Exercise Intensity and Activity Energy Expenditure of Professional Golf Players in Official Competitive Setting.

BACKGROUND: Research regarding the physical needs of professional golf players is lacking. With advances in wearable technology, it has become easier to analyze physiological responses such as heart rate (HR) to determine activity energy expenditure (AEE). The purpose of the study was to evaluate exercise intensity (EI) and AEE during 4 consecutive tournament's golf rounds using a popular wrist-based HR monitoring. HYPOTHESIS: Wearable systems for HR monitoring can be used to provide an accurate estimate of energy expenditure. STUDY DESIGN: Cross-sectional study. LEVEL OF EVIDENCE: Level 3. METHODS: A total of 20 male professional golfers participated in the study. Each player was monitored during an official tournament consisting of 4 rounds of 18 holes. EI and AEE were determined using HR wrist monitoring (Whoop Strap 2.0). We calculated the percentage of HRmax (%HRmax) and the percentage of HRres (%HRres) and the AEE in kcal/min using Keytel's formula. RESULTS: The calculated mean %HRmax and %HRres for the study population were 56.4% ± 1.8% and 40.5% ± 2.6%, respectively. Considering American College of Sports Medicine guidelines, these average percentages correspond to a moderate EI. The average caloric expenditure was 5.4 ± 0.4 kcal/min and 1555.8 ± 157.8 kcal per round considering an average golf round duration of 288.3 ± 19.5 minutes. CONCLUSION: A professional player's golf round is moderate physical activity. The AEE of this activity was equal to 5.4 cal/min, which is moderate energy consumption. CLINICAL RELEVANCE: These data could help golf coaches and conditioning coaches to have a better understanding of the load placed on golfers during tournaments.

A century of exercise physiology: lung fluid balance during and following exercise.

PURPOSE: This review recalls the principles developed over a century to describe trans-capillary fluid exchanges concerning in particular the lung during exercise, a specific condition where dyspnea is a leading symptom, the question being whether this symptom simply relates to fatigue or also implies some degree of lung edema. METHOD: Data from experimental models of lung edema are recalled aiming to: (1) describe how extravascular lung water is strictly controlled by "safety factors" in physiological conditions, (2) consider how waning of "safety factors" inevitably leads to development of lung edema, (3) correlate data from experimental models with data from exercising humans. RESULTS: Exercise is a strong edemagenic condition as the increase in cardiac output leads to lung capillary recruitment, increase in capillary surface for fluid exchange and potential increase in capillary pressure. The physiological low microvascular permeability may be impaired by conditions causing damage to the interstitial matrix macromolecular assembly leading to alveolar edema and haemorrhage. These conditions include hypoxia, cyclic alveolar unfolding/folding during hyperventilation putting a tensile stress on septa, intensity and duration of exercise as well as inter-individual proneness to develop lung edema. CONCLUSION: Data from exercising humans showed inter-individual differences in the dispersion of the lung ventilation/perfusion ratio and increase in oxygen alveolar-capillary gradient. More recent data in humans support the hypothesis that greater vasoconstriction, pulmonary hypertension and slower kinetics of alveolar-capillary O2 equilibration relate with greater proneness to develop lung edema due higher inborn microvascular permeability possibly reflecting the morpho-functional features of the air-blood barrier.

The birth of experimental physiology.

The year 2023 marks the 300th anniversary of the death of Antonio Maria Valsalva (1666-1723). Valsalva was a leading physician across the 17th and 18th centuries, specifically for his focus on experimental physiology, the science dealing with the normal functioning of bodily organs as a basis for a better understanding of diseases, symptoms, and care. He used a top-down systematic approach typical of the Enlightenment, rather than a heuristic one ("trial-and-error"), which became feasible after the long-lasting ban on dissecting human corpses was lifted. Valsalva's main interest was exploring the complex structure of the human ear, to which he dedicated a specific treatise, De Aure Humana. He understood the issues inherent in the imbalance in pressure between the outer and inner ear and found ways to exploit it to get rid of purulent fluid by deliberately raising the inside pressure with his maneuver. Time was however not yet ripe to see the broader importance that the Valsalva maneuver would achieve, not just in otorhinolaryngology, but also in cardiology and other fields of medicine. Although Valsalva's name is usually associated with his maneuver, his contributions to the history of medicine were broader: he discovered several anatomical parts (i.e., the sinuses of Valsalva), built the basis for the development of pathological anatomy, introduced advances in surgery, and promoted compassionate care of patients affected by mental diseases.NEW & NOTEWORTHY Antonio Maria Valsalva (1666-1723) was a pioneer in experimental physiology between the 17th and 18th centuries. The Valsalva maneuver is still a popular academic topic and has broad applications not only in physiology research, but also in the diagnosis and therapy of various diseases. The celebration of 300 years from his death could be a timely occasion to commemorate the scientific works of this illustrious scientist.

Role of the Air-Blood Barrier Phenotype in Lung Oxygen Uptake and Control of Extravascular Water.

The air blood barrier phenotype can be reasonably described by the ratio of lung capillary blood volume to the diffusion capacity of the alveolar membrane (Vc/Dm), which can be determined at rest in normoxia. The distribution of the Vc/Dm ratio in the population is normal; Vc/Dm shifts from ∼1, reflecting a higher number of alveoli of smaller radius, providing a high alveolar surface and a limited extension of the capillary network, to just opposite features on increasing Vc/Dm up to ∼6. We studied the kinetics of alveolar-capillary equilibration on exposure to edemagenic conditions (work at ∼60% maximum aerobic power) in hypoxia (HA) (PIO2 90 mmHg), based on an estimate of time constant of equilibration (τ) and blood capillary transit time (Tt). A shunt-like effect was described for subjects having a high Vc/Dm ratio, reflecting a longer τ (>0.5 s) and a shorter Tt (<0.8 s) due to pulmonary vasoconstriction and a larger increase in cardiac output (>3-fold). The tendency to develop lung edema in edemagenic conditions (work in HA) was found to be directly proportional to the value of Vc/Dm as suggested by an estimate of the mechanical properties of the respiratory system with the forced frequency oscillation technique.

Heart rate variability, postural sway and electrodermal activity in competitive golf putting.

BACKGROUND: Stressful conditions during competitive golf putting may result in impaired performance, producing physiological changes. Nevertheless, simultaneous measurements of postural sway (PS), heart rate variability (HRV) and electrodermal activity (EDA) during a competitive golf putting have not yet been examined. This study aims at describing if changes in PS, HRV and EDA during golf putting, might affect the golfer's performance. METHODS: Based on EGA-handicap, 40 amateur golfers were divided in 2 groups. They competed in an indoor round of golf putting. PS, EDA, HRV and putting performance (SCORE) were recorded at basal and during competition. RESULTS: During the putting round, a significant increase in low-frequency power (LF) and decrease in high-frequency power (HF) was found in Group A, leading to an increased LF/HF ratio. The heart rate increased significantly more in Group A than in Group B, but the stress index (SI) remained lower in this group. EDA significantly increased in both groups, with no statistical difference between groups. No statistical difference in SCORE was observed. CONCLUSIONS: Despite the significant differences observed between the two groups, both at baseline and in response to competition, no variation of the studied variables was associated with a better putting performance.

Giovanni Maria Lancisi (1654-1720) and the modern cardiovascular physiology.

Giovanni Maria Lancisi (1654-1720) was one of the most important Italian physicians of the modern age. Orphaned of his mother, he spent his early years in the city of Orvieto; when he was 12, his father brought him back to Rome and enrolled him to study medicine at the Sapienza University in Rome. His dedication to study and work soon led him to increasingly important positions. Within a few years, the fame of Lancisi became such that he was appointed the personal physician of three popes. In De Subitaneis Mortibus (1707), he described the pathophysiology of heart diseases, identifying the cause of sudden deaths in structural anomalies of the heart, lungs, and brain. He also wrote about cerebral localizations and first discussed the physiological mechanisms of urine formation and excretion. In 1717, Lancisi described the pathogenesis of malaria and the close correlation between its onset and the swampy waters of the Tiber River, proposing the draining of marshes to eradicate malaria. In the posthumous De Motu Cordis et Aneurysmatibus (1728) he described for the first time heart dilatation and aneurysms of the great vessels, providing a fundamental contribution to the history of cardiovascular physiology. Proof of his interest in medical education is the establishment of an academy and the donation of a library to the hospital, bridging the gap between theory and practice in medical training. Over the centuries, Lancisi's memory has faded, but his work is still relevant for anyone practicing the medical profession.

Pulmonary Interstitial Matrix and Lung Fluid Balance From Normal to the Acutely Injured Lung.

This review analyses the mechanisms by which lung fluid balance is strictly controlled in the air-blood barrier (ABB). Relatively large trans-endothelial and trans-epithelial Starling pressure gradients result in a minimal flow across the ABB thanks to low microvascular permeability aided by the macromolecular structure of the interstitial matrix. These edema safety factors are lost when the integrity of the interstitial matrix is damaged. The result is that small Starling pressure gradients, acting on a progressively expanding alveolar barrier with high permeability, generate a high transvascular flow that causes alveolar flooding in minutes. We modeled the trans-endothelial and trans-epithelial Starling pressure gradients under control conditions, as well as under increasing alveolar pressure (Palv) conditions of up to 25 cmH2O. We referred to the wet-to-dry weight (W/D) ratio, a specific index of lung water balance, to be correlated with the functional state of the interstitial structure. W/D averages ∼5 in control and might increase by up to ∼9 in severe edema, corresponding to ∼70% loss in the integrity of the native matrix. Factors buffering edemagenic conditions include: (i) an interstitial capacity for fluid accumulation located in the thick portion of ABB, (ii) the increase in interstitial pressure due to water binding by hyaluronan (the "safety factor" opposing the filtration gradient), and (iii) increased lymphatic flow. Inflammatory factors causing lung tissue damage include those of bacterial/viral and those of sterile nature. Production of reactive oxygen species (ROS) during hypoxia or hyperoxia, or excessive parenchymal stress/strain [lung overdistension caused by patient self-induced lung injury (P-SILI)] can all cause excessive inflammation. We discuss the heterogeneity of intrapulmonary distribution of W/D ratios. A W/D ∼6.5 has been identified as being critical for the transition to severe edema formation. Increasing Palv for W/D > 6.5, both trans-endothelial and trans-epithelial gradients favor filtration leading to alveolar flooding. Neither CT scan nor ultrasound can identify this initial level of lung fluid balance perturbation. A suggestion is put forward to identify a non-invasive tool to detect the earliest stages of perturbation of lung fluid balance before the condition becomes life-threatening.

Differences in alveolo-capillary equilibration in healthy subjects on facing O2 demand.

Oxygen diffusion across the air-blood barrier in the lung is commensurate with metabolic needs and ideally allows full equilibration between alveolar and blood partial oxygen pressures. We estimated the alveolo-capillary O2 equilibration in 18 healthy subjects at sea level at rest and after exposure to increased O2 demand, including work at sea level and on hypobaric hypoxia exposure at 3840 m (PA ~ 50 mmHg). For each subject we estimated O2 diffusion capacity (DO2), pulmonary capillary blood volume (Vc) and cardiac output ([Formula: see text]). We derived blood capillary transit time [Formula: see text] and the time constant of the equilibration process ([Formula: see text], ß being the slope of the hemoglobin dissociation curve). O2 equilibration at the arterial end of the pulmonary capillary was defined as [Formula: see text]. Leq greately differed among subjects in the most demanding O2 condition (work in hypoxia): lack of full equilibration was found to range from 5 to 42% of the alveolo-capillary PO2 gradient at the venous end. The present analysis proves to be sensible enough to highlight inter-individual differences in alveolo-capillary equilibration among healthy subjects.

Rodolfo Margaria and the First Walk on the Moon.

INTRODUCTION: During the Cold War years, the Space Race was largely supported by the efforts of many engineers and scientists, in particular human physiologists. Rodolfo Margaria (1901-1983), director of the Institute of Human Physiology at the University of Milan, was one of the most eminent and focused his studies on the mechanics of human locomotion in subgravity, in particular on the Moon's surface. Long before the real Moon landing, Margaria was able to correctly theorize how astronauts would walk on lunar soil, what would be the optimal pattern of progression, as well as determine the optimum and maximum speed at one-sixth of the Earth's gravity. On 21st July 1969 at 02:56 UTC, great excitement was aroused by the television images of Neil Armstrong's first steps on the Moon. Instead of walking, he moved around making small leaps, as expected from Margaria and colleagues.Grasso GS, Beretta EP, Miserocchi GA, Riva MA. Rodolfo Margaria and the first walk on the Moon. Aerosp Med Hum Perform. 2019; 90(11):982-985.

Impact of Hanging Motionless in Harness on Respiratory and Blood Pressure Reflex Modulation in Mountain Climbers.

Harness hang syncope (HHS) is a risk that specifically affects safety of harness users in mountain climbing. Aims: To evaluate individual patterns of breathing resulting from deranged cardiovascular reflexes triggering a syncopal event when a mismatch between cerebral O2 demand and supply is present. Results: Forty healthy participants [aged 39.1 (8.2) years] were enrolled in a motionless suspension test while hanging in harness. Respiratory gas exchange values were analyzed to assess the pattern of breathing (EpInWel, respiratory elastic power) and cardiovascular parameters were monitored (BP, blood pressure). Four participants experienced HHS after 30.0 (7.6) minutes, with an early manifestation of loss of control of both a sustainable EpInWel and BP, starting after 10-12 minutes. Among the other participants, two different reactions were observed during suspension: (1) group G1 tolerated 32.7 (11.4) minutes of suspension by a favorable adaptation of the EpInWel and BP parameters and (2) group G2 showed significantly shorter time of suspension 24.0 (10.4) minutes with unfavorable increase in EpInWel and BP. Conclusions: Greater resistance to HHS occurs in people developing less marked fluctuations of both respiratory and cardiovascular reflex responses. Conversely, wider fluctuations both in control of EpInWel and BP were observed in the event of decreased suspension tolerance or in syncopal events.

Air blood barrier phenotype correlates with alveolo-capillary O2 equilibration in hypobaric hypoxia.

The O2 diffusion limitation across the air blood barrier (DO2 and subcomponents Dm and Vc) was evaluated in 17 healthy participants exposed to hypobaric hypoxia (HA, 3840m, PIO2 ∼90mmHg). A 10% decrease in alveolar volume (VA) in all participants suggested the development of sub-clinical interstitial lung edema. In >80% of participants DO2/VA increased, reflecting an individual strategy to cope with the hypoxia stimulus by remodulating Vc or Dm. Opposite changes in Dm/Vc ratio were observed and participants decreasing Vc showed reduced alveolar blood capillary transit time. The interplay between diffusion and perfusion (cardiac output) was estimated in order to investigate the individual adaptive response to hypoxia. It appears remarkable that despite individual differences in the adaptive response to HA, diffusion limitation did not exceed ∼11% of the alveolar-venous PO2 gradient, revealing an admirable functional design of the air-blood barrier to defend the O2 diffusion/perfusion function when facing hypobaric hypoxia corresponding to 50mmHg decreased PAO2.

Reappraisal of DLCO adjustment to interpret the adaptive response of the air-blood barrier to hypoxia.

DLCO measured in hypoxia must be corrected due to the higher affinity (increase in coefficient θ) of CO with Hb. We propose an adjustment accounting for individual changes in the equation relating DLCO to subcomponents Dm (membrane diffusive capacity) and Vc (lung capillary volume): 1/DLCO=1/Dm+1/θVc. We adjusted the individual DLCO measured in hypoxia (HA, 3269m) by interpolating the 1/DLCO to the sea level (SL) 1/θ value. Nineteen healthy subjects were studied at SL and HA. Based on the proposed adjustment, DLCO increased in HA in 53% of subjects, reflecting the increase in Dm that largely overruled the decrease in Vc. We hypothesize that a decrease in Vc (buffering microvascular filtration) and the increase in Dm (possibly resulting from a decrease in thickness of the air-blood barrier) represent the anti-edemagenic adaptation of the lung to hypoxia exposure. The efficiency of this adaptation varied among subjects as DLCO did not change in 31% of subjects and decreased in 16%.

Mild training program in metabolic syndrome improves the efficiency of the oxygen pathway.

In sedentary patients suffering of metabolic syndrome, we evaluated the effects of mild exercise program (EP) on the efficiency of the oxygen delivery system. The prescription of exercise (40 min/session, 3 times/week) was tailored at workload corresponding to ∼90% individual anaerobic threshold (AT). EP improved significantly by ∼10% peak values of oxygen consumption (VO2) and heart rate (HR). Furthermore, in response to steady state workload at 90% AT, EP shortened the time constant of VO2, HR and the ratio VO2/HR (reflecting arterio-venous O2 concentration difference) by ∼6s. EP also decreased the elastic respiratory work due to a change in breathing pattern implying a larger contribution of respiratory rate, at the expense of tidal volume during exercise hyperventilation. In all subjects the perceived fatigue (Borg) decreased after training. This study supports a positive effect of a mild EP for the adaptive response of the oxygen chain to face metabolic needs compatible with daily life in patients affected by metabolic syndrome.

Regional differences in bronchial reactivity assessed by respiratory impedance.

We used the Impulse Oscillometric System (IOS) to gain information concerning the distribution of hyper-reactivity along the bronchial tree during methacholine challenge test (MCT). 37 subjects underwent MCT until reaching the provocative dose (PD20). At each dose, we estimated respiratory resistance at 5 and 20Hz (R5, R20), and reactance at 5Hz (X5). In non-responsive subjects (N=14) no changes in R5, R20, and X5 were observed during MCT. In responsive subjects, a wide spectrum of responses was found concerning frequency dependence and PD20. We describe two phenotypes representing the extremes of response. For PD20>400µg (N=13), MCT caused equal changes of resistance/reactance on varying oscillation frequencies, suggesting a homogeneous bronchoconstriction along the bronchial tree. For PD20<200µg (N=10), a remarkable frequency dependence was observed, with increase in R5, no change in R20, and decrease in X5, suggesting hyper-responsiveness of the distal airways paralleled by a change in visco-elastic properties of lung parenchyma.

Inter-individual differences in control of alveolar capillary blood volume in exercise and hypoxia.

We compared by non-invasive technique the adaptive response of alveolar capillary network to edemagenic conditions (exercise and high altitude [HA, PIO2 107mmHg] in subjects with different resting sea level (SL) capillary blood volume (normalized to alveolar volume, Vc/Va): Group 1 (N=10, Vc/Va=16.1±6.8ml/L- mean±SD) and Group 2 (N=10, Vc/Va=25±7.7). In Group 1 Vc/Va remained unchanged in HA at rest and increased during exercise at SL (26.3±8.6) and HA (28.75±10.2); in Group 2 Vc/Va significantly decreased in HA (19±6) and did not increase in exercise at SL and HA. We hypothesize that Group2 exerts a tight control on Vc/Va being more exposed to the risk of lung edema due to inborn greater microvascular permeability. Conversely, Group 1 appears more resistant to lung edema given the large capillary recruitment in the most edemagenic condition. The 4-fold increase in frequency dependence of respiratory resistance in Group2 in HA stems for greater proneness for lung water perturbation compared to Group 1.

Consensus definitions to promote an evidence-based approach to management of the pleural space. A collaborative proposal by ESTS, AATS, STS, and GTSC.

The present project involved a collective effort agreed by the European Society of Thoracic Surgeons, the American Association for Thoracic Surgery, the Society of Thoracic Surgeons, and the General Thoracic Surgery Club to assemble a joint panel of experts to review the available data and address ambiguous aspects of chest tube definitions and nomenclature. The task force was composed of 11 invited participants, identified for their expertise in the area of chest tube management. The subject was divided in different topics, which were in turn assigned to at least two experts. The draft reports written by the experts on each topic were distributed to the entire expert panel, and comments solicited in advance of the meetings. During the meetings, the drafts were reviewed, discussed, and agreed on by the entire panel. Standardized definitions and nomenclature were proposed for the following topics related to chest tube management: pleural and respiratory mechanics after pulmonary resection; external suction versus no external suction; fixed versus variable suction; objective air leak evaluation; objective fluid drainage evaluation; and chest drain: type, number, and size. A standardized set of definitions and nomenclature were proposed to set a scientifically based framework with which to evaluate existing studies and to more clearly formulate questions, parameters, and outcomes for future studies.

Respiratory mechanics and fluid dynamics after lung resection surgery.

Thoracic surgery that requires resection of a portion of lung or of a whole lung profoundly alters the mechanical and fluid dynamic setting of the lung-chest wall coupling, as well as the water balance in the pleural space and in the remaining lung. The most frequent postoperative complications are of a respiratory nature, and their incidence increases the more the preoperative respiratory condition seems compromised. There is an obvious need to identify risk factors concerning mainly the respiratory function, without neglecting the importance of other comorbidities, such as coronary disease. At present, however, a satisfactory predictor of postoperative cardiopulmonary complications is lacking; postoperative morbidity and mortality have remained unchanged in the last 10 years. The aim of this review is to provide a pathophysiologic interpretation of the main respiratory complications of a respiratory nature by relying on new concepts relating to lung fluid dynamics and mechanics. New parameters are proposed to improve evaluation of respiratory function from pre- to the early postoperative period when most of the complications occur.

Hypoxia-induced modifications in plasma membranes and lipid microdomains in A549 cells and primary human alveolar cells.

We evaluated the response to mild hypoxia exposure of A549 alveolar human cells and of a continuous alveolar cell line from human excised lungs (A30) exposed to 5% O(2) for 5 and 24 h. No signs of increased peroxidation and of early apoptosis were detected. After 24 h of hypoxia total cell proteins/DNA ratio decreased significantly by about 20%. Similarly, we found a decrease in membrane phospholipid and cholesterol content. The membrane fluidity assessed by fluorescence anisotropy measurements was unchanged. We also prepared the detergent resistant membrane fraction (DRM) to analyze the distribution of the two types of lipid microdomains, caveolae and lipid rafts. The DRM content of Cav-1, marker of caveolae, was decreased, while CD55, marker of lipid rafts, increased in both cell lines. Total content of these markers in the membranes was unchanged indicating remodelling of their distribution between detergent-resistant and detergent-soluble fraction of the cellular membrane. The changes in protein markers distribution did not imply changes in the corresponding mRNA, except in the case of Cav-1 for A30 line. In the latter case we found a parallel decrease in Cav-1 and in the corresponding mRNA. We conclude that an exposure to a mild degree of hypoxia triggers a significant remodelling of the lipid microdomains expression, confirming that they are highly dynamic structures providing a prompt signalling platform to changes of the pericellular microenvironment.

Biochemical and morphological changes in endothelial cells in response to hypoxic interstitial edema.

BACKGROUND: A correlation between interstial pulmonary matrix disorganization and lung cellular response was recently documented in cardiogenic interstitial edema as changes in the signal-cellular transduction platforms (lipid microdomains: caveoale and lipid rafts). These findings led to hypothesize a specific "sensing" function by lung cells resulting from a perturbation in cell-matrix interaction. We reason that the cell-matrix interaction may differ between the cardiogenic and the hypoxic type of lung edema due to the observed difference in the sequential degradation of matrix proteoglycans (PGs) family. In cardiogenic edema a major fragmentation of high molecular weight PGs of the interfibrillar matrix was found, while in hypoxia the fragmentation process mostly involved the PGs of the basement membrane controlling microvascular permeability. Based on these considerations, we aim to describe potential differences in the lung cellular response to the two types of edema. METHODS: We analysed the composition of plasma membrane and of lipid microdomains in lung tissue samples from anesthetized rabbits exposed to mild hypoxia (12 % O2 for 3-5 h) causing interstitial lung edema. Lipid analysis was performed by chromatographic techniques, while protein analysis by electrophoresis and Western blotting. Lipid peroxidation was assessed on total plasma membranes by a colorimetric assay (Bioxytech LPO-586, OxisResearch). Plasma membrane fluidity was also assessed by fluorescence. Lipid microdomains were isolated by discontinuous sucrose gradient. We also performed a morphometric analysis on lung cell shape on TEM images from lung tissue specimen. RESULTS: After hypoxia, phospholipids content in plasma membranes remained unchanged while the cholesterol/phospholipids ratio increased significantly by about 9% causing a decrease in membrane fluidity. No significant increase in lipid peroxidation was detected. Analysis of lipid microdomains showed a decrease of caveolin-1 and AQP1 (markers of caveolae), and an increase in CD55 (marker of lipid rafts). Morphometry showed a significant decrease in endothelial cell volume, a marked increase in the cell surface/volume ratio and a decrease in caveolar density; epithelial cells did not show morphological changes. CONCLUSION: The biochemical, signaling and morphological changes observed in lung endothelial cell exposed to hypoxia are opposite to those previously described in cardiogenic edema, suggesting a differential cellular response to either type of edema.

Endothelial cells as early sensors of pulmonary interstitial edema.

We studied responses of endothelial and epithelial cells in the thin portion of the air-blood barrier to a rise in interstitial pressure caused by an increase in extravascular water (interstitial edema) obtained in anesthetized rabbits receiving saline infusion (0.5 ml.kg(-1).min(-1) for 3 h). We obtained morphometric analyses of the cells and of their microenvironment (electron microscopy); furthermore, we also studied in lung tissue extracts the biochemical alterations of proteins responsible for signal transduction (PKC, caveolin-1) and cell-cell adhesion (CD31) and of proteins involved in membrane-to-cytoskeleton linkage (alpha-tubulin and beta-tubulin). In endothelial cells, we observed a folding of the plasma membrane with an increase in cell surface area, a doubling of plasmalemma vesicular density, and an increase in cell volume. Minor morphological changes were observed in epithelial cells. Edema did not affect the total plasmalemma amount of PKC, beta-tubulin, and caveolin-1, but alpha-tubulin and CD-31 increased. In edema, the distribution of these proteins changed between the detergent-resistant fraction of the plasma membrane (DRF, lipid microdomains) and the rest of the plasma membrane [high-density fractions (HDFs)]. PKC and tubulin isoforms shifted from the DRF to HDFs in edema, whereas caveolin-1 increased in DRF at the expense of a decrease in phosphorylated caveolin-1. The changes in cellular morphology and in plasma membrane composition suggest an early endothelial response to mechanical stimuli arising at the interstitial level subsequently to a modest (approximately 5%) increase in extravascular water.