Disease relevance of Lung Compliance

• Chronic expression of TGF-alpha in the lungs of newborn transgenic mice caused remodeling of the developing lung during the period of postnatal alveolarization, resulting in markedly enlarged parenchymal airspace, pulmonary fibrosis, and physiological abnormalities including airway obstruction and increased lung compliance [1].
• Effective alveolar volume, diffusing capacity for carbon monoxide (DCOsb), volume-corrected diffusing capacity (D/VA), static lung compliance (Cst), and lung distensibility were measured in 16 sheep seropositive for maedi-visna virus (MVV) immediately before they were killed [2].
• The larger decrease in lung compliance in SP-B(+/-) mice was associated with increased severity of pulmonary edema, hemorrhage and inflammation, lung permeability and protein leakage into the alveolar space [3].
• 1 The intravenous administration of E. coli endotoxin (2.0 mg/kg) in cats anaesthetized with sodium pentobarbitone resulted in immediate pulmonary hypertension and reductions in lung compliance and systemic arterial PO2 [4].
• This study demonstrates that beclomethasone by nebulization (1) reduced airway resistance in oxygen-dependent neonates with bronchopulmonary dysplasia, (2) improved dynamic lung compliance, as reported with parenterally administered glucocorticoids, and (3) produced no apparent increase in the incidence of infection [5].

High impact information on Lung Compliance

• Samples exposed to FeCl2 + H2O2 had significantly diminished surface tension lowering ability in vivo as indicated by their reduced ability to improve lung compliance of surfactant-deficient fetal rabbits [6].
• Lung compliance, pulmonary function, surfactant pool size, glucose and FFA levels were significantly decreased in adrenalectomized animals [7].
• Complete deficiency of SP-B in mice and humans results in lethal, neonatal respiratory distress syndrome and is characterized by a virtual absence of lung compliance, highly disorganized lamellar bodies, and greatly diminished levels of SP-C mature peptide; in contrast, lung structure and function in SP-C null mice is normal [8].
• Lung morphology, surfactant proteins B-D, lung tissue, alveolar phospholipid pool sizes and composition, and lung compliance in SP-A(-/-) mice were unaltered [9].
• Eighteen patients with progressive pulmonary dysfunction, diminished vital capacity (VC), and/or decreased static lung compliance (Cst) were treated with cyclophosphamide and corticosteroids for 1 year [10].

Chemical compound and disease context of Lung Compliance

• The data show that conventional doses of furosemide can (1) cause metabolic alkalosis and reduce ventilation; (2) increase the PaCO2, which reflects changes in acid-base status and not changes in lung function; and (3) increase lung compliance, perhaps by decreasing lung water [11].
• Our data show that alpha 1-AT treatment prevented the reduced lung compliance observed in the untreated hyperoxia-exposed neonatal rats, as well as the right ventricular hypertrophy and the associated vascular changes of medial hypertrophy of muscular arteries and muscularization of distal arteries [12].
• The relative activities of three bronchoconstrictive mediators of anaphylaxis, prostaglandin (PG) D2, PGF2 alpha and histamine, were investigated in anesthetized dogs using two different measures of peripheral lung reactivity: resistance to flow through collateral airways (Rcoll) and dynamic lung compliance (Cdyn) [13].
• 4 These results may suggest that TXA2 is responsible for the endotoxin-induced pulmonary arterial hypertension but that some other arachidonic acid derivative (prostaglandin F2 alpha) is responsible for the reduced lung compliance that follows the acute administration of E. coli endotoxin [14].
• Therefore, we measured EELV, total lung resistance (RL), dynamic lung compliance (Cdyn), DE, and minute ventilation (VE) in anesthetized rats during normoxia and hypoxia (10% O(2)) before (control) and after administration of atropine or saline [15].

Biological context of Lung Compliance

• Inhalation of either 20 ppm NO or terbutaline produced similar reduction in pulmonary resistance and increase in lung compliance [16].
• The changes in airway resistance and dynamic lung compliance induced by 50 micrograms/ml were reduced approximately 60% and 25%, respectively, by pretreatment with atropine (1 mg/kg, i.v., -10 min) [17].
• Prior to diuresis functional residual capacity decreased from mean +/- SEM of 16.2 +/- 2 to 13.3 +/- 1.2 ml/kg, and dynamic lung compliance decreased from 2.5 +/- 0.3 to 1.8 +/- 0.3 ml/cm H2O (P less than 0.05), indicating that the respiratory disease was worsening [18].
• 1 The characteristics of vanadate-induced bronchoconstriction and airways hyperreactivity were observed in spontaneously breathing anaesthetized guinea-pigs by measurement of airways resistance (Raw) and dynamic lung compliance (Cdyn) [19].
• The lung compliance derived from pressure volume curves was also significantly higher in the aminophyllin-treated group when compared with controls at 27 days of gestation (0.023 +/- 0.0005 ml/cm H2O, mean +/- SEM vs 0.010 +/- 0.0002) and at 28 days of gestation (0.048 +/- 0.0003 vs 0.035 +/- 0.0006) [20].

Anatomical context of Lung Compliance

• During the study, percent change from baseline of peak airway pressure, total lung compliance of the lung and chest wall, and blood lactate levels appeared to be significantly smaller in dogs pretreated with CoQ10 than in controls [21].
• RESULTS: Endotoxin caused decreases in peripheral leukocyte counts, lung compliance, and arterial oxygen tension, and increases in the lung wet-to dry-weight ratio, polymorphonuclear cell counts in BALF, and albumin, C3a, C5a, tumor necrosis factor alpha, interleukin-1 beta, and thromboxane B2 concentrations in BALF [22].
• Stimulation of pulmonary C-fibers (PCs) by capsaicin and of rapidly adapting receptors (RARs) by reduced lung compliance reflexly increases airway submucosal gland secretion in dogs [23].
• In this genetic mouse model of obesity, the results suggested that respiratory complications associated with the obese phenotype, including rapid breathing pattern at baseline, diminished lung compliance, and abnormal respiratory muscle adaptations, are attenuated with prolonged leptin treatment [24].
• Effects of atropine on the responses of rapidly adapting pulmonary stretch receptors and dynamic lung compliance to sodium cyanide-induced hyperpnea [25].

Associations of Lung Compliance with chemical compounds

• Airway reactivity was assessed by the concentration of inhaled histamine required to produce a 40% reduction in dynamic lung compliance (Cdyn40) [26].
• Dose-response curves were obtained for aerosols of acetylcholine (ACh), prostaglandin F2alpha (PGF2alpha), histamine (H), and 5-hydroxytryptamine (5-HT) on pulmonary resistance (Rp) and dynamic lung compliance (Cdyn) in Ascaris-hypersensitive dogs [27].
• Lack of recruitment resulted in reduced overall survival (59% nonrecruited vs. 100% recruited, p < 0.05), increased microvascular leak, greater impairment of oxygenation and lung compliance, increased PVR, and elevated plasma lactate [28].
• In both the liquid ventilation groups the lung compliance improved with the instillation of perfluorodecalin (from 0.46 SD 0.18 to 0.62 SD 0.09 ml/cm H(2)O/kg in the PLV alone group at 1 h, p < 0.05 compared with the control group) and remained stable for the remainder of the study [29].
• Furthermore, the static lung compliance, the intrapulmonary high-energy phosphates, lactate, and pyruvate were measured [30].

Gene context of Lung Compliance

• IA endotoxin caused rapid and sustained increases in SP mRNAs that preceded the increase in alveolar saturated phosphatidylcholine processing of SP-B and improved lung compliance in prematurely delivered lambs [31].
• Thus during E. coli pneumonia in mice, the lack of signaling from TNF-alpha and IL-1 decreases inflammation and preserves lung compliance [32].
• Despite normal survival, pulmonary function studies demonstrated a consistent decrease in lung compliance in SP-B(+/-) mice [33].
• Lung volume-to-body weight ratios and lung compliance were increased in adult TGF-alpha transgenic mice, whereas tissue and airway elastance were reduced [34].
• In addition, the low lung compliance measured in anesthetized, ventilated TNFR1(+/+) mice on day 7 after BMT was restored to baseline during TNFR1 deficiency [35].

Analytical, diagnostic and therapeutic context of Lung Compliance

• 1. Anaesthetized dogs were given aerosols of 5-hydroxytryptamine (5-HT), histamine and acetylcholine; the effects on the changes in total lung resistance (RL) and dynamic lung compliance (Cdyn) produced by electrical stimulation of the peripheral cervical vagi, and I.V. histamine and acetylcholine were studied [36].
• Pulmonary function tests revealed mild but not significant changes in O2 and CO2 alveolar exchange efficiency and lung compliance (P-V curve) of treated animals in comparison to pair fed controls [37].
• OBJECTIVE: We used the premature rabbit model of surfactant deficiency to test the hypothesis that perinatal administration of terbutaline would lead to increased secretion of surfactant into the alveolar space and increase lung compliance during mechanical ventilation [38].
• Spirometry, total lung capacity (TLC), diffusing capacity (Dco), static lung compliance (Cst), and tests of respiratory muscle function (peak inspiratory pressure [PIP] and the maximum change in transdiaphragmatic pressure [delta PDI] during a diaphragmatic Müeller maneuver) were obtained [39].
• Analysis of lung lavage revealed that SGS alone decreased cholesterol and the cholesterol/DSPC ratio which might be expected to decrease lung compliance [40].

References