Pulmonary Distensibility Research Articles

Correlation between Pulmonary Artery Pressure and Vortex Duration Determined by 4D Flow MRI in Main Pulmonary Artery in Patients with Suspicion of Chronic Thromboembolic Pulmonary Hypertension (CTEPH).

Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the causes of pulmonary hypertension (PH) and requires invasive measurement of the mean pulmonary artery pressure (mPAP) during right heart catheterisation (RHC) for the diagnosis. 4D flow MRI could provide non-invasive parameters to estimate the mPAP. Twenty-five patients with suspected CTEPH underwent cardiac MRI. Mean vortex duration (%), pulmonary distensibility, right ventricular volumes and function were measured using 4D flow MRI and cine sequences, and compared with the mPAP measured by RHC. The mPAP measured during RHC was 33 ± 16 mmHg (10–66 mmHg). PH (defined as mPAP > 20 mmHg) was present in 19 of 25 patients (76%). A vortical flow was observed in all but two patients (92%) on 4D flow images, and vortex duration showed good correlation with the mPAP (r = 0.805; p < 0.0001). Youden index analysis showed that a vortex duration of 8.6% of the cardiac cycle provided a 95% sensitivity and an 83% specificity to detect PH. Reliability for the measurement of vortex duration was excellent for both intra-observer ICC = 0.823 and inter-observer ICC = 0.788. Vortex duration could be a useful parameter to non-invasively estimate mPAP in patients with suspected CTEPH.

Assessment of pulmonary hemodynamics and stress-induced pulmonary hypertension in clinical practice

Pulmonary hypertension (PH) is currently determined by the mean pulmonary artery pressure (PAPmean) increase, which in turn is associated with a number of parameters, such as cardiac output (CO), pulmonary vascular resis-tance (PVR) and left atrial pressure. Therefore, changes in PAP mean during exercise cannot be discussed apart from the listed indicators. Probably, this was one of the reasons for the absence of an accurate hemodynamic de-termination of stress-induced PH. However, today it has been revealed that PAP at rest increases only when ≥50% of pulmonary microcirculation is off, and for the earliest detection of the problem it is advisable to use factors that lead to increase of CO and PVR, one of them is exercise. Moreover, clinicians often observe that the anamnesis of PH starts from complaints, associated with exercise. Mo-dern non-invasive technologies (stress-echocardiogra-phy, cardiopulmonary exercise testing) provide very de-tailed data not only about the pulmonary circulation, but also about ventilator function, blood gas composition, structural and functional changes in the heart. Stress-in-duced PH is defined as combination of normal mean pulmonary artery pressure values (PAPmean &lt;25 mm Hg) at rest and increase of PAPmean &gt;30 mm Hg during exercise, as well as PVR &gt;3 WU, however, this definition isn’t generally accepted. As an alternative, to determine stress-induced PH, it was proposed to evaluate PAPmean/CO curve, that excludes the influence of peak hemody-namic parameters. The pulmonary vessels distensibility and ventriculo-arterial coupling represent promising pa-rameters for complete characterization of the pulmonary circulation changes during exercise.

ASSOCIATION OF ADIPOKINES AND OBESITY-RELATED PATHWAYS WITH LUNG FUNCTION AND PULMONARY VASCULAR DISTENSIBILITY

SESSION TITLE: Pulmonary Manifestations of Systemic Disease Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: October 18-21, 2020 PURPOSE: Obesity has multifactorial effects on lung function and pulmonary hypertension. The contributions of adipose related cytokine (adipokine) pathways to alterations in lung function remain unclear. In this context, we examined the role of adipokines and obesity-related biomarkers in relationship to pulmonary function and dynamic pulmonary vascular response to exercise. METHODS: We examined patients who underwent clinically indicated cardiopulmonary exercise testing (CPET) with invasive hemodynamic monitoring at Massachusetts General Hospital between December 2006 and June 2017. We excluded patients with low LVEF or who failed to reach adequate exercise threshold (defined at RER>1.0). We examined the association of adiponectin, leptin, resistin, IL6, CRP, and insulin resistance (HOMA-IR) with pulmonary function (% predicted FEV1, FVC, FEV1/FVC, TLC and DLCO) using multivariable linear regression. Analyses were adjusted for age, sex, BMI, smoking status, diabetes, prior MI, and heart failure. Adipokines were log-transformed and standardized. RESULTS: Among 695 individuals (mean age 57 years, 60% women), we found that leptin, CRP and HOMA-IR were all associated with lower FEV1, FVC, TLC and DLCO (multivariable p<0.05 for all), with minimal effect on FEV1/FVC ratio indicating restrictive physiology. For example, a 1-SD higher leptin level was associated with a 3% lower FEV1, 2.7% lower FVC, 4.5% lower TLC and 3.5% lower DLCO (p<0.05 for all). By contrast, adiponectin was associated with lower FEV1 and FEV1/FVC ratio (p<0.05 for both), indicating obstructive physiology. In addition, leptin, resistin, IL6, CRP, and HOMA-IR were associated with lower peak VO2 (p<=0.001 for all). When examining measures of pulmonary vascular function, we observed that higher adiponectin, IL6, and CRP were associated with worse pulmonary distensibility, and higher leptin, IL6, and CRP were associated with worse pulmonary artery compliance (p<0.05 for all). CONCLUSIONS: Adipokines and obesity-related pathways including leptin, IL6, CRP, and HOMA-IR were associated with worse pulmonary function in a pattern suggestive of restrictive physiology, in addition to worse functional capacity. IL6 and CRP were associated with both a lower pulmonary artery distensibility and compliance. CLINICAL IMPLICATIONS: Adipokine and obesity-related biomarkers were associated with restrictive lung physiology demonstrated by a reduction in % predicted FEV1, FVC, TLC and DLCO. In addition, higher levels of adipokines, in particular IL6 and CRP, demonstrated worsening pulmonary distensibility as well as pulmonary compliance indicating a negative effect on the pulmonary vascular system. These results may shed light onto potential mechanisms by which obesity can lead to lung disease and pulmonary hypertension. DISCLOSURES: No relevant relationships by Robyn Farrell, source=Web Response No relevant relationships by Jennifer Ho, source=Web Response No relevant relationships by Emily Lau, source=Web Response no disclosure on file for Gregory Lewis; No relevant relationships by Elizabeth Liu, source=Web Response Owner/Founder relationship with Patch Please note: >$100000 Added 04/06/2020 by Rajeev Malhotra, source=Web Response, value=Ownership interest Consultant relationship with Third Pole Please note: $1001 - $5000 Added 04/06/2020 by Rajeev Malhotra, source=Web Response, value=Consulting fee Consultant relationship with MyoKardia Please note: $20001 - $100000 Added 04/06/2020 by Rajeev Malhotra, source=Web Response, value=Consulting fee No relevant relationships by Jenna McNeill, source=Web Response No relevant relationships by Matthew Nayor, source=Web Response No relevant relationships by John Sbarbaro, source=Web Response No relevant relationships by Mark Schoenike, source=Web Response No relevant relationships by Emily Zern, source=Web Response

¿El reflujo gastroesofágico y la aspiración de contenido gástrico están implicados en la etiopatogenia y la progresión de la fibrosis pulmonar idiopática?

ABSTRACT Gastroesophageal reflux (GERD) and hidden aspiration of gastric contents are probably involved in the pathogenesis and progression of idiopathic pulmonary fibrosis (IPF). The pathological mechanisms involved are decreased pulmonary distensibility and consequent increase of intrathoracic negative pressure during inspiration, as well as decreased control mechanisms of esophageal motility or lower esophageal sphincter. The prevalence of GERD and oesophageal dysmotility was higher in patients with IPF as compared with general population. Among patients with IPF, 67-76% demonstrated abnormal oesophageal acid exposure. However, no relationship was demonstrated between severity of GERD and severity of IPF. Data are scant on outcomes of antireflux treatment in patients with IPF. Actually, some data suggests that antacid treatment may be deleterious in some IPF patients. After analyzing all the relevant evidence found to date, a causal relationship between GERD, gastric content aspiration and IPF pathogenesis cannot be established. There is scant evidence examining antireflux treatment in idiopathic pulmonary fibrosis patients.

Respiratory Rehabilitation in Interstitial Lung Diseases

Introduction: The interstitial lung diseases (ILD) are mainly characterized by: dry cough, dyspnea and exercise desaturation. These symptoms are due, among other causes, to the lack of pulmonary distensibility and to the alteration of the gas exchange. The objective of this study is to demonstrate the effects that a respiratory rehabilitation program (RRP) has in a group of patients with ILD. Method: prospective cohort study that was approved by the Maule Health Service Ethics Committee and all Patients signed an informed consent, which were 10 (3 men, 7 women), age: 72.4±7.9 years with diagnosis of ILD, specifically 7 with usual interstitial pneumonia(UIP), of which three are associated with rheumatoid arthritis(RA), 3 to idiopathic pulmonary fibrosis(IPF) and 1 to chronic hypersensitivity pneumonitis(CHP), 2 with nonspecific interstitial pneumonia (NSIP) and 1 cryptogenic organizing pneumonia(COP), which were subjected to a RRP based on aerobic training of the respiratory and peripheral musculature, during 36 sessions of 60 minutes each, 3 times a week. The measured variables pre and post training were: body mass index(BMI), forced vital capacity(FVC), distance walked through the six minute walking test(6MWT), dyspnea through the modified scale of the medical research council(MMRC), strength of the inspiratory musculature through the maximal inspiratory pressure(MIP), initial saturation of oxygen(ISO2), final saturation of oxygen(FSO2), desaturation of oxygen(DO2) measured with pulse oximetry, diffusing capacity of the lung for carbon monoxide(DLCO) and quality of life through Saint George Respiratory Questionnaire (SGRQ). The statistical analysis was Carried Out with the program SPSS version 23. Results: significant changes (p<0.05) in: FVC, 6MWT, mMRC, MIP, and SGRQ. Non-significant changes (p˃0.05) in: BMI, ISO2, FSO2, DO2, and DLCO. Conclusion: our RRP improved lung function, exercise capacity, dyspnea, respiratory muscle strength and quality of life of the subjects intervened.

Overbuilt for exercise or not: how do lung structure and distensibility impact exercise capacity?

Cardiacoutput,muscleoxygendeliveryand oxygen extraction are hypothesized to limit maximal oxygen consumption ( ˙ VO2max )i n healthy individuals. Much work aiming to address the long-standing question of cardiac output limitation has focused on the capacity of the left ventricle to increase stroke volume with substantially less focus on the importance of the right ventricle. The right ventricle is thin-walled, crescent shaped and generally less resistant to afterload stress than the left ventricle. While the increase in mean pressure encountered by the left ventricle during exercise is ∼25%, the right ventricle encounters a threeto four-fold increase in mean pulmonary vascular pressure. Indeed, elite endurance athletes experience acute right ventricular dysfunction and show evidence of right ventricular fibrosis after a race (3‐11 h) although left ventricular structure and function are unaffected (La Gerche et al. 2012). Within our group, we have frequently discussed how the right ventricle might be limited in its ability to increase cardiac output in the face of hypertensive pulmonary vascular pressures and find the question of whether right ventricular afterload stress impacts exercise capacity in healthy individuals breathing room air to be intriguing. Thus, we were excited to have the opportunity to discuss the recent paper entitled ‘Pulmonary vascular distensibility predicts aerobic capacity in healthy humans’, published (Lalande et al. 2012). Here, Lalande et al. hypothesized that the distensibility of the pulmonary vasculature predicts ˙ VO2max in healthy humans.

Chronic Obstructive Pulmonary Disease (COPD) is associated with pulmonary artery stiffness - the MESA COPD study

Background This study seeks to evaluate indices of pulmonary artery (PA) stiffness in patients with COPD and compare with normal controls. We hypothesize that patients with COPD would have increased pulmonary artery stiffness. To test this we determine the pulmonary artery area change (distensibility in %) by cardiac MRI and relate the distensibility to a wide range of severity of COPD. Methods The MESA COPD Study recruited 290 patients (135 patients of various COPD severity and 155 controls) from four field centers in the US, age 50-79 years with ≥10 pack-years of smoking, all free of clinical cardiovascular disease. COPD was defined on post-bronchodilator spirometry by GOLD criteria (FEV1/FVC 80% = mild, 50-80%=moderate, <50%=severe). All participants underwent full-lung CTs. Percent emphysema was defined as the percentage of total voxels within the lung field that fell below -910 Hounsfield units. MRI studies were performed using 1.5T scanners. To measure ventricular function, the entire heart was imaged in short-axis orientation using a retrospectively gated steady-state free precession sequence. Phase-contrast images of the pulmonary arteries were obtained using a segmented fast gradient echo sequence with free breathing and analyzed quantitatively using dedicated software (FLOW, Medis). Distensibility of the pulmonary vessels (in %) are measured by the following formula, 100×(maximum PA area-minimum PA area)/minimum PA area. The base model (model 1) was adjusted for age, gender, height, weight, race/ethnicity and cohort of selection, given relationships of COPD severity to the pulmonary distensibility. We then additionally adjusted for smoking status, pack-years, diabetes mellitus, hypertension, oxygen saturation, LDL, HDL and statin use (model 2).

Pulmonary compliance and lung volume varies with ecomorphology in anuran amphibians: implications for ventilatory-assisted lymph flux

Vertical movement of lymph from ventral regions to the dorsally located lymph hearts in anurans is accomplished by specialized skeletal muscles working in concert with lung ventilation. We hypothesize that more terrestrial species with greater lymph mobilization capacities and higher lymph flux rates will have larger lung volumes and higher pulmonary compliance than more semi-aquatic or aquatic species. We measured in situ mean and maximal compliance (Δvolume/Δpressure), distensibility (%Δvolume/Δpressure) and lung volume over a range of physiological pressures (1.0 to 4.0 cmH(2)O) for nine species of anurans representing three families (Bufonide, Ranidae and Pipidae) that span a range of body masses and habitats from terrestrial to aquatic. We further examined the relationship between these pulmonary variables and lymph flux for a semi-terrestrial bufonid (Rhinella marina), a semi-aquatic ranid (Lithobates catesbeianus) and an aquatic pipid (Xenopus laevis). Allometric scaling of pulmonary compliance and lung volume with body mass showed significant differences at the family level, with scaling exponents ranging from ∼0.75 in Bufonidae to ∼1.3 in Pipidae. Consistent with our hypothesis, the terrestrial Bufonidae species had significantly greater pulmonary compliance and greater lung volumes compared with semi-aquatic Ranidae and aquatic Pipidae species. Pulmonary distensibility ranged from ∼20 to 35% cmH(2)O(-1) for the three families but did not correlate with ecomorphology. For the three species for which lymph flux data are available, R. marina had a significantly higher (P<0.001) maximal compliance (84.9±2.7 ml cmH(2)O(-1) kg(-1)) and lung volume (242.1±5.5 ml kg(-1)) compared with L. catesbeianus (54.5±0.12 ml cmH(2)O(-1) kg(-1) and 139.3±0.5 ml kg(-1)) and X. laevis (30.8±0.7 ml cmH(2)O(-1) kg(-1) and 61.3±2.5 ml kg(-1)). Lymph flux rates were also highest for R. marina, lowest for X. laevis and intermediate in L. catesbeianus. Thus, there is a strong correlation between pulmonary compliance, lung volume and lymph flux rates, which suggests that lymph mobilization capacity may explain some of the variation in pulmonary compliance and lung volume in anurans.

Breath-Hold Diving

Extensive breath-hold (BH) diving imposes high pulmonary stress by performing voluntary lung hyperinflation maneuvers (glossopharyngeal insufflation, GI), hyperinflating the lung up to 50% of total lung capacity. Breath-hold durations of up to 10 min without oxygen support may also presume cerebral alterations of respiratory drive. Little is known about the long-term effects of GI onto the pulmonary parenchyma and respiratory adaptation processes in this popular extreme sport. Lung function assessments and subsequent measures of pulmonary static compliance were obtained for 5 min after GI in 12 elite competitive breath-hold divers (BHD) with a mean apnea diving performance of 6.6 yr. Three-year follow-up measurements were performed in 4 BHD. Respiratory drive was assessed in steady-state measurements for 6% and 9% CO2 in ambient air. Short-term pulmonary stress effects for static compliance during GI (13.75 L·kPa) could be confirmed in these 12 divers without exhibiting permanent changes to the lungs' distensibility (7.41 L·kPa) or lung function parameters as confirmed by the follow-up measurements and for 4 BHD after 3 yr (P>0.05). Respiratory drive was significantly reduced in these BHD revealing a characteristic breathing pattern with a significant increase in VE and mouth occlusion pressure (P0.1) between free breathing and 6% CO2, as well as between 6% CO2 and 9% CO2 (all P<0.001). BH diving with performance of GI does not permanently alter pulmonary distensibility or impair ventilatory flows and volumes. A blunted response to elevated CO2 concentrations could be demonstrated, which was supportive of the hypothesis that CO2 tolerance is a training effect due to BH diving rather than being an inherited phenomenon.

Pulmonary distensibility and flow dynamics in systemic sclerosis using velocity encoded magnetic resonance imaging

Pulmonary distensibility and flow dynamics in systemic sclerosis using velocity encoded magnetic resonance imaging

Commentaries on Viewpoint: Use of mean airspace chord length to assess emphysema

to the editor: Although mean airspace chord length ( L m) lacks the elegance of some stereology methods and requires careful attention to technique ([4][1]), Mitzner ([3][2]) argues that L m has utility in studying experimental emphysema. Clearly, L m reflects the dimensions of alveoli but is not a

Value of MR phase-contrast flow measurements for functional assessment of pulmonary arterial hypertension

Goals of our study were to compare the pulmonary hemodynamics between healthy volunteers and patients with pulmonary arterial hypertension (PAH) and correlate MR flow measurements with echocardiography. Twenty-five patients with PAH and 25 volunteers were examined at 1.5 T. Phase-contrast flow measurements were performed in the ascending aorta and pulmonary trunk, resulting in the following parameters: peak velocity (cm/s), average blood flow (l/min), time to peak velocity (ms), velocity rise gradient and pulmonary distensibility (cm(2)). The bronchosystemic shunt was calculated. In PAH patients transthoracic echocardiography and right-heart catheterization (RHC) served as the gold standard. In comparison to volunteers, the PAH patients showed significantly reduced pulmonary velocities (P = 0.002), blood flow (P = 0.002) and pulmonary distensibility (P = 0.008). In patients, the time to peak velocity was shorter (P<0.001), and the velocity rise gradient was steeper (P = 0.002) than in volunteers. While in volunteers the peak velocity in the aorta was reached earlier, it was the reverse in patients. Patients showed a significant bronchosystemic shunt (P = 0.01). No meaningful correlation was found between MRI measurements and echocardiography or RHC. MRI is a feasible technique for the differentiation between PAH and volunteers. Further studies have to be conducted for the absolute calculation of pressure estimates.

Monitorización de la función respiratoria en el niño con ventilación mecánica (II): complianza, resistencia, hiperinsuflación dinámica, espacio muerto y trabajo respiratorio

Several parameters can be used to study respiratory mechanics in children on mechanical ventilation. Compliance is a measure of the distensibility of the respiratory system. In mechanical ventilation two measures of compliance can be used. Static compliance (pulmonary distensibility) can be measured in volume modes by the application of an inspiratory pause with the respiratory system at rest (sedated patients without inspiratory effort). Dynamic compliance does not require an inspiratory pause and the respiratory system need not be at rest. Compliance can be calculated numerically or expressed graphically in the volume-pressure curve. Many respirators can calculate inspiratory and expiratory airway resistance (including endotracheal tube resistance). Several measures can be used to detect dynamic hyperinflation (intrinsic PEEP, auto-PEEP, trapped air volume) after application of an expiratory pause. The latest respirators can perform these measurements almost automatically. Work of breathing and respiratory effort can also be analyzed by measuring several parameters (pressure-time product, imposed work of breathing, P 0.1, maximum inspiratory pressure). However, these measures have not yet been standardized in children.

A risk-benefit assessment of natural and synthetic exogenous surfactants in the management of neonatal respiratory distress syndrome.

Alveolar surfactant is central to pulmonary physiology. Quantitative and qualitative surfactant abnormalities appear to be the primary aetiological factors in neonatal respiratory distress syndrome (RDS) and exogenous replacement of surfactant is a rational treatment. Available exogenous surfactants have a natural (mammal-derived lung surfactants) or synthetic origin. Pharmacodynamic and clinical studies have demonstrated that exogenous surfactants immediately improve pulmonary distensibility and gas exchange; however, this is achieved more slowly and with more failures with synthetic surfactants. The ensuing advantageous haemodynamic effects are not so striking and they include an inconvenient increased left to right ductal shunt. Two strategies of administration have been used: prophylactic or rescue therapy to treat declared RDS. All methods of instillation require intubation. In addition to the early benefits (improved gas exchange and reduced ventilatory support) the incidence of classical complications of RDS, especially air leak events, is decreased except for the uncommon problem of pulmonary haemorrhage. The incidence of bronchopulmonary dysplasia is neither uniformly nor significantly reduced although the severity appears to be lessened. The overall incidence of peri-intraventricular haemorrhages is not diminished although separate trials have shown a decreased rate. The most striking beneficial effect of exogenous surfactants is the increased survival (of about 40%) of treated very low birthweight neonates. A small number of adverse effects has been described. The long term outcome of survivor neonates with RDS treated with surfactants versus control neonates with RDS not treated with surfactants is similar in terms of physical growth, at least as good in terms of respiratory status, with a similar or slightly better neurodevelopmental outcome. There is not clear benefit of exogenous surfactant therapy in extremely premature infants (< 26 weeks gestational age, birthweight < 750 g). The potential risks of contamination, inflammatory and immunogenic reaction and the inhalation of platelet activating factor remain a theoretical concern of surfactant therapy which has not been confirmed in clinical practice. The optimal timing of treatment favours prophylaxis over rescue treatment and early rescue treatment rather than delayed therapy. Meta-analyses suggest the clinical superiority of natural surfactant extracts over a synthetic one (colfosceril palmitate). The economic impact of surfactant therapy is favourable and the costs per quality-adjusted life year (QALY) for surviving surfactant treated infants are low. In conclusion, the mid and long term benefit/risk ratio clearly favours the use of exogenous surfactants to prevent or to treat RDS in neonates who have a gestational age of > 26 weeks or a birthweight of > 750 g, especially with the prophylactic strategy using natural surfactant extracts.

Large lungs and growth hormone: an increased alveolar number?

Previous physiological studies suggest that increased lung growth in patients with acromegaly is associated with either a normal or above normal pulmonary transfer factor. These findings can be interpreted to suggest either alveolar hypertrophy or hyperplasia as the mechanism for lung growth in this condition. Since the ventilated airspaces retain normal elastic properties, we wanted to determine whether the mechanism for lung growth in acromegaly is the result of an increased alveolar number rather than size. Measurements of pulmonary distensibility (K) (an index of alveolar size), elastic recoil, single-breath carbon monoxide transfer factor and carbon monoxide transfer coefficient (KCO), pulmonary capillary blood volume and alveolar membrane diffusing capacity, together with chest width, were compared in nonsmoking, acromegalic and normal men and women, with and without an increased lung size. Pulmonary transfer factor was normal for all groups studied, regardless of lung size. However, KCO was inversely related to total lung capacity (% predicted) for all subjects and KCO (% predicted) was inversely related to chest width in men. Pulmonary capillary blood volume (% predicted) was inversely related to total lung capacity (% predicted) for subjects with large lungs. Pulmonary distensibility (K), membrane diffusing capacity and elastic recoil were within the normal range. These findings suggest normal alveolar size, alveolar membrane surface area and mechanical function in subjects with large lungs. They also suggest that KCO may not be a reliable guide to the interpretation of the mechanism of lung growth in individuals with disproportionately large lungs, and may be reduced because not all the alveoli are perfused. The normal values for pulmonary distensibility found in all our individuals with large lungs, including acromegalics, suggest that lung growth has been achieved by an increased alveolar number rather than size. However, morphometric studies of the lungs of nonsmoking, acromegalic subjects without lung disease, are required to substantiate this finding.

Hemodynamic changes during prolonged laparoscopic surgery.

7 healthy pigs, anesthetized with ketamine/azaperon/thiopentone and ventilated with O2/N2O by volume control, underwent anterior resection of the descending colon by laparoscopic view. During operation of pneumoperitoneum by inflating CO2 to an abdominal pressure of 14 mm Hg was installed. Immediately (+2 min) after the onset of insufflation, both systemic and pulmonary arterial pressure increased. However, pulmonary artery pressure started to decrease after 10 min, whereas systemic arterial pressure remained elevated until the end of the experimental protocol. Left ventricular (LV) pressure and LV dp/dt increased in parallel with the systemic arterial pressure. Peak inspiratory pressure and central venous pressure increased in parallel with the abdominal pressure. Blood gas analysis of arterial and pulmonary blood demonstrated increased pCO2 associated with mild acidosis. Arterial pO2 did not change significantly indicating that the decreased pulmonary distensibility did not endanger the oxygenation. Pulmonary pO2 and pulmonary O2 saturation increased early (+10 min) after start of insufflation and were stable during the 2 h of observation indicating either increased cardiac output or decreased O2 extraction. We conclude that the sharp initial rise of both arterial pressures could be the effect of a mechanical action, whereas sustained hemodynamic alterations would involve complex regulatory mechanisms like an increase of sympathetic activity, baroreceptor control, or a response to acidosis. The acute and, in the systemic circulation, stable increase of ventricular afterload should be considered in patients with underlying cardiac diseases such as ischemic heart disease or valvular dysfunction or in patients taking drugs which interfere with normal compensatory processes.

Direct measurement of pulmonary microvascular distensibility.

Pulmonary vascular distensibility has an important influence on pulmonary hemodynamics. Although many measurements of distensibility have been made on large pulmonary vessels, there is less information on microvascular distensibility. We have measured the distensibility of the smallest (< 70-microns-diam) precapillary arterioles and postcapillary venules. Isolated dog lobes, at 2.5 cmH2O transpulmonary pressure, were perfused at low flows, which caused the arteriovenous pressure gradient to be very small and thereby permitted accurate estimation of microvascular pressure. As microvascular pressure was systematically varied between 0 and 30 mmHg, subpleural microvascular diameters were determined from computer-enhanced images obtained by videomicroscopy. Arteriolar and venular distensibilities were not different from each other. The microvascular pressure-diameter relationship was alinear with distensibility coefficients of 1-3% mmHg-1, values that are of the same order of magnitude as previously measured distensibilities of 100- to 1,000-microns-diam canine pulmonary vessels.

The large lungs of elite swimmers: an increased alveolar number?

In order to obtain further insight into the mechanisms relating to the large lung volumes of swimmers, tests of mechanical lung function, including lung distensibility (K) and elastic recoil, pulmonary diffusion capacity, and respiratory mouth pressures, together with anthropometric data (height, weight, body surface area, chest width, depth and surface area), were compared in eight elite male swimmers, eight elite male long distance athletes and eight control subjects. The differences in training profiles of each group were also examined. There was no significant difference in height between the subjects, but the swimmers were younger than both the runners and controls, and both the swimmers and controls were heavier than the runners. Of all the training variables, only the mean total distance in kilometers covered per week was significantly greater in the runners. Whether based on: (a) adolescent predicted values; or (b) adult male predicted values, swimmers had significantly increased total lung capacity ((a) 145 +/- 22%, (mean +/- SD) (b) 128 +/- 15%); vital capacity ((a) 146 +/- 24%, (b) 124 +/- 15%); and inspiratory capacity ((a) 155 +/- 33%, (b) 138 +/- 29%), but this was not found in the other two groups. Swimmers also had the largest chest surface area and chest width. Forced expiratory volume in one second (FEV1) was largest in the swimmers ((b) 122 +/- 17%) and FEV1 as a percentage of forced vital capacity (FEV1/FVC)% was similar for the three groups. Pulmonary diffusing capacity (DLCO) was also highest in the swimmers (117 +/- 18%). All of the other indices of lung function, including pulmonary distensibility (K), elastic recoil and diffusion coefficient (KCO), were similar. These findings suggest that swimmers may have achieved greater lung volumes than either runners or control subjects, not because of greater inspiratory muscle strength, or differences in height, fat free mass, alveolar distensibility, age at start of training or sternal length or chest depth, but by developing physically wider chests, containing an increased number of alveoli, rather than alveoli of increased size. However, in this cross-sectional study, hereditary factors cannot be ruled out, although we believe them to be less likely.

Plasma elastin-derived peptide levels in normal adults, children, and emphysematous subjects. Physiologic and computed tomographic scan correlates.

Pulmonary emphysema is likely to be the result of elastic tissue digestion by unrestrained elastase activity in the lung. Elastin breakdown by elastases results in the release of soluble elastin fragments (EDP), which may be measured in plasma by an ELISA. Plasma EDP levels measured using an ELISA were determined in the following groups: disease-free children (n = 24), 0.162 +/- 0.082 ng/ml; disease-free adult nonsmokers (n = 114), 1.74 +/- 0.8 ng/ml; smokers (n = 68), 2.76 +/- 4.59 ng/ml; reformed smokers (n = 43), 1.91 +/- 1.14 ng/ml. Adults with established pulmonary emphysema (n = 50), as defined by bullous formation on the chest radiograph, had levels of 50.83 +/- 24.8 ng/ml, significantly higher than the disease-free groups at p < 0.01. Pulmonary emphysema can be reflected by pulmonary function tests, especially those that measure the pulmonary elastic properties, and by computed tomographic (CT) scan percent emphysema score. We therefore examined the relationship of plasma EDP to these other indicators of pulmonary emphysema in a separate group of 26 subjects using elastic recoil measurements (K), and a further group of 30 subjects with CT scan percent emphysema score. A significant correlation of p < 0.001 was shown for plasma EDP and K and a significant correlation of p < 0.01 was shown for plasma EDP and CT scan percent emphysema score, these correlations suggesting that plasma EDP levels are indicators of the loss of pulmonary distensibility and of mild to moderate pulmonary emphysema. These findings suggest that pulmonary emphysema is characterized by active elastin breakdown.

Estimating alveolar surface area during life

Alveolar surface area (Sa) may be derived from measurements of total lung capacity (TLC) and mean linear intercept (Lm), an estimate of average airspace size. Because the index of pulmonary distensibility, K, is a function of Lm, we were able to derive Lm from ln K using their respective age regressions and estimated Sa in 147 healthy subjects. K was obtained from exponential analysis of static pressure-volume data. TLC was measured in a body plethysmograph. As an estimate of airspace size, the value used for Lm was shown to be appropriate for the air-inflated lung at TLC. In 95 men (mean age 40 ± 16 SD years), Sa was 118 (SD 22)m 2 and in 52 women (mean age 38 ± 17 SD years) it was 91 (SD 18) m 2 and Sa decreased with age ( P<0.001). In a morphometric study, Thurlbeck ( Am. Rev. Respir. Dis. 95: 765–773, 1967) obtained smaller values for Sa (owing to the use of a smaller lung volume) and a similar decrease in Sa with age as that found here. Providing a standardised methodology is used for measurement of K, the present method allows a reasonable estimate of Sa to be obtained during life.