Biomedical subjects

G Saumon

Publications and source records attributed to G Saumon.

At least 55 records · Page 3Linked to original sources

PubMed1989

Cellular effects of beta-adrenergic and of cAMP stimulation on potassium transport in rat alveolar epithelium.

Alveolar fluid absorption is greatly enhanced by cAMP and by beta-adrenergic agonists via an increase in Na+ transport. Little is known about K+ homeostasis under these circumstances. We studied K+ transport across alveolar epithelium in isolated perfused rat lungs stimulated either by dibutyryl-cAMP or isoproterenol. K+ fluxes and the apparent permeability of 86Rb across the epithelium (alveoli to plasma) were interpreted according to a model involving two types of cells, B and L, distinguished by the location of Na+-K+-ATPases (basal and luminal). Water is considered to be absorbed by B cells in a solute-coupled process energized by a basolateral Na+-K+-ATPase that is stimulated by isoproterenol and cAMP. K+ transport out of the alveoli is due to the activity of a Na+-K+-ATPase located in the apical membrane of L cells. In the present study net transport rate of K+ was -0.5 +/- 0.15 nmol/s, n = 20 (out of alveoli) in control conditions. When the epithelium was stimulated by dibutyryl-cAMP (10(-4) mol/l) net absorption of K+ reversed to net 'secretion' into alveoli (3.2 +/- 0.31 nmol/s), fluid absorption was not stimulated. K+ 'secretion' was abolished by apical Ba2+, indicating it was due to opening of apical K+ channels. Basolateral ouabain reversed net K+ 'secretion' to net absorption indicating that K+ entry into alveoli was dependent on activity of B cell basolateral Na+-K+-ATPase (masking simultaneous K+ removal by apical L cell Na+-K+-pump). When larger concentrations of dibutyryl-cAMP (10(-3) mol/l) or when isoproterenol were used to stimulate the epithelium there was a tripling of fluid absorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗

PubMed1989

Exercise tolerance in chronic obstructive pulmonary disease: importance of active and passive components of the ventilatory system.

We investigated which components of ventilatory function are related to exercise tolerance in chronic obstructive pulmonary disease (COPD) patients. Physical characteristics, usual lung function, timing and neuromuscular components of ventilation were measured in 113 outpatients in whom FEV1/VC was less than 75% of the predicted value and exercise was limited by breathlessness. These variables were used to predict the maximum work load during progressive bicycle exercise. The prediction was obtained using a stepwise procedure in men and women separately. Among the variables selected, age, body weight, FEV1/VC, PImax, and P0.1/VT/TI accounted for 79% of the variability in maximum performance in men. The predictive model was statistically verified and was stable. The mean prediction error was 12 Watts. Among these variables, P0.1/VT/TI, PImax, and FEV1/VC were the main determinants of maximum work load (MWL). These results show that exercise limitation in COPD is related to impairment of both the active (inspiratory muscles) and passive (respiratory impedance) components of the ventilatory system. The same conclusions concerning passive components are proposed for women, despite a smaller population which prevented verification of the prediction.

Adult↗

PubMed1988

Apical sodium-sugar transport in pulmonary epithelium in situ.

The presence of an apical sodium-coupled transport system for D-glucose in lung alveolar epithelial cells has been demonstrated in lungs instilled with Ringer's fluid and perfused with either blood or Ringer's fluid (Basset et al. (1987) J. Physiol. 384, 325-345). The direction of transport is from alveoli towards interstitium. The characteristics of the system were evaluated in similar preparations by use of sugar analogues such as alpha-methyl-glucopyranoside, 2-deoxyglucose, 3-O-methylglucose and L-glucose. The main finding was the presence of a transport system for alpha-methylglucopyranoside and 2-deoxyglucose in the apical cell membrane. This system was unaffected by phloretin. Both alpha-methylglucopyranoside and 2-deoxyglucose transports were inhibited by phloridzin and by the presence of glucose (10(-2) mol.l-1). Competition was demonstrated between D-glucose and alpha-methylglucopyranoside or 2-deoxyglucose, but not for 3-O-methylglucose or L-glucose. 3-O-Methylglucose was cleared as slowly as L-glucose. The results comply partly with those known from intestinal epithelium and kidney proximal tubular epithelium, but the handling of 3-O-methylglucose was different. The relative transport rates of Na+ and glucose are compatible with a Na+: glucose coupling ratio larger than one.

Animals↗

PubMed1988

Doppler echocardiographic measurement of mitral flow volume: validation of a new method in adult patients.

Instantaneous intracardiac flow volumes can be calculated as the product of instantaneous flow velocity and instantaneous orifice area. This was accounted for in a new method of measuring stroke volume and cardiac output in the mitral orifice by pulsed Doppler echocardiography. This method was compared with simultaneous thermodilution in 30 adult patients in sinus rhythm without substantial atrioventricular or pulmonary valve abnormalities. The mitral orifice was assimilated to a conduit with 1) an ellipse-shaped inlet and outlet, 2) the same (and constant) long axis for the inlet and outlet ellipses (that is, the mediolateral anulus diameter measured on apical four chamber views), and 3) a varying outlet short axis (that is, the mitral anteroposterior leaflet separation derived from left parasternal M-mode recordings). This method design avoided the need for a short-axis view of the whole circumference of the mitral outlet orifice, which is difficult to obtain in many adult patients. The mitral flow velocity was recorded from the apex under two-dimensional guidance, within the mitral canal, close to the outlet section. Integration of instantaneous mitral leaflet separation multiplied by instantaneous flow velocity was performed using Simpson's rule. In addition to the proposed "instantaneous orifice area" method (method A), a "mean orifice area" method (method B) was also compared with thermodilution. In this simplified method, mitral flow was the product of mean orifice area and the diastolic mitral velocity integral, both derived from the same recordings as for method A.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Potassium transport across rat alveolar epithelium: evidence for an apical Na+-K+ pump.

1. Experiments were performed on rat lungs into which various solutions were instilled whilst the lungs were perfused with either whole blood or Ringer solution. Instillation of ion-free glucose solution led to a net flux of fluid and ions into the alveolar spaces. K+ ions entered faster than Na+ ions and reached a concentration about twice that in the perfusate. Ouabain in the perfusate (basolateral side) prevented the rise in alveolar K+ concentration above that in the perfusate, indicating a transcellular pathway. Ba2+ in the instillate (apical side) hindered the entry of K+ into alveoli, suggesting the presence of apical K+ channels. 2. When Ringer solution was instilled, K+ was continuously removed from the alveoli and the K+ concentration in the instillate remained constant or decreased slightly depending on the rate of fluid absorption. The net K+ efflux from alveoli to blood was 0.23 pmol/(cm2 s). When Ba2+ was added to the instillate the net K+ efflux increased to 0.36 pmol/(cm2 s). Apical ouabain reversed the K+ flux resulting in a net K+ flux of 0.19 pmol/(cm2 s) into the alveoli. This suggests the presence of an Na+-K+-ATPase located in the apical membrane of some alveolar cells. 3. The K+ transport from instillate (Ringer solution) to perfusate was traced by means of 86Rb which was added to the instillate. Ouabain in the instillate did not affect fluid absorption but reduced the apparent 86Rb permeability by 50% although the paracellular permeability (estimated with [3H]mannitol) was unaffected. This also indicates the presence of an apical Na+-K+-ATPase. When ouabain was added to the perfusate, the apparent 86Rb permeability doubled. These findings indicate that recirculation of 86Rb (and K+) occurs due to the activity of both apical and basolateral Na+-K+-ATPases. 4. When ouabain was placed on both sides of the epithelium, preventing transcellular transport, the passive 86Rb permeability was 10.3 x 10(-8) cm/s (assuming an alveolar surface area of 5000 cm2). This value agrees with the passive permeabilities for mannitol, Na+ and Cl- suggesting that the paracellular pathway acts as a water-filled neutral channel. 5. We conclude that K+ is 'secreted' into the alveoli and is also removed from the alveoli, both processes being energized by Na+-K+-ATPases placed on the basolateral and apical sides, respectively. It is likely that two functionally different cell types exist in the alveolar membrane. One type ('B cell') has a Na+-K+-ATPase located at the basolateral membrane and K+ channels situated luminally.(ABSTRACT TRUNCATED AT 400 WORDS)

Absorption↗

PubMed1988

High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure.

The respective roles of high pressure and high tidal volume to promote high airway pressure pulmonary edema are unclear. Positive end-expiratory pressure (PEEP) was shown to reduce lung water content in this type of edema, but its possible effects on cellular lesions were not documented. We compared the consequences of normal tidal volume ventilation in mechanically ventilated rats at a high airway pressure (HiP-LoV) with those of high tidal volume ventilation at a high (HiP-HiV) or low (LoP-HiV) airway pressure and the effects of PEEP (10 cm H2O) on both edema and lung ultrastructure. Pulmonary edema was assessed by extravascular lung water content and microvascular permeability by the drug lung weight and the distribution space of 125I-labeled albumin. HiP-LoV rat lungs were not different from those of controls (7 cm H2O peak pressure ventilation). By contrast, the lungs from the groups submitted to high volume ventilation had significant permeability type edema. This edema was more pronounced in LoP-HiV rats. It was markedly reduced by PEEP, which, in addition, preserved the normal ultrastructural aspect of the alveolar epithelium. This was in striking contrast to the diffuse alveolar damage usually encountered in this type of edema. To our knowledge, this constitutes the first example of a protective effect of PEEP during permeability edema.

Animals↗

PubMed1987

cAMP and beta-adrenergic stimulation of rat alveolar epithelium. Effects on fluid absorption and paracellular permeability.

The absorption of fluid (bicarbonate-buffered Ringer with 10 mmol/l glucose) instilled into rat lungs is a Na+-coupled process that takes place through two apical transport systems: an amiloride-sensitive Na+ transport and a Na+-glucose co-transport. Fluid absorption in isolated, perfused rat lungs and the permeability to 3H-mannitol of alveolar epithelium were studied in control conditions and during stimulation of the alveolar epithelium by cAMP or isoproterenol. cAMP led to a threefold increase in the rate of fluid absorption and to an increase in the paracellular permeability. A similar response was found following beta-adrenergic stimulation obtained with isoproterenol in the perfusate. The increase in fluid transport was due to enhancement of the amiloride-sensitive component of Na+ transport. The Na+-glucose co-transport which accounts for about 60% of fluid absorption in control conditions was depressed, possibly as a consequence of a depolarization of the apical alveolar cell membrane. Fluid absorption was reduced by 40% by apical amiloride (10(-4) mol/l) in control lungs and to an even larger extent in isoproterenol-stimulated lungs; it was completely abolished by amiloride in cAMP stimulated lungs. Since the Na+-glucose co-transport was still operative, this suggests that a secretory process was triggered. This was confirmed in experiments in which both kinds of transport were inhibited with a combination of amiloride and glucose-free Ringer. In these conditions fluid balance was zero in unstimulated lungs whilst fluid entry into alveoli was observed in isoproterenol and cAMP stimulated lungs.

Absorption↗

PubMed1987

Significance of active ion transport in transalveolar water absorption: a study on isolated rat lung.

1. Experiments were performed on isolated rat lungs perfused with Ringer solutions containing red cells. The goal was to clarify the role of active transport of Na+ for the absorption of fluid across the alveolar membrane, and to characterize active and passive pathways. 2. Partially degassed lungs were filled with 5 ml of an isotonic Ringer solution containing 125I-labelled albumin in order to calculate the fluid movement, and 22Na+ or 36Cl- for measurement of ion fluxes. Passive non-electrolyte permeability was determined in all experiments using [3H]mannitol. 3. The average rate of fluid absorption in phosphate-buffered instillates was 134 nl/s (S.E., 18.5; n = 14). With ouabain (10(-4) M) in the perfusate the fluid absorption rate fell to 57 nl/s (S.E., 8.2; n = 18). Amiloride (10(-3)-10(-4) M) in the instillate reduced the absorption to 75 nl/s (S.E., 8.6; n = 16). These results show that fluid absorption depends on transcellular transport of Na+ and that alveolar epithelial cells have a Na+ entry system in the luminal membrane and a Na+-K+ pump in the abluminal membrane. 4. The transcellular ion transport operates in parallel with a paracellular, passive leak that allows mannitol to pass with a permeability surface area product of 1.2 X 10(-4) ml/s, corresponding to a permeability coefficient of 2.4 X 10(-8) cm/s, assuming an alveolar surface area of 5000 cm2. 5. The passive fluxes of Na+ were 9.4 pmol/(cm2s) (S.E., 1.3; n = 25) in the direction from alveoli to perfusate and 8.0 pmol/(cm2s) (S.E., 0.86; n = 6) from perfusate to plasma. The passive fluxes of Cl- in the two directions were not significantly different either. Thus the transalveolar electrical potential difference is too small to affect ion movements measurably. 6. The passive permeability to Na+ was 6.7 X 10(-8) cm/s and to Cl- was 10.2 X 10(-8) cm/s (alveolar surface area assumed to be 5000 cm2). The ratio of the permeabilities is close to the ratio of the diffusion coefficients in free solution, suggesting a neutral or weakly charged paracellular channel. 7. We conclude that the alveolar epithelium performs solute-coupled fluid transport from alveoli to plasma, and that it shows many features that are common to other fluid-transporting epithelia; with an approximate surface area of 100 m2 in humans it constitutes one of the largest epithelial surfaces in the body.(ABSTRACT TRUNCATED AT 400 WORDS)

Absorption↗

PubMed1987

Fluid absorption by rat lung in situ: pathways for sodium entry in the luminal membrane of alveolar epithelium.

1. The purpose of the investigation was to characterize the luminal membrane and the paracellular pathway of rat lung alveolar epithelium. Experiments were performed on lungs in situ instilled with isotonic, buffered Ringer solution and perfused with blood from a donor rat using cross-circulation technique. 2. The rate of active Na+ transport was 4.4 pmol/(cm2s). The fluid absorption was 156 nl/s, and was unaffected by the presence of protein in the instillate (166 nl/s). In the absence of Na+, fluid absorption was zero. Amiloride (10(-3) M) reduced fluid absorption by 60%. Amiloride, combined with absence of D-glucose, arrested fluid absorption completely. Phloridzin at the luminal side reduced fluid absorption whilst phloretin had no effect. Amiloride together with phloridzin (10(-3) M) also arrested absorption. Thus, there are two entry systems for Na+ in the luminal membrane: Na+ channels and a Na+-D-glucose symport. These results show that alveolar fluid absorption is due to cellular activity. 3. Substitution of Cl- with gluconate not only stopped fluid absorption, but led to slight reversal of net fluid movement. 4. Passive unidirectional flux of Na+, determined with 22Na+, was 9.9 pmol/(cm2s) and that of Cl-, determined with 36Cl-, was 12.4 pmol/(cm2s). These fluxes were based on an assumed alveolar surface area of 5000 cm2. Transference numbers calculated from these figures are close to those in free solution, suggesting a neutral or weakly charged intercellular junctional pathway. The D-mannitol permeability in the paracellular pathway was 1.7 X 10(-8) cm/s. 5. It is a consequence of the proposed mechanism for fluid absorption that it becomes inoperative if the normally high reflexion coefficients for Na+ and Cl- are lowered in pathological states. In such conditions pulmonary oedema may develop depending on the net balance of passive mechanical and colloid-osmotic forces. 6. An explanation of the reversal of fluid transport at the time of birth is presented.

Absorption↗

PubMed1987

Na and nonelectrolyte entry into inner ear fluids of the rat.

Kinetics of hydrophilic solute entry into endolymph (EL), perilymph (PL), and cerebrospinal fluid (CSF) were studied after intravenous administration (sodium, urea, glycerol, mannitol, sucrose) and cerebral lateral ventricle injection (urea, sucrose) of tracers in anesthetized rats. Samples of cochlear EL, PL of scala vestibuli (PLV), PL of scala tympani (PLT), and cisternal CSF were obtained. The data showed slow entry of tracers in PLV, PLT, and CSF as follows: Na greater than urea greater than mannitol approximately sucrose; slower entry of mannitol and sucrose in PLT and CSF than in PLV; 1 h delayed peak of radioactivity in PLV compared with the immediate peaks in PLT and CSF after CSF injection, and the value of PLV peak was 13% that in CSF; extremely slow entry of nonelectrolytes in EL. These results indicate that PLV originates mainly from plasma across a blood-perilymph barrier that restricts the entry of small hydrophilic solutes. The blood-perilymph barrier is most likely composed of an endothelial barrier associated with an epithelial secretion. The latter could be located at the vasculo-epithelial zone of the spiral limbus.

Animals↗

PubMed1987

Facilitated transfer of glucose from blood into perilymph in the rat cochlea.

The transport of glucose into cochlear endolymph, perilymph of scala vestibuli and perilymph of scala tympani, and cerebrospinal fluid (CSF) was studied after intravenous administration of tracers of D-glucose, L-glucose, and 3-O-methyl-D-glucose in anesthetized rats. The data showed that D-glucose concentrations in perilymph of scala vestibuli, perilymph of scala tympani, and CSF were approximately 50%, and in endolymph less than 10%, that in plasma; D-glucose concentration in perilymph of scala vestibuli, perilymph of scala tympani, and CSF increased as a linear function of that in plasma; D-glucose entry into perilymph of scala vestibuli, perilymph of scala tympani, and CSF was more rapid than that of L-glucose; after infusion of 3-O-methyl-D-glucose, but not after that of mannitol, both the D-glucose concentration ratio of perilymph over plasma and D-glucose transfer into perilymph were lowered. These results indicate that D-glucose enters into perilymph of scala vestibuli by a facilitated transport, possibly located at the blood-perilymph barrier.

3-O-Methylglucose↗

PubMed1986

Smoking and interstitial lung disease. The effect of cigarette smoking on the incidence of pulmonary histiocytosis X and sarcoidosis.

Cigarette smoking produces marked alterations in the lung parenchyma and in the population of immune and inflammatory cells present in the lower respiratory tract. These cigarette-induced changes appear to influence the incidence of two different interstitial lung diseases, histiocytosis X and sarcoidosis. Smoking is a strong risk factor for the development of pulmonary histiocytosis X, since the incidence of smoking is very high among patients with histiocytosis X: 90% of the patients with histiocytosis X were smokers; 46% of the controls were smokers (p less than .001). In contrast, smoking appears to reduce the incidence of sarcoidosis: 31% of the patients with sarcoidosis were smokers (p less than .05 compared to controls). In an effort to understand how cigarette smoking influences the incidence of these two disorders, we compared the numbers and types of immune and inflammatory cells recovered by bronchoalveolar lavage from nonsmoking and smoking controls and patients with histiocytosis X and sarcoidosis. Although nonsmoking patients with histiocytosis X did not have a significant increase in the number of alveolar macrophages recovered by lavage (p greater than .2 compared to normals), smoking patients had an increase in the number of alveolar macrophages similar to that observed in the control population. In contrast, the number of macrophages recovered from patients with sarcoidosis who smoked was considerably less than that observed in normal smokers (p less than .05 comparing patients with sarcoidosis and controls who smoked 1-20 cigarettes/day). This difference in the intensity of the cigarette-induced macrophage alveolitis observed in the two patient groups may be important in explaining the opposite effects of cigarette smoking on the incidence of histiocytosis X and sarcoidosis.

Adult↗

PubMed1985

Servo-controlled air pump for calibration of respiratory measurement systems.

We describe a servo-controlled piston pump driven by a stepping motor. The analogue controller is a single non-linear second-order feedback loop with adjustable speed and acceleration limits. This system, designed to simulate slowly-moving, active and non-linear systems, can be used as a low (0-6.5 litre s-1) flow volume generator in calibration procedures.

Calibration↗

PubMed1985

Intermittent positive-pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in rats.

The mechanisms by which intermittent positive-pressure ventilation with high inflation pressure (HIPPV) induces pulmonary edema remain uncertain. In this study we investigated the physiologic and anatomic changes related to HIPPV at 45 cmH2O peak inspiratory pressure in rats. Edema was quantified by the extravascular lung water obtained from postmortem weighing and by 22Na distribution space. Pulmonary microvascular permeability was assessed by dry lung weight and fractional albumin uptake. After only 5 min of HIPPV, there was a significant increase in Na space, dry lung weight, and fractional albumin uptake when compared with that in control rats mechanically ventilated at 7 cmH2O peak inspiratory pressure. These changes suggest that edema may be due at least in part to alterations in microvascular permeability. Moderate peribronchovascular edema was present. At the ultrastructural level, some endothelial cells were found detached from their basement membrane. This lesion has been previously described in other types of pulmonary microvascular injury. The above findings remained almost unchanged after 10 min of HIPPV. After 20 min of HIPPV, we observed the outpouring of a high protein content alveolar flooding accompanied by a further significant increase in fractional albumin uptake and dry lung weight. Additional anatomic damage appeared including epithelial lesions and hyaline membranes. Thus, HIPPV edema presents all the features of high permeability edema. These results may be of concern in the ventilatory management of patients with acute respiratory failure in order to avoid additional damages induced by local overinflation.

Animals↗

PubMed1984

Automatic monitoring of breath-to-breath occlusion pressure and ventilatory parameters during CO2 rebreathing.

A computerized system for occlusion pressure measurement during a rebreathing test is described. The system is implemented on an Apple II microcomputer. A set of programs allows calibration, data acquisition during the experiment, and fast automatic processing of the various parameters of ventilation and occlusion pressure versus end tidal PCO2. The use of a limited memory system is made possible by an electronic interface which allows preprocessing of the mouth pressure. In addition, that device drives a new simple electromagnetic valve with low flow resistance and dead space.

Biomedical Engineering↗

PubMed1984

Electrochemical heterogeneity of the cochlear endolymph: effect of acetazolamide.

The electrochemical composition of endolymph (EL) of two adjacent cochlear turns was studied in anesthetized rats. Differences in [K]EL, [Cl]EL, and endocochlear potential (EP) were found between the basal turn (165.6 +/- 3.0 mM, n = 14; 144.6 +/- 2.1 mM, n = 14;96.6 +/- 1.9 mV, n = 5, respectively) and the middle turn (155.7 +/- 2.5 mM, n = 15; 133.2 +/- 1.5 mM, n = 15; 87.0 +/- 1.6 mV, n = 6, respectively). The pH values of inner ear fluids were evaluated with 5,5-dimethyloxazolidine-2,4-dione: EL pH of either turn was not different from blood and perilymph (PL) pH. Acetazolamide (40 mg X kg body wt-1) reduced EP and [Cl]EL at each turn by about 20 and 6%, respectively, but [K]EL was unchanged. The electrochemical differences between the two turns persisted. Acetazolamide produced a 0.2-unit decrease in blood pH while the pH values of EL and PL remained unchanged. These results suggest the existence of an electrochemical gradient within EL from the base to the apex of the cochlea involving K+ and Cl- concentrations. H+ and HCO-3 do not appear to participate in this gradient, and the acid-base status in EL could be maintained both by active H+ transport into EL and by HCO-3 formation in the cochlear epithelium.

Acetazolamide↗

PubMed1984

The relationship between disease duration and noninvasive pulmonary explorations in sarcoidosis with erythema nodosum.

In order to investigate the initial course of pulmonary sarcoidosis, the following investigations were carried out in 14 nonsmoking patients with Logfren 's syndrome 3 to 12 wk after the onset of erythema nodosum (EN): bronchoalveolar lavage (BAL) (cellular and protein components), serum assays of lgG and of the activity of angiotensin-converting enzyme (SACE), and pulmonary function tests. These results were related to the disease duration, estimated by the time lapse separating the onset of EN from the investigations. All patients but one showed a large increase in the percentage of lymphocytes (%-L) in BAL fluid (more than 30%). Although each patient was evaluated only once, and thus this work was not an actual longitudinal study, a linear relationship between lymphocyte count per milliliter of recovered fluid during BAL (L-count) and disease duration was found during the first 8 wk (r = 0.78, p less than 0.01), suggesting a fast-developing alveolitis. The delayed rise in SACE level may indicate a secondary activation of macrophages; SACE and L-count were well related, either up to 8 wk (SACE versus L-count: r = 0.84, p less than 0.01) or up to 12 wk (SACE versus L-count: r = 0.61, p less than 0.01). Serum lgG levels were found to follow the L-count (serum lgG versus L-count: r = 0.79, p less than 0.01) and appeared to be a reliable index of disease activity. Respiratory function showed a univocal pattern, with a marked decrease in all of the patients in carbon monoxide diffusing capacity (DLCO), contrasting with normal lung volumes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1982

Pulmonary sarcoidosis with an alveolar radiographic pattern.

Thirty-three cases of sarcoidosis (4.4% of 746 patients) showed an alveolar radiological pattern. A study of pulmonary function was carried out in 25 patients and compared with that of 46 patients with the interstitial radiological type of sarcoidosis. Twenty-two cases have been followed up from one to six years after the initial examination. The radiographic lesions were most often bilateral and included nodules greater than 15 mm with ill-defined margins or diffuse, infiltrative, non-retractile opacities with fluffy margins. Bilateral mediastinal lymph nodes were present in 27 patients. In 20 patients an associated reticulation was found on radiography. In four patients an open lung biopsy was done. The granulomatous nodules were identical to those found in other forms of sarcoidosis, although they were more confluent in the affected areas. Clinical and functional findings did not differ from those in the more common forms of sarcoidosis. Alveolar sarcoidosis has a sudden course. The alveolar radiological patterns always disappeared, with or without steroid treatment, while reticular patterns persisted in four patients. Rapid radiological changes were observed. Some functional abnormalities persisted in cases that were followed. It is concluded that alveolar sarcoidosis is a distinct acute form of sarcoidosis.

Adolescent↗