Respiratory mechanics in men following a deep air dive

1986 ◽  
Vol 61 (2) ◽  
pp. 734-740 ◽  
Author(s):  
P. W. Catron ◽  
J. Bertoncini ◽  
R. P. Layton ◽  
M. E. Bradley ◽  
E. T. Flynn

The mechanical properties of the lungs were measured in 10 men before and after a simulated air dive to 285 ft of seawater (87 m). The objective was to determine whether a dive likely to produce pulmonary bubble emboli would alter lung mechanics. Lung function was measured predive and at 1, 2, 3, 6, 7, and 23 h postdive. Measurements of lung function were also made at identical times on a control day when no dive was made. Each set of measurements included precordial Doppler signals, pulmonary resistance, quasistatic lung compliance, forced vital capacity (FVC), forced expired volume after 1.0 s (FEV 1.0), the ratio of FEV 1.0 to FVC (FEV 1.0/FVC%), and maximal airflow after 50 and 75% of the vital capacity had been expired (Vmax50 and Vmax75, respectively). Base-line measurements of pulmonary resistance and quasistatic compliance were normal in all subjects. FVC and FEV 1.0 were greater than predicted for most subjects and were increased proportionately so that the FEV 1.0/FVC% was normal. Following the dive, bubble signals were heard in four subjects, and two subjects had mild symptoms of decompression sickness. No subject demonstrated any alteration in lung function that could be attributed to the dive. We concluded that stressful decompressions capable of producing “silent” pulmonary bubble emboli do not alter lung mechanics.

1978 ◽  
Vol 44 (3) ◽  
pp. 479-482 ◽  
Author(s):  
A. Wanner ◽  
M. E. Reinhart

Most currently used animal models of allergic airway diseases differ from human asthma in that induced bronchospasm in the former is not accompanied by pulmonary hyperinflation. In the present investigation, we chose unsedated, restrained sheep to determine the effect of cholinergic bronchial provocation on respiratory mechanics, functional residual capacity (FRC), and arterial blood gases. Seven animals had been actively sensitized by intramuscular injections of Ascaris suum extract, and four untreated animals served as controls. After inhalation of nebulized 1% methacholine solution, mean pulmonary resistance increased significantly in the sensitized sheep from a base line of 2.4 +/- 0.7 (SD) cmH2O/(l/s) to a peak value after 5 min of 7.9 +/- 4.0 cmH2O/(l/s). This was accompanied by a significant increase of mean FRC from 0.99 +/- 0.14 liters to 1.31 +/- 0.24 liters. The observed changes were transient, and after 60 min, pulmonary resistance and FRC had returned to base-line values. No significant changes occurred in static lung compliance, PaO2, PaCO2, and pH. In the control animals, methacholine provocation did not produce changes in pulmonary function. These results indicate that, in sensitized conscious sheep, induced bronchospasm is associated with pulmonary hyperinflation.


1996 ◽  
Vol 81 (2) ◽  
pp. 964-975 ◽  
Author(s):  
R. Pellegrino ◽  
O. Wilson ◽  
G. Jenouri ◽  
J. R. Rodarte

To elucidate differences in lung mechanics, we investigated the relative changes of partial forced expiratory flows at 50 and 30% of vital capacity, pulmonary resistance (RL), dynamic elastance (Edyn), and the effects of a deep inhalation (DI) on maximal flows, Edyn, and RL in eight asthmatic and eight normal individuals during bronchial challenges with methacholine, histamine, and ATP. RL was partitioned into inspiratory and expiratory resistance. Different constrictor agents did not induce specific patterns of response. For a given decrement of flow at 50 and 30% vital capacity, RL increased significantly more in normal than in asthmatic individuals. The ratio of inspiratory to expiratory RL was always < 1 at baseline but became > 1 in the majority of asthmatic and normal individuals when RL exceeded 12.2 +/- 0.9 cmH2O.1–1.s, suggesting that tidal inspiration may have induced transient bronchodilation in more constricted subjects. In asthmatic individuals, DI had a significantly smaller effect on flow but not on RL compared with normal individuals. The recovery of RL and Edyn after DI was faster than Edyn for both normal and asthmatic individuals. These findings are consistent with the idea that asthmatic individuals have a stronger peripheral response to agonists than normal individuals.


Respiration ◽  
2020 ◽  
pp. 1-8
Author(s):  
Pierre-Henri Aussedat ◽  
Nader Chebib ◽  
Kais Ahmad ◽  
Jean-Charles Glerant ◽  
Gabrielle Drevet ◽  
...  

<b><i>Background:</i></b> Video-assisted surgical lung biopsy (SLB) is performed in 10–30% of cases to establish the diagnosis of idiopathic pulmonary fibrosis (IPF). <b><i>Objectives:</i></b> The aim of the study was to analyze the impact of SLB on lung function in patients eventually diagnosed with IPF. <b><i>Methods:</i></b> This is an observational, retrospective, monocentric study of all consecutive patients eventually diagnosed with IPF in multidisciplinary discussion who underwent SLB over 10 years in a specialized center. The primary end point was the variation in forced vital capacity (FVC) before and after the SLB. The secondary end points were the variations in forced expiratory volume in one second (FEV1), total lung capacity (TLC), carbon monoxide diffusion capacity (DLCO), and morbidity and mortality associated with the SLB. <b><i>Results:</i></b> In 118 patients who underwent SLB and were diagnosed with IPF, a relative decrease in FVC of 4.8% (<i>p</i> &#x3c; 0.001) was found between measurements performed before and after the procedure. The mean FVC decrease was 156 ± 386 mL in an average period of 185 days, representing an annualized decline of 363 ± 764 mL/year. A significant decrease was also observed after SLB in FEV1, TLC, and DLCO. Complications within 30 days of SLB occurred in 14.4% of patients. Two patients (1.7%) died within 30 days, where one of them had poor lung function. Survival at 1 year was significantly poorer in patients with FVC &#x3c;50% at baseline. <b><i>Conclusion:</i></b> In this uncontrolled study in patients ultimately diagnosed with IPF, SLB was followed by a significant decline in FVC, which appears to be numerically greater than the average decline in the absence of treatment in the literature. <b><i>Summary at a Glance:</i></b> This study evaluated the change in lung function in 118 consecutive patients diagnosed with idiopathic pulmonary fibrosis by surgical lung biopsy. Forced vital capacity decreased by 156 ± 386 mL in a mean of 185 days between the last measurement before and first measurement after biopsy, representing an annualized decline of 363 ± 764 mL/year.


2009 ◽  
Vol 297 (4) ◽  
pp. L641-L649 ◽  
Author(s):  
Min Yee ◽  
Patricia R. Chess ◽  
Sharon A. McGrath-Morrow ◽  
Zhengdong Wang ◽  
Robert Gelein ◽  
...  

Despite its potentially adverse effects on lung development and function, supplemental oxygen is often used to treat premature infants in respiratory distress. To understand how neonatal hyperoxia can permanently disrupt lung development, we previously reported increased lung compliance, greater alveolar simplification, and disrupted epithelial development in adult mice exposed to 100% inspired oxygen fraction between postnatal days 1 and 4. Here, we investigate whether oxygen-induced changes in lung function are attributable to defects in surfactant composition and activity, structural changes in alveolar development, or both. Newborn mice were exposed to room air or 40%, 60%, 80%, or 100% oxygen between postnatal days 1 and 4 and allowed to recover in room air until 8 wk of age. Lung compliance and alveolar size increased, and airway resistance, airway elastance, tissue elastance, and tissue damping decreased, in mice exposed to 60–80% oxygen; changes were even greater in mice exposed to 100% oxygen. These alterations in lung function were not associated with changes in total protein content or surfactant phospholipid composition in bronchoalveolar lavage. Moreover, surface activity and total and hydrophobic protein content were unchanged in large surfactant aggregates centrifuged from bronchoalveolar lavage compared with control. Instead, the number of type II cells progressively declined in 60–100% oxygen, whereas levels of T1α, a protein expressed by type I cells, were comparably increased in mice exposed to 40–100% oxygen. Thickened bundles of elastin fibers were also detected in alveolar walls of mice exposed to ≥60% oxygen. These findings support the hypothesis that changes in lung development, rather than surfactant activity, are the primary causes of oxygen-altered lung function in children who were exposed to oxygen as neonates. Furthermore, the disruptive effects of oxygen on epithelial development and lung mechanics are not equivalently dose dependent.


1983 ◽  
Vol 55 (1) ◽  
pp. 92-99 ◽  
Author(s):  
J. M. Hinson ◽  
A. A. Hutchison ◽  
M. L. Ogletree ◽  
K. L. Brigham ◽  
J. R. Snapper

To examine the role of circulating granulocytes in the airway changes caused by endotoxemia, we measured the response of chronically instrumented unanesthetized sheep to endotoxemia before and after granulocyte depletion with hydroxyurea. Granulocyte depletion did not affect the increases in mean pulmonary arterial pressure caused by endotoxin [peak pressure 59 +/- 8 cmH2O +/- (SE) control, 51 +/- 8 cmH2O granulocyte depleted]. However, the early (30-60 min after endotoxin) airway response to endotoxemia was markedly attenuated. Without granulocyte depletion, endotoxin caused dynamic compliance (Cdyn) to decrease to 41 +/- 10% of the base-line value and total lung resistance (RL) to increase to 283 +/- 61% of base line. When animals were granulocyte depleted, endotoxin decreased Cdyn to 69 +/- 6% (P less than 0.05) of base line and increased RL to 141 +/- 20% of base line (P less than 0.05). Granulocyte depletion also attenuated the effect of endotoxin on arterial oxygenation. During the maximum airway response to endotoxin, the alveolar-to-arterial oxygen gradient was 47 +/- 5 Torr in control studies and 32 +/- 2 Torr in granulocyte depleted studies (P less than 0.05). We conclude that interaction of granulocytes with the lung contributes to the changes in lung mechanics observed following endotoxemia and that the early pulmonary hypertension and the early alterations in lung mechanics caused by endotoxemia are caused by separate processes.


1990 ◽  
Vol 69 (6) ◽  
pp. 2034-2042 ◽  
Author(s):  
S. F. Quan ◽  
R. J. Lemen ◽  
M. L. Witten ◽  
D. L. Sherrill ◽  
R. Grad ◽  
...  

We measured changes with growth in lung function and airway reactivity after acute canine parainfluenza virus type 2 (CPI2, n = 5), canine adenovirus type 2 (CAV2, n = 7), and sequential CAV2-CPI2 (n = 6) infections or no infection (controls, n = 6) in beagle puppies (age approximately 79 days). In the CPI2 and CAV2 groups, a lower respiratory illness developed by day 3 postinfection with clinical recovery by day 14. In the CAV2-CPI2 group, puppies were inoculated initially with CAV2 and 12 days later with CPI2. In this group, illness persisted until day 14 after infection with CPI2. Lung resistance (RL), dynamic (Cdyn) and static (Cst) lung compliance, functional residual capacity (FRC), and responsiveness to aerosolized histamine were measured before infection and at periodic intervals until 239 +/- 43 days of age. Lung function data were analyzed using a longitudinal random effects model. In all groups, FRC, Cst, and Cdyn increased with age. In all infected groups, the regression slopes for Cdyn were steeper than in controls. RL decreased linearly with age without group slope differences. Histamine reactivity increased with age, but there were no differences in slope among groups. Lung pathological studies showed areas of obliterative bronchiolitis and chronic small airways inflammation particularly in the CAV2 and CAV2-CPI2 groups. Thus, viral bronchiolitis produces chronic small airways inflammation in beagle puppies and alters the changes in lung function occurring with growth. Histamine reactivity increases with age and is not modified by viral infection.


1979 ◽  
Vol 47 (2) ◽  
pp. 418-424 ◽  
Author(s):  
J. W. Ramsdell ◽  
P. F. Georghiou

We studied the effect of prolonged airways obstruction induced by extended cholinergic stimulation in five anesthetized, mechanically ventilated dogs. A continuous intravenous metacholine infusion was utilized to maintain pulmonary resistance (RL) at 200--1500% preinfusion levels for 13--23 h. At maximum RL (18.86 +/- 7.74 vs. 2.09 +/- 0.18 (mean +/- SD) cmH2O/ (L/S) PREINfusion; P less than 0.01), dynamic lung compliance (Cdyn) fell from 67.5 +/- 14.6 to 32.7 +/- 11.6 ml/cmH2O (P less than 0.005) and arterial partial pressure of oxygen (PaO2) fell modestly from 95.8 +/- 6.1 Torr preinfusion to 83.2 +/- 12.7 Torr (P less than 0.05). Tachyphylaxis to methacholine developed, requiring increases in infusion rates to maintain elevated RL. Abnormalities in lung function resolved promptly upon termination of the infusion. Two similarly instrumented control animals ventilated for 19 and 25 h without metacholine infusion had no change in RL, Cdyn, or PaO2. Histological examination of the lungs revealed no differences between infused and control animals. In spite of marked increases in RL, prolonged cholinergic stimulation produced only mild changes in gas exchange and no sustained changes in lung function or structure.


1990 ◽  
Vol 69 (1) ◽  
pp. 245-250 ◽  
Author(s):  
J. M. Fouke ◽  
R. A. DeLemos ◽  
M. J. Dunn ◽  
E. R. McFadden

Short-term exposure to 0.5 parts per million (ppm) ozone has been shown to cause an increase in respiratory resistance in primates that can be diminished by 50% with pretreatment with cromolyn sodium. Because of the known membrane-stabilizing effects of cromolyn and the resultant inhibition of mediator production, we hypothesized a role for the products of arachidonic acid (AA) metabolism in these events. We exposed five adult male baboons to 0.5 ppm ozone on two occasions, once with cromolyn pretreatment and once without. Pulmonary resistance (RL) was monitored and bronchoalveolar lavage (BAL) was performed before and after each exposure. The BAL was analyzed for a stable hydrolysis product of prostacyclin, 6-keto-prostaglandin (PG) F1 alpha, PGE2, a stable hydrolysis product of thromboxane (Tx) A2, TxB2, and PGF2 alpha. RL increased after ozone exposure (1.62 +/- 0.23 to 3.77 +/- 0.51 cmH2O.l-1.s, difference 2.15; P less than 0.02), and this effect was partially blocked by cromolyn (1.93 +/- 0.09 to 3.18 +/- 0.40 cmH2O.l-1.s, difference 1.25; P less than 0.02). The base-line levels of the metabolites of AA in the BAL were as follows (in pg/ml): 6-keto-PGF1 alpha 72.78 +/- 12.6, PGE2 145.92 +/- 30.52, TxB2 52.52 +/- 9.56, and PGF2 alpha 22.28 +/- 5.42. Ozone exposure had no effect on the level of any of these prostanoids (P = NS). These studies quantify the magnitude of cyclooxygenase products of AA metabolism in BAL from baboon lungs and demonstrate that changes in the levels of these mediators in BAL are not prerequisites for ozone-induced increases in respiratory resistance.(ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 69 (2) ◽  
pp. 728-733 ◽  
Author(s):  
M. R. Banerjee ◽  
J. H. Newman

The purpose of this study was to measure airway and hemodynamic effects of atrial natriuretic peptide (ANP) and its efficacy in counteracting the changes in lung mechanics that occur with aerosol histamine and carbachol. Synthetic human alpha-ANP was injected into the pulmonary arteries of awake sheep chronically instrumented for measurement of lung mechanics and hemodynamics (n = 7). Base-line dynamic lung compliance (Cdyn) and pulmonary resistance (RL) did not change after ANP injection. On separate days, the dose required to reduce Cdyn to 65% of base line (ED65Cdyn) to progressive doses of aerosol histamine and the dose required to increase RL by 100% of the base-line values (ED200RL) to progressive doses of aerosol carbachol were determined. ANP was given as bolus injections of 1, 5, and 10 micrograms/kg 3 min after either the ED65Cdyn or ED200RL doses of histamine and carbachol, respectively, and the airway response was monitored for 10 min. ANP significantly reversed the rise in RL after carbachol administration (n = 10). This action of ANP was not altered by cyclooxygenase inhibition with ibuprofen. ANP did not reverse the reduction in Cdyn caused by either histamine (n = 7) or carbachol. The bronchodilating effect of ANP appears to be more prominent in the larger central airways than in the peripheral airways. The hemodynamic effects of ANP were similar to those reported by others. Heart rate and cardiac output had a biphasic response, with an initial rise followed by a drop below the base line. Systemic arterial and left atrial pressures decreased significantly. Pulmonary arterial pressure did not change significantly.(ABSTRACT TRUNCATED AT 250 WORDS)


1983 ◽  
Vol 55 (3) ◽  
pp. 1008-1014 ◽  
Author(s):  
W. A. LaFramboise ◽  
R. D. Guthrie ◽  
T. A. Standaert ◽  
D. E. Woodrum

Dynamic lung compliance (CL), inspiratory pulmonary resistance (RL), and functional residual capacity (FRC) were measured in 10 unanesthetized 48 h-old newborn monkeys and seven 21-day-old infant monkeys during acute exposures to an equivalent level of hypoxemia. End-expiratory airway occlusions were performed and the pressure developed by 200 ms (P0.2) was utilized as an index of central respiratory drive. P0.2 demonstrated a sustained increase throughout the period of hypoxemia on day 2 despite the fact that minute ventilation (VI) initially increased but then fell back to base-line levels. Dynamic lung compliance fell and FRC increased by 5 min of hypoxemia in the newborns. The 21-day-old monkeys exhibited a sustained increase in both VI and P0.2 throughout the hypoxic period with no change in CL and FRC. RL did not change at either postnatal age during hypoxemia. These data indicate that the neonatal monkey is subject to changes in pulmonary mechanics (decreased CL and increased FRC) during hypoxemia and that these changes are eliminated with maturation.


Sign in / Sign up

Export Citation Format

Share Document