Pulmonary Airflow Research Articles

Viscous airflow through a rigid tube with a compliant lining: a simple model for the air-mucus interaction in pulmonary airways.

The respiratory tract of mammals is lined with a layer of mucus, described as viscoelastic semi-solid, above a layer of watery serous fluid. The interaction of these compliant layers with pulmonary airflow plays a major role in lung clearance by two-phase gas-liquid flow and in increased flow resistance in patients with obstructive airway diseases such as cystic fibrosis, chronic bronchitis and asthma. Experiments have shown that such coupled systems of flow-compliant-layers are quite susceptible to sudden shear instabilities, leading to formation of relatively large amplitude waves at the interface. Although these waves enhance the lung clearance by mobilizing the secretions, they increase the flow resistance in airways. The objective of this paper is to understand the basic interaction mechanism between the two media better by studying airflow through a rigid pipe that is lined by a compliant layer. The mathematical model that has been developed for this purpose is capable of explaining some of the published experimental observations. Wave instability theory is applied to the coupled air-mucus system to explore the stability of the interface. The results show that the onset flow speed for the initiation of unstable surface waves, and the resulting wavelength, are both very sensitive to mucus thickness. The model predicts that the instabilities initiate in the form of propagating waves for the elastic mucus where the wave speed is about 40 percent of the flow speed. The wavelength and phase speed to air velocity ratio are shown to increase with increasing mucus thickness.(ABSTRACT TRUNCATED AT 250 WORDS)

Laryngeal biomechanics: An overview of mucosal wave mechanics

The biomechanics of wave propagation in viscoelastic materials can be useful in understanding the nature of normal and pathologic vocal fold vibration. Mucosal wave movement is the primary means by which the larynx transforms the egressive pulmonary air flow into sound. This short tutorial describes a number of concepts fundamental to the understanding of the vocal fold traveling wave. The displacement velocity of the vocal folds is shown to be proportional to the wave speed, which in turn is proportional to the elastic modulus or stiffness of the vocal folds. Finally, a few cases of unilateral paralysis are used to demonstrate how vocal fold stiffness, entrainment, and degree of vocal fold closure interact to create the complex vibratory patterns that occur in disordered laryngeal states. It is emphasized that surgical voice restoration must consider these properties of the mucosal wave to improve phonatory function.

A specific endothelin-1 antagonist blocks inhaled endothelin-1-induced bronchoconstriction in sheep

In this study we used conscious sheep to compare the relative potencies of inhaled endothelin- (ET) 1 and ET-3 and to determine whether a newly described selective ET-1 receptor antagonist, [diaminopropionic acid1-Asp15]ET-1 ([Dpr1-Asp15]ET-1), when given as an aerosol blocks ET-1-induced bronchoconstriction. Partial concentration-response curves to ET-1 and ET-3 were obtained by measuring the change in pulmonary airflow resistance (RL) after aerosol challenge. Both ET-1 (n = 6) and ET-3 (n = 4) caused concentration-dependent (10(-10)-10(-7) bronchoconstriction, but ET-3 was 400-fold less potent than ET-1. Pretreatment (30 min) with 25 breaths of 5 x 10(-8) M [Dpr1-Asp15]ET-1 caused a 100-fold rightward shift of the ET-1 concentration-response curve. The activity of the ET-1 antagonist (25 breaths of 5 x 10(-8) M) was compared with that of various control peptides (25 breaths of 10(-8) M). ET-1 (50 breaths of 10(-7) M) caused an increase in RL of 133 +/- 33% (SE) over baseline. [Dpr1-Asp15]ET-1 significantly inhibited this response by 54%. No protection was seen with a monocyclic control peptide or a thrombin receptor peptide. There was, however, a small protective effect (38%, P < 0.05) seen with [Dpr1-Asp15]ET-3, a structurally homologous ET-3 antagonist. [Dpr1-Asp15]ET-1 had no effect on carbachol (n = 3) or leukotriene D4-induced bronchoconstriction. Thus inhaled ET-1 and, to a lesser extent, ET-3 cause concentration-dependent bronchoconstriction in conscious sheep.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship of pulmonary arterial pressure and airflow obstruction to emphysema

Guinea pigs were exposed to cigarette smoke for 6 mo, after which lung and cardiac function and lung morphology were examined. The smoke-exposed animals were divided into two groups on the basis of final pulmonary arterial pressure. We found that the smoke-exposed animals with increased pulmonary arterial pressure had a moderate degree of airflow obstruction compared with the normotensive smoke group, which showed only mild airflow obstruction, and with the control group. Both smoke groups had similar degrees of emphysema. Although both smoke groups had an increased percentage of muscularized small arterioles, only the group with increased pulmonary arterial pressure had an altered flow-pressure response to dobutamine. We conclude that although cigarette smoke appears to induce changes in the vascular structure and to produce emphysematous lung destruction, the increased pulmonary arterial pressure in guinea pigs chronically exposed to smoke is not directly related to either of these findings. Instead, it appears that there is a dynamic alteration of both the airways, producing airflow obstruction, and the vasculature, producing increased pulmonary arterial pressure.

Diagnosis of obstructive airways disease from the clinical examination

To determine the operating characteristics of history and physical examination items for pulmonary airflow obstruction. Prospective observational study. Medical Preoperative Evaluation Clinic at the Durham Veterans Affairs Medical Center. Consecutive patients referred for outpatient medical preoperative risk assessment. None. Number of years the patient had smoked cigarettes, patient-reported wheezing [LR+ (likelihood ratio for finding present) = 3.1; LR- (likelihood ratio for finding absent) = 0.58], and auscultated wheezing (LR+ = 12; LR- = 0.87) were independent predictors of obstructive airways disease from the history and physical examination. Forced expiratory time and peak expiratory flow rate, both measured by the clinician at the bedside, were additional independent predictors of airflow obstruction. A nomogram using patient-reported wheezing, number of years the patient had smoked, and auscultated wheezing was developed and validated (area under receiver operating characteristic curve = 0.78; p = 0.0001) for the bedside prediction of obstructive airways disease. Peak expiratory flow rate can be substituted for auscultated wheezing with similar predictive ability. The results of bedside clinical examinations predict the presence of obstructive airways disease. A nomogram based on a combination of four bedside findings predicts airflow obstruction as well as clinicians' overall clinical impressions.

Techniques for drug delivery to the airways, and the assessment of lung function in animal models

A common approach to understanding the mechanisms underlying clinical asthma and in new drug development is to mimic the disease in animal models. When developing animal models of pulmonary diseases, such as asthma, the experimentally induced disease may be characterized in terms of pathophysiological changes induced (e.g., inflammation, smooth muscle contraction) or by the indices of lung function that are affected by such changes. Similarly, the effects of drugs can be assessed in terms of the reversal of disease- or mediator-induced changes in lung function. Small animals, such as the guinea pig and rat, are commonly used for the assessment of lung function in models of pulmonary diseases, such as asthma, and to evaluate the effects of drugs. A variety of techniques, differing in their level of sophistication, has been developed to measure parameters of lung function in small laboratory animals. Simple techniques involve the visual assessment of the response of a conscious animal to bronchoconstriction induced by an inhaled spasmogen or antigen. This technique is rapid but gives results that are difficult to interpret in physiological terms. Bronchospasm can be better assessed in anesthetized, mechanically ventilated animals by recording bronchial tone as changes in either 1) ventilation circuit pressure or 2) air overflow as the lungs are inflated. These techniques are widely used but because they require surgical intervention they are not suited to long-term or repeat studies. In addition, they give only a limited indication of the physiological changes that affect airway caliber. To improve the models available, researchers have subsequently developed techniques that use the same physiological principles as some of the tests applied to the assessment of lung function in humans. These techniques allow the measurement of parameters of respiratory mechanics, such as lung compliance and airway resistance, that determine the relationship between pulmonary pressure changes and air flow into and out of the lungs. Continued development has resulted in models that use nonsurgical plethysmographic techniques. These allow the long-term or repeated measurement of lung function in conscious animals under minimal restraint. In the treatment of asthma, inhalation is the preferred route of administration of a drug as it allows rapid drug delivery to the site of action. Systematic effects are reduced, and the therapeutic dose is minimized. Drugs are generally inhaled as either nebulized liquids or dry-powder formulations. Because drug inhalation requires patient cooperation, techniques have been modified to allow drug delivery to the airways of experimental animals. Nebulizers of dry-powder generators can be used to deliver drugs either directly to the airways of anesthetized, tracheostomized animals or into an exposure chamber. If required, then some techniques allow lung function changes to be simultaneously measured. Alternatively, drugs can be administered by intratracheal instillation to the lungs of anesthetized animals. The pharmacological effects of anti-asthma drugs are partly dependent on the dose delivered to the lungs and the distribution in the airways. A variety of noninvasive and invasive techniques are used to measure drug deposition in experimental animals. Noninvasive methods allow the time course of distribution, absorption, and elimination to be followed. This review, therefore, discusses the various techniques most commonly used to deliver drugs to the airways of animals and to assess drug deposition, and the methods used to assess lung function in these models.

Persistence of enhanced aerosol deposition in the lung after recovery from carbachol-induced airway obstruction

Time course recovery from induced airway obstruction by carbachol infusion (CI; 0.2 microgram.kg-1.min-1 for 40 min), carbachol aerosol (CA; 10 breaths of 2% solution), and histamine aerosol (HA; 25-50 breaths of 5% solution) challenge was investigated in conscious sheep (n = 6 each). Total lung aerosol deposition and airway caliber as assessed by pulmonary airflow resistance (RL) were measured every 20-30 min up to 4 h after the challenges. Aerosol deposition was measured by monitoring aerosol concentration continuously with a laser aerosol photometer while the sheep rebreathed 1.0-micron-diam inert oil droplets delivered by a 0.25-liter bag-in-box system driven by a respiratory pump at a breathing frequency of 30 breaths/min. Total accumulated deposition at the fifth breath (AD5) as percentage of the initial aerosol concentration was determined and used as an aerosol deposition index. Percent changes in AD5 from baseline were compared with corresponding changes in RL. Both RL and AD5 increased after Cl, CA, and HA: 192-477% for RL and 23-44% for AD5 (P less than 0.05). Mean RL return to baseline values 1 h after CI and HA and 2 h after CA. Mean AD5 returned to baseline at 1 h post-HA. In contrast, mean AD5 remained elevated for 2-4 h after CI and CA (P less than 0.05), and the increased AD5 could not be reversed by a bronchodilator aerosol. The persistence of enhanced aerosol deposition long after the return of RL to baseline suggests that complete recovery of airway conditions after CI and CA takes much longer than predicted by RL.(ABSTRACT TRUNCATED AT 250 WORDS)

Breathing in Rana Pipiens: the Mechanism of Ventilation

ABSTRACT The mechanism and pattern of ventilation in unrestrained Rana pipiens were investigated by simultaneous measurements of pulmonary pressure, buccal pressure and air flow at the nostrils. The buccal cavity was ventilated continuously at a rate of 90±3.2 oscillations min−1 by low-amplitude pressure swings above and below atmospheric. The lungs were ventilated intermittently by the buccal pump at a rate of 6.3±0.8 breaths min−1. Expiration of gas from the nostrils occurred on two occasions during a lung ventilation. Ventilation of the lungs was achieved by precise timing of two valves, the nostrils and glottis. The timing of the valves determined the volume of expiratory flow on these two occasions and its relationship to inspiratory flow. Thus, the breathing movements could cause inflation, deflation, or no change in the lung volume. Periodically the lung was inflated by a sequence of successive breaths. During inflations the nostrils closed simultaneously with glottal opening and almost no gas was expired during the first expiratory phase. This caused a complete mixing of buccal contents and pulmonary gas and this mixture was pumped back into the lung. Deflations were characterized by a delay in nostril closing that resulted in a large outflow of gas from the lung and buccal cavity during the first phase of expiration. More gas left the system than was pumped into the lungs. The results suggest that coherent air flow from glottis to nostrils, as required by the ‘jet stream’ hypothesis of Gans et al. (1969), is not likely to occur.

Respiratory effects of pollution

Atmospheric pollution is increasingly responsible for chronic airway disease. Although outdoor pollution has decreased somewhat in recent years, indoor pollution has increased. Outdoor pollution results essentially from the combustion of coal and other fuels used for heating, industrial production and motor vehicles. The major sources of indoor pollution are heating and cooking devices. The main pollutants are suspended particulates, SO 2, NO 2 in indoor pollution and ozone which is linked to the photochemical effects. Transient increases in pollution cause transient decreases in pulmonary airflow. Chronic pollution seems to lead to an increase in the prevalence of lower and upper respiratory airway symptoms. In young children early exposure to pollution contributes to the development of chronic airways disease later in life. Asthmatics are at greater risk for pollution-related complications and several pollutants are known to increase bronchial reactivity. Further efforts are needed to reduce in pollution indoor and outdoor environments in particular with regard to tobacco smoke and especially for children. pollution / airway diseases.

Capsaicin and histamine antagonist‐sensitive mechanisms in the immediate allergic reaction of pig airways

The airway vascular and bronchial responses were studied in pigs sensitized with Ascaris suum. Ascaris, histamine (H) and capsaicin aerosol all induced a clear-cut increase in blood flow in the nasal, laryngeal and bronchial circulation with a decrease in vascular resistance of 20-40%. When delivered to the lung both ascaris and histamine, but not capsaicin, caused pulmonary airflow obstruction with increase in resistance and a fall in dynamic compliance of 40-70%. After pretreatment of pigs with a combination of the H1- and H2-receptor antagonists terfenadine and cimetidine, the vascular and bronchial responses were strongly reduced to both histamine (by greater than 77%) and ascaris (by greater than 58%), but not to capsaicin aerosol. The bronchoconstriction to histamine was found to be mediated by H1-receptors only, while both H1- and H2-antagonists were necessary to block the vasodilatory response, with H2-receptors being more important in the bronchial circulation and H1-receptors being more important in the laryngeal and nasal circulation. Furthermore, when pigs were pretreated with capsaicin systemically 2 days before the experiment, the vasodilation was decreased upon capsaicin (by 80%), ascaris (by greater than 40%) and histamine (by greater than 50%) aerosol challenge. When histamine was administered intravenously the desensitizing effect of capsaicin pretreatment was much less pronounced. The effect of capsaicin desensitization on the pulmonary obstruction upon ascaris and histamine challenge was limited to a 60% reduction of the fall in dynamic compliance and a delayed peak in resistance upon ascaris challenge. We conclude that histamine is one of the main vasodilatory mediators released upon allergen challenge at three different levels of the pig airways. A considerable part of the histamine effect is indirect and probably due to activation of capsaicin-sensitive sensory nerves.

Aerosol deposition in the lung with asymmetric airways obstruction: in vivo observation

Both the total and regional aerosol deposition were measured in six adult sheep before and after an induction of asymmetric airway obstructions, either by local instillation of carbachol solution (CS, 0.1%) distal to the right main bronchus or inhalation challenge of the right lung with carbachol aerosol (CA, 10 breaths). Total lung deposition was determined by monitoring inert monodisperse aerosols [1.0 micron mass median aerodynamic diam (MMAD)] breath-by-breath, at the mouth, by means of a laser aerosol photometer. Cumulative aerosol deposition over the first five breaths as a percent of the initial aerosol concentration (AD5) was used as a deposition index. Regional deposition pattern was determined by scintigraphic images of sulfur-colloid aerosol (1.5 microns MMAD) tagged with 99mTc. Radioactivity counts in the right (R) and left lung (L) were expressed as a percent of the whole lung count. Half-lung AD5 was then determined by multiplying AD5 by fractional radioaerosol depositions in R or L. Pulmonary airflow resistance (RL mean +/- SE), as determined by an esophageal balloon technique, increased by 111 +/- 28 and 250 +/- 96% after CA and CS, respectively (P less than 0.05). AD5 also increased in all the sheep tested by 29 +/- 3 and 52 +/- 8%, respectively, after CA and CS (P less than 0.05). Radioaerosol deposition pattern was even at base line (R/L = 51:49) but shifted toward the unchallenged L after CS (R/L = 40:60). Deposition pattern after CA was variable: a shift toward L in three, no change in one, and a shift toward the R lung in two sheep.(ABSTRACT TRUNCATED AT 250 WORDS)

Ethnic Differences in the Prevalence of Pulmonary Airflow Obstruction Among Grain Workers

World Health Organization data suggest that British males over 45 have a higher death rate from chronic bronchitis, emphysema, and asthma combined than do other Europeans. Although widely supposed that this is due to particularly unfavorable environmental factors in the British Isles, as well as a higher rate of tobacco consumption, ethnicity itself may be a significant factor in determining risk of obstructive airways disease. To test this hypothesis, we have analyzed the prevalence of airflow obstruction (100 x FEV1:FVC less than 68% and FEV1 less than 84 percent predicted) in Saskatchewan grain workers of British, German, and Eastern European ancestry using the Mantel-Haenszel odds ratio (OMH) and stepwise logistic regression. We found that the British grain workers had a significantly greater prevalence of airflow obstruction (OMH = 3.2; p less than 0.01) than the Eastern Europeans. We also found that ethnic origin made a significant contribution to the estimation of risk of airflow obstruction among grain workers independent of the effects of age and smoking.

Airway responsiveness to inhaled and intravenous carbachol in sheep: effect of airway mucus.

Excessive airway mucus can alter both the mass and site of aerosol deposition, which, in turn, may affect airway responsiveness to inhaled materials. In six prone sheep, we therefore measured pulmonary airflow resistance (RL) and cumulative aerosol deposition during five standard breaths (AD5) at base line and 3 min after inhalation challenge with 2% carbachol in buffered saline (10 breaths, tidal volume = 500 ml) or after an intravenous loading dose of carbachol (3 micrograms/kg) followed by a constant infusion of 0.3 micrograms.kg-1.min-1 with and without instillation of 20 ml of a mucus simulant (MS) into the distal end of each of the main bronchi or 30 ml of MS into the right main bronchus only by means of a flexible fiber-optic bronchoscope. Before carbachol challenge, RL did not change with MS into either both lungs or one lung only. AD5 increased from 36 +/- 2% (SE) before to 42 +/- 2% after MS instillation into both lungs (P less than 0.05) but remained unchanged after MS into one lung. After carbachol inhalation, RL increased significantly by 154 +/- 20 before and 126 +/- 25% after MS into both lungs and 162 +/- 24 before and 178 +/- 31% after MS into one lung (P less than 0.05). When the percent increase in RL was normalized for total aerosol deposition (% delta RL/AD5), the normalized values were lower after MS (3.0 +/- 0.5) than before MS (4.4 +/- 0.3) into both lungs (P less than 0.05) but were not significantly different before and after MS into the right lung only.(ABSTRACT TRUNCATED AT 250 WORDS)

LUNG LOBE COLLAPSE

The radiographic changes caused by collapse of lung lobes in pulmonary disease, pneumothorax, and pleural effusion depend on the lobar recoiling force and local pleural pressure. Differences in the tendency of normal lung lobes or regions to collapse depend on the relative surface‐to‐volume ratio, determined by shape and size of the region or lobe. This ratio affects the physiologic parameters of pulmonary interdependence, compliance, and collateral air flow. Pulmonary surfactant increases compliance, particularly at low volumes, maintains alveolar stability, and assists in maintaining capillary patency and preventing pulmonary edema. Its loss due to lung injury increases collapsing forces. In the presence of pneumothorax or pleural effusion, diseases that cause lobar collapse produce localized air or fluid entrapment that is a diagnostic sign of the presence of the underlying pulmonary disease.

Pulmonary Airflow Obstruction following Lymphography

In a series of 27 patients a significant mean decrease of forced expiratory volume in one second (FEV1) was recorded at 1/2, 2, 4 and 24 hours after lymphography with an oily contrast medium, with a maximum mean decrease at 4 hours after injection. The decrease of FEV1 was greater in patients given large amounts of contrast medium at high injection speed. Furthermore, an excessive decrease was observed in patients with metastatic lymph nodes, while a less marked decrease of FEV1 was observed in patients treated with aspirin. No serious clinical side effects were observed. It is recommended that the injection speed and the total amount of contrast medium be limited as far as possible, especially in patients with severe airflow obstruction or with metastases in the lymphatic system. Oral administration of aspirin may limit the decrease in FEV1 following lymphography.

Oronasal distribution of respiratory airflow

The oronasal distribution of respiratory airflow was determined during incrementally graded submaximal exercise in 30 (14 M, 16 F) healthy adult volunteers. Nasal airflow was measured by a pneumotachograph attached to a nasal mask. Oral airflow was determined as the difference between nasal airflow and total pulmonary airflow, the latter being measured by a head-out exercise body plethysmograph. The two airflow signals were sampled every 20 msec by a microprocessor, which calculated the oral and nasal minute volumes (separating inspiration and expiration) and produced an on-line print-out of the results. Twenty subjects (‘normal augmenters’) switched from nasal to oronasal breathing at a V̇ e of 35.3±10.8 l·min −1, four subjects (‘mouth breathers’) habitually breathed oronasally, five subjects (‘hose breathers’) persistently breathed through the nose only, and one subject showed no consistent nose/mouth breathing pattern. After the switch to oronasal breathing, the nasal portion of V̇ e decreased suddenly to 57% of total V̇ e , oral minute volume increased rapidly, equalling nasal minute volume at a V̇ e 45 l·min −1, and accounting for 61% of the total ventilation at high respiratory minute volumes (90 l·min −1). During oronasal breathing, normal augmenters inspired some 2 l·min −1 more nasally than they expired. Similarly, the nasal inspiration of mouth breathers expiration by 2 l·min −1 at rest, but the difference increased to 13.5 l·min −1 at a V̇ e of 81.5·min −1.

The switching point from nasal to oronasal breathing

The switching point from nasal to oronasal breathing during incrementally graded submaximal exercise was determined in 30 (14 M, 16 F) healthy adult volunteers. Nasal airflow was measured by a pneumotachograph attached to a nasal mask. Oral airflow was determined as the difference between nasal airflow and total pulmonary airflow, the latter being measured by a head-out exercise body plethysmorgraph. The airflow and pressure signals were sampled every 20 msec by a microprocessor, which calculated respiratory volumes and nasal work of breathing, and produced an on-line print-out. Twenty of the 30 subjects (normal augmenters) switched from nasal to oronasal breathing at submaximal exercise of 105.0 W (SD = 30.1), four subjects (mouth breathers) breathed habitually oronasally, five subjects (nose breathers) persistently through the nose only, and one subject showed no consistent nose/mouth breathing pattern. In normal augmenters, the onset of oronasal breathing ( V ̇ e ± 10.8 1 · min −1 ) was quite consistent individually, but varied considerably between individuals without showing a significant sex difference. The factors most closely related to the switching point were rating of perceived exertion of breathing and nasal work of breathing.

Altered function and histology in guinea pigs after inhalation of diesel exhaust

Health effects of inhaled diesel engine exhaust were evaluated in infant guinea pigs following 4 and 8 weeks of exposure. Animals were exposed to 1 part exhaust diluted by 13 parts clean air for 20 hr/day, 7 days/week. Lung function, electrocardiogram, growth rate, and histopathology were assessed following exposure. After 4 weeks, animals exposed to irradiated exhaust, showed a 35% increase in pulmonary air flow resistance, and a small but significant decrease in heart rate. Necropsy, after 8 weeks, showed exhaust exposed animals to have black discoloration of the lungs and increased lung to body weight ratios. Microscopic examination of the lungs from these animals revealed black particulate material in the cytoplasm of alveolar macrophages and in draining lymph nodes.

Nasopulmonary reflex: evaluation in the nonparalyzed and paralyzed anesthetized dog.

Changes in the pulmonary mechanics of various animal species have been observed after nasal stimulation. In reviewing the methods of these studies, we found that often the respiratory patterns were not controlled well enough to permit conclusions about changes in resistance and compliance. To further investigate the possibility of a nasopulmonary reflex, we first studied the effect of nasal stimulation on pulmonary mechanics in anesthetized, nonparalyzed dogs. In this group of 35 dogs, we found that nasal stimulation typically produced marked changes in breathing patterns, a large transient increase (150%) in pulmonary airflow resistance, but no change in compliance. This response to nasal stimulation could be abolished by interrupting either the trigeminal or the vagus nerves. In an additional group of 12 anesthetized, paralyzed dogs, we found no changes in resistance or compliance after nasal stimulation. From this observation, we concluded that nasal stimulation produced changes in breathing patterns that led to alterations in resistance without an actual change in the intrinsic behavior of the pulmonary airways.

Exercise-Aggravated Hypoxemia and Orthodeoxia in Cirrhosis

A syndrome characterized by hypoxemia aggravated by exercise, orthodeoxia, hypocapnia, and evidence of hyperdynamic circulation, but otherwise normal indices of pulmonary air flow, volume, and distribution of ventilation has been observed as an infrequent complication of hepatic cirrhosis. An illustrative case is described, the features of which support the presence of a shunt or shunt-like mechanism consisting of low-resistance vascular communications within the lung. We suggest that this may represent the existence of a hepatopulmonary syndrome analogous to the hepatorenal syndrome.