronic obstructive pulmonary disease (COPD) or alpha 1-antitrypsin deficiency (alpha 1-AD). Es,L, in normal lungs, is the bulk modulus, and was systematically greater than PL.dEs,L/dPL increased with VL.PL at Es,L = 30 cm H2O decreased with age in normal lungs, but Es,L at PL = 8 cm H2O showed no age relationship. In both COPD and alpha 1-AD Es,L and dEs,L/dPL were increased compared to normal lungs. We conclude that Es,L is a curvilinear function of PL in normal lungs, COPD and alpha 1-AD, and is systematically greater than PL. The increase in Es,L and dEs,L/dPL in COPD and alpha 1-AD compared to normals probably represents two distinct abnormalities in the elastic properties of emphysematous lungs: (1) an increase in resting length of alveolar walls accounting for hyperinflation, and (2) a decrease in extensibility of alveolar walls once they become stressed. Using total lung capacity (TLC) as an index of the former and Es,L as an index of the latter, we showed no correlation between either and FEV1. Thus abnormalities in lung elastic properties in emphysema do not account for chronic expiratory flow limitation in emphysema. Furthermore, the increased values of Es,L in emphysema suggest that emphysematous airspaces are poorly ventilated. As they are presumably poorly perfused, emphysema per se may not disturb ventilation perfusion ratios seriously.

Respiratory mechanics determined by flow interruption during passive expiration in cats

We used the interrupter technique to measure the resistance Rinit (equal to the initial change ΔPinit in tracheal pressure divided by flow at interruption) during expiration in six normal anaesthetized-paralyzed cats. By performing interruptions at different points in expiration we found Rinit in each cat to be linearly dependent on flow. By allowing the cats to expire through two different resistances we were also able to demonstrate a volume dependence of Rinit in four of the cats. In addition, we obtained a secondary pressure change Δdif in each cat, as the magnitude of the slow change in tracheal pressure in the 2 sec following interruption of flow. ΔPdif was approximately constant over most of the expired volume range, and represented the difference between the static elastic recoil pressure of the respiratory system and the pressure driving flow at any volume during a passive expiration. ΔPdif became larger than ΔPinit towards the end of expiration. Since previously used methods for measuring respiratory system resistance have employed varying combinations of ΔPinit and ΔPdif as the resistive pressure drop, it is clear that measurements of resistance must be made with standard techniques under standard conditions if they are to be compared.

Lung mechanics and their relationship to lung volumes in pulmonary sarcoidosis

Pulmonary sarcoidosis was studied with respect to lung mechanical properties and to the influence of these on lung volumes. Sixty-six patients, with histological support for the diagnosis of sarcoidosis, and radiological signs of pulmonary involvement, i.e., stage II or III, were studied. The static pressure/volume (P/V) curves showed that the static elastic recoil pressure (PelL) tended to be increased at a given percentage of predicted total lung capacity (TLC). Reduction of static lung compliance (CstL) was a typical finding. At maximal inspiration PelL was abnormally low in 20 subjects, including in the main those with recent onset of the disease and older patients. The possibility of a greater inflammatory activity at the site of mechanical receptors in the lungs and airways of these patients is proposed. Pulmonary resistance, measured at a given PelL, was usually increased signifying bronchial involvement. TLC, residual volume (RV) and functional residual capacity (FRC) were lower in current smokers and ex-smokers than in lifelong nonsmokers. This may be due to synergistic effects of the inflammatory processes caused by smoking and sarcoidosis. A reduced vital capacity (VC) mainly reflected a low CstL but also obstruction with increased RV. Forced expiratory volume in one second (FEV1) reflected lung stiffness and obstruction equally. Lung mechanics revealed functional abnormalities which were not obvious from the standard tests, particularly in patients with respiratory symptoms.

Cardiopulmonary function after lobectomy or pneumonectomy for pulmonary neoplasm

Resection of pulmonary tissue for bronchial carcinoma causes a decrease in vital capacity of 15% after lobectomy and 35-40% following pneumonectomy. After operation the lung becomes stiffer and elastic recoil pressure and transdiaphragmatic pressure at TLC increase. Maximum effort tolerance decreases after pneumonectomy with a normal pulmonary artery pressure at rest and an increase in pulmonary artery pressure and in pulmonary vascular resistance on effort, compared to preoperative values. Cardiac output and stroke volume during effort show a decrease after operation with an increase in peripheral arterial blood pressure and in peripheral vascular resistance. Arterial oxygen saturation on effort decreases after pneumonectomy, possibly due to the absolute decrease in diffusing capacity. When comparing resting and exercise values at identical work loads, increases in systemic arterial blood pressure, pulmonary and systemic vascular resistance and arteriovenous oxygen difference were similar although generally less pronounced after lobectomy compared to pneumonectomy; cardiac output, stroke volume and oxygen consumption showed the same tendency to decrease after lobectomy and pneumonectomy.

Volume and pressure during transient added resistance

Total respiratory resistance (Rrs) can be computed from measurements of flow before and during a brief period of added resistance. This ‘added resistance’ method does not require measurement of total driving pressure (Pt). One of the assumptions of this method is that the change in Pt (ΔPt) is negligible during the time of increased resistance. To evaluate this assumption we measured both the volume exhaled during a brief imposition of an external resistor, and the total respiratory compliance (Crs) of 7 healthy volunteers. The mean volume exhaled was 18.6 ml, and the mean Crs was 88 ml/cm H 2O. The volume exhaled divided by Crs gives the change in total static elastic recoil pressure (ΔPel,rs), which is one component of ΔPt. The mean ΔPel, rs was 0.22 cm H 2O. Since the pressure exerted by contraction of inspiratory muscles (Pmus,I) opposes Pel,rs, we also estimated ΔPmus,I and subtracted it from ΔPel,rs to obtain ΔPt. The computed mean ΔPt during the time of added resistance was 0.045 cm H 2O. This value is quite small in relation to Pt during a spontaneous expiration at rest. We also studied 13 subjects with Chronic Obstructive Pulmonary Disease and found no significant effect of transient added resistance on intraesophageal pressure. We conclude that the assumption of negligible ΔPt should not prevent the added resistance method from being very useful, particularly when simplicity of equipment and testing procedure are important.

Lung function in workers exposed to soft paper dust.

In a cross-sectional study, 13 nonsmoking men with heavy exposure to paper dust were compared with 14 unexposed men, mainly office workers, employed at the same paper mill. They were studied using questionnaires, physical examinations, pulmonary function studies, and chest radiographs. Among those exposed there was an increased lung elastic recoil pressure (Pel) compared with controls which was significant (p less than 0.05) at the maximal level of total lung capacity (100% TLC). Furthermore, among the exposed workers there was also a significantly (p less than 0.05) decreased residual volume (RV). Two of the exposed men underwent lung biopsies, one of which showed fibrotic alveolar walls. Among the exposed there was also a significant (p less than 0.05) predominance of symptoms from the lower respiratory tract. We suggest that the observed pulmonary function impairment taken together with the histological examination of the lung biopsies are signs of a nonspecific reaction to high levels of paper dust.

Elastic recoil pressure arising from surface tension in hamster lungs treated with intratracheal bleomycin.

Lung elastic recoil pressure arising from surface tension (Ps) was evaluated in normal and bleomycin-treated lungs. Twenty two male golden hamsters were separated into a control group (group A, n = 10) and a bleomycin group (group B, n = 12). Group B was given a single intratracheal instillation of bleomycin and group A was given normal saline as a control. Thirty days after instillation, three cycles of static air -and saline-filled pressure-volume curves (P-V curve) were measured. Ps was graphically derived from air- and saline-filled P-V curves. The Ps of groups A and B were compared at the same lung volumes. Mean body weight and nose-to-tail length of the two groups did not differ significantly. Total lung capacity, defined as lung air volume at a transpulmonary pressure of 25 cmH2O, was significantly smaller in group B (mean +/- S.E. was 4.08 +/- 0.20 ml) than in group A (mean +/- S.E. was 5.23 +/- 0.12 ml) (p less than 0.01). The Ps of group B was significantly larger than that of group A at all lung volumes studied (p less than 0.01-0.05). These results indicate that the lung elastic recoil pressure component due to the surface tension was increased by intratracheal instillation of bleomycin in hamsters.