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PubMed1986

[Interstitial pulmonary emphysema in mechanically ventilated newborn infants. Study of the course of the disease].

106 (15.7%) of 675 artificially ventilated newborn developed interstitial pulmonary emphysema (PIE). Basic lung diseases were: IRDS, neonatal pneumonia, shock lung, meconium aspiration, hypoplasia of the lungs and other miscellaneous disorders of the chest. PIE developed in 68% of patients within 8 hours following artificial respiration. At the beginning of PIE both lungs were concerned in 41.5% of patients, one lobe of both lungs was affected in 32.1%. PIE was located in one lung in 8.5% and in only one lobe in 17.9%. Maximum of PIE was seen within 5 days after initiating respiration in 76.7% of the patients. Persistent PIE developed in 28.7% of the patients. Persistent PIE of both lungs was seen in 11 cases, PIE of one lung in 8 cases and persistent lobar emphysema in another 8. Pulmonary pseudocysts developed in 22 (20.8%) of the patients.

Female↗
PubMed1983

[Planimetric determination of lung volume and its significance in the radiological diagnosis of pulmonary emphysema].

The volume of the lungs of 102 patients with emphysema and of 33 normal individuals, aged between 30 and 79 years, was determined with the use of a digital planimeter from routine chest x-rays in two planes. Contrary to the values obtained by a helium dilution method, the volumes, as determined by planimetry, did not show a linear relationship with age, but showed an increase after the age of 60. This agrees with the results of total body plethysmography, carried out by Amrein et al. The planimetric method of Harris, Pratt and Kilburn is a simple and rapid method for demonstrating, even in the presence of regional ventilatory abnormalities, total volume with sufficient accuracy, which complements and quantifies the radiological diagnosis of emphysema.

Adult↗
PubMed1983

[Therapy of progressive interstitial lobar emphysema].

Progressive pulmonary interstitial lobar emphysema is a complication of artificial ventilation in infants with RDS. Several types of conservative approaches are suggested. In 3 of our cases the rapid progression of emphysema makes lobectomy necessary.

Female↗
PubMed1984

Role of the parasympathetic system in airway obstruction due to emphysema.

To study the relative contributions of parasympathetic and sympathetic mechanisms in airway obstruction in patients with emphysema, we gave supramaximal doses of anticholinergic and adrenergic agents in sequence and in combination. Serial doses of one agent were administered to achieve a plateau of bronchodilatation; after that the other agent was administered. The plateau achieved with the anticholinergic agent (atropine methonitrate) was significantly higher than that achieved with the adrenergic agent (salbutamol). When the adrenergic agent was given first, additional bronchodilatation was achieved with subsequent use of the anticholinergic agent. When the anticholinergic agent was given first, no additional bronchodilatation was achieved with subsequent administration of the adrenergic agent. When both agents were given simultaneously, the degree of bronchodilatation was virtually identical to that obtained with the anticholinergic agent alone. Tests sensitive to small-airway and large-airway function and lung volumes gave essentially the same results. Thus, all achievable bronchodilatation was obtained with the anticholinergic agent alone. These results suggest that the two classes of agents produce bronchodilatation through a common cholinergic pathway in emphysema, and support the concept that parasympathetic activity is the dominant reversible component of airway obstruction in this disease.

Aged↗
PubMed1998

Relation between preoperative inspiratory lung resistance and the outcome of lung-volume-reduction surgery for emphysema.

BACKGROUND: Surgery to reduce lung volume has recently been reintroduced to alleviate dyspnea and improve exercise tolerance in selected patients with emphysema. A reliable means of identifying patients who are likely to benefit from this surgery is needed. METHODS: We measured lung resistance during inspiration, static recoil pressure at total lung capacity, static lung compliance, expiratory flow rates, and lung volumes in 29 patients with chronic obstructive lung disease before lung-volume-reduction surgery. The changes in the forced expiratory volume in one second (FEV1) six months after surgery were related to the preoperatively determined physiologic measures. A response to surgery was defined as an increase in the FEV1 of at least 0.2 liter and of at least 12 percent above base-line values. RESULTS: Of the 29 patients, 23 had some improvement in FEV1 including 15 who met the criteria for a response to surgery. Among the variables considered, only preoperative lung resistance during inspiration predicted changes in expiratory flow rates after surgery. Inspiratory lung resistance correlated significantly and inversely with improvement in FEV1 after surgery (r=-0.63, P<0.001). A preoperative criterion of an inspiratory resistance of 10 cm of water per liter per second had a sensitivity of 88 percent (14 of 16 patients) and a specificity of 92 percent (12 of 13 patients) in identifying patients who were likely to have a response to surgery. CONCLUSIONS: Preoperative lung resistance during inspiration appears to be a useful measure for selecting patients with emphysema for lung-volume-reduction surgery.

Adult↗
PubMed2000

Increased metalloproteinase activity, oxidant production, and emphysema in surfactant protein D gene-inactivated mice.

Targeted ablation of the surfactant protein D (SP-D) gene caused chronic inflammation, emphysema, and fibrosis in the lungs of SP-D (-/-) mice. Although lung morphology was unperturbed during the first 2 weeks of life, airspace enlargement was observed by 3 weeks and progressed with advancing age. Inflammation consisted of hypertrophic alveolar macrophages and peribronchiolar-perivascular monocytic infiltrates. These abnormalities were associated with increased activity of the matrix metalloproteinases, MMP2 and MMP9, and immunostaining for MMP9 and MMP12 in alveolar macrophages. Hydrogen peroxide production by isolated alveolar macrophages also was increased significantly (10-fold). SP-D plays a critical role in the suppression of alveolar macrophage activation, which may contribute to the pathogenesis of chronic inflammation and emphysema.

Animals↗
PubMed1998

Latent alpha1-antichymotrypsin. A molecular explanation for the inactivation of alpha1-antichymotrypsin in chronic bronchitis and emphysema.

alpha1-Antichymotrypsin is an acute phase protein that protects the tissues from damage by proteolytic enzymes, but previous studies have shown that alpha1-antichymotrypsin within the lungs of patients with chronic bronchitis and emphysema is intact but inactive as an inhibitor. Ammonium sulfate fractionation followed by blue Sepharose and DNA-Sepharose chromatography was used to isolate small amounts of intact, monomeric but inactive alpha1-antichymotrypsin from the plasma of 30 healthy blood donors. This species had a higher DNA binding affinity with more anodal electrophoretic mobility than native alpha1-antichymotrypsin and was conformationally stable against thermal denaturation, 8 M urea, and 7 M guanidinium chloride. The protein was unable to accept synthetic reactive loop peptides, and the reactive loop was resistant to proteolytic cleavage at the P5-P4 bond but could be cleaved between P1' and P3'. These data suggest that this new alpha1-antichymotrypsin species was in a conformation similar to those of the crystallographically determined latent serpins, plasminogen activator inhibitor-1 and antithrombin. alpha1-Antichymotrypsin from lung lavage migrated with the same electrophoretic mobility as the putative latent alpha1-antichymotrypsin, suggesting that this is the inactive conformation described previously in the lungs of patients with chronic bronchitis and emphysema. This conformational transition of alpha1-antichymotrypsin, from an active to an inactive state, within the lung may play an important role in the pathogenesis of chronic lung disease.

Bronchitis↗
PubMed2002

Prenatal, but not postnatal, inhibition of fibroblast growth factor receptor signaling causes emphysema.

Although fibroblast growth factor (FGF) signaling is required for the formation of the lung in the embryonic period, it is unclear whether FGF receptor activity influences lung morphogenesis later in development. We generated transgenic mice expressing a soluble FGF receptor (FGFR-HFc) under conditional control of the lung-specific surfactant protein C promoter (SP-C-rtTA), to inhibit FGF activity at various times in late gestation and postnatally. Although expression of FGFR-HFc early in development caused severe fetal lung hypoplasia, activation of the transgene in the postnatal period did not alter alveolarization, lung size, or histology. In contrast, expression of the transgene at post-conception day E14.5 decreased lung tubule formation before birth and caused severe emphysema at maturity. FGFR-HFc caused mild focal emphysema when expressed from E16.5 but did not alter alveolarization when expressed after birth. Although FGF signaling was required for branching morphogenesis early in lung development, postnatal alveolarization was not influenced by FGFR-HFc.

Animals↗
PubMed2003

Pneumonitis and emphysema in sp-C gene targeted mice.

SP-C-deficient (SP-C -/-) mice developed a severe pulmonary disorder associated with emphysema, monocytic infiltrates, epithelial cell dysplasia, and atypical accumulations of intracellular lipids in type II epithelial cells and alveolar macrophages. Whereas alveolar and tissue surfactant phospholipid pools were increased, levels of other surfactant proteins were not altered (SP-B) or were modestly increased (SP-A and SP-D). Analysis of pressure-volume curves and forced oscillatory dynamics demonstrated abnormal respiratory mechanics typical of emphysema. Lung disease was progressive, causing weight loss and cardiomegaly. Extensive alveolar remodeling was accompanied by type II cell hyperplasia, obliteration of pulmonary capillaries, and widespread expression of alpha-smooth muscle actin, indicating myofibroblast transformation in the lung parenchyma. Dysplastic epithelial cells lining conducting airways stained intensely for the mucin, MUC5A/C. Tissue concentrations of proinflammatory cytokines were not substantially altered in the SP-C (-/-) mice. Production of matrix metalloproteinases (MMP-2 and MMP-9) was increased in alveolar macrophages from SP-C (-/-) mice. Absence of SP-C caused a severe progressive pulmonary disorder with histologic features consistent with interstitial pneumonitis.

Animals↗
PubMed1989

Prevention of emphysema. Importance of early identification.

If emphysema is identified early, much can be done to prevent or even reverse its progress. Smokers must be helped to stop smoking, and early, aggressive therapy with bronchodilators (plus corticosteroids, if needed) should be instituted. By preventing emphysema, the desperate cost of progressive respiratory insufficiency and curtailment of the pleasurable activities of daily living can be avoided.

Bronchodilator Agents↗
PubMed2000

Oxidative mechanisms in tobacco smoke-induced emphysema.

Cigarette smoking is well established as the cause of the majority of cases of emphysema. However, the mechanisms by which exposure of the lung to smoke causes the destruction of the lung parenchyma are not known. Oxidation probably contributes to the progression of this disease in several different ways. Oxidants present in the smoke itself or those generated by inflammatory cells in response to the particulate phase of the smoke inactivate proteinase inhibitors, and the increased inflammatory cells produce and release additional proteinases. The expression and activity of metalloproteinases, which have recently been implicated in the pathogenesis of emphysema, are regulated by redox status. Finally, oxidative damage to structural proteins may potentiate their degradation by the increased proteolytic burden.

Animals↗
PubMedDate not supplied

Maternal nicotine exposure during gestation and lactation of rats induce microscopic emphysema in the offspring.

The aim of this study was thus to determine whether maternal nicotine exposure during gestation and lactation will result in early emphysema in the lungs of the offspring. Female rats received nicotine subcutaneously during gestation and lactation. Nicotine administration commenced 1 day after mating and lasted until weaning on postnatal day 21. The offspring were exposed to nicotine via the placenta and mother's milk only. Lung tissue of the neonates was collected for analysis on postnatal days 14, 21, 35 and 42. The results show that maternal nicotine exposure had no effect on the total alveolar count (Na), mean alveolar volume (Valv), and airspace wall surface area per unit volume of lung tissue (AWUV) of the 14- and 21-day-old rat pups. However, the Na of the 35- and 42-day-old control animals was higher than that of the nicotine exposed animals. The Valv of the 35- and 42-day-old nicotine exposed rat pups was however larger than that of the control animals, whereas the AWUV of the 35- and 42-day-old control animals were bigger than that of the nicotine-exposed animals of the same age. The scanning electron micrographs showed a gradual flattening of the alveoli. It is therefore concluded that maternal nicotine exposure induced changes at gene level that renders the lungs of the offspring more susceptible to emphysema-like lesions.

Animals↗
PubMed2005

Aerosolized hyaluronan limits airspace enlargement in a mouse model of cigarette smoke-induced pulmonary emphysema.

This study was designed to determine if aerosolized hyaluronan (HA) could prevent airspace enlargement and elastic fiber injury in a mouse model of cigarette smoke-induced pulmonary emphysema. Compared to untreated/smoked controls, HA-treated animals showed statistically significant reductions in mean linear intercept (54 versus 65 microm; P < .001) and elastic fiber breakdown products (desmosine and isodesmosine) in bronchoalveolar lavage fluid (0.3 versus 7.0 ng/mL; P < .05). As in previous studies, the aerosolized HA showed preferential binding to elastic fibers, suggesting that it may protect them from injury. These findings support further investigation of the potential use of HA as a treatment for pulmonary emphysema.

Adjuvants, Immunologic↗
PubMedDate not supplied

Noninvasive assessment of pulmonary emphysema using dynamic contrast-enhanced magnetic resonance imaging.

Emphysema tends to be complicated by diffuse abnormalities in the pulmonary peripheral microvasculature. The aim of this study was to evaluate whether dynamic contrast-enhanced magnetic resonance imaging (MRI) could provide a valid assessment of pulmonary blood flow as an indicator of the severity of emphysema. To do this, the authors compared MRI data with the pathological findings in lung tissue. Dynamic contrast-enhanced MRI is a noninvasive method and can be used to repeatedly monitor clinicopathological severity. Using MRI clear pulmonary vascular information can be obtained easily, and the relative pulmonary blood flow in the lung parenchyma can be quantified.

Animals↗
PubMed2006

Beneficial effects of autologous bone marrow mononuclear cell transplantation against elastase-induced emphysema in rabbits.

The authors investigated whether autologous bone marrow mononuclear cell (BMC) transplantation via the left and right main bronchi would mitigate elastase-induced pulmonary emphysema in rabbits. Four weeks after elastase administration, rabbits also receiving BMCs showed significantly better pulmonary function (FVC, FEV100, FEVPEF) and smaller alveolar airspaces, as indicated by a smaller mean linear intercept, than those receiving porcine pancreatic elastase (PPE) (200 U/kg) alone via the left and right main bronchi. BMCs also significantly reduced cell counts in bronchoalveolar lavage fluid, the incidence of apoptotic (TUNEL-positive) cells and matrix metalloproteinase (MMP)-2 expression, while increasing numbers of proliferative (Ki-67-positive) cells. Thus, BMCs may inhibit the progression to emphysema by attenuating inflammation, MMP-2 expression, and apoptosis, while enhancing alveolar cell proliferation.

Animals↗
PubMed2005

Pulmonary function tests versus computed tomography in sheep with experimental emphysema.

The authors explored the relative utility of pulmonary function tests (PFTs) and computed tomography (CT) to characterize the progression of papain induced emphysema in sheep (n = 12). PFT included plethysmography (FRC(pleth)), helium dilution (FRC(He)), and expired reserve volume (ERV). Following papain, FRC(pleth) and FRC(He) were unchanged; ERV decreased hence residual volume increased significantly (RV + 270 mL, +86%, P = .02). In contrast, FRC by CT increased in 10 of 12 sheep (+264 mL +21%, P = .008). We conclude that plethysmography was insensitive to emphysema, but the effect on ERV (i.e., trapped gas volume) and FRC by CT were very similar, and in line with the morphologic changes in this animal model.

Animals↗
PubMedDate not supplied

Emphysema and metalloelastase expression in mouse lung induced by cigarette smoke.

Cigarette smoke (CS) causes pulmonary emphysema in humans and elastin degradation plays a key role in its pathogenesis. Previous studies on CS-exposed animals have been equivocal and have not clearly demonstrated the progression of the disease. In this study, morphometry was used to assess lung modifications to alveolar septa, airspaces, elastic and collagen fibers, and alveolar macrophages. Male (n = 40) C57/BL6 mice were exposed 3 times/day, whole body, to CS from three cigarettes for 10, 20, 30, or 60 days. Control groups (n = 10) were sham-smoked or received no exposure (day 0, n = 10). Morphometry included measurements of volume fraction of alveolar septa and airspaces, elastic and collagen fibers, and surface fraction of elastic fibers and alveolar septa. Morphometrical differences in mice after 60 days of exposure were greater than those after 10, 20, or 30 days, suggesting a progression of the disease. Inflammatory lesions in the lungs of mice contained significantly more metalloelastase (MMP-12) in macrophages at 10, 20, and 30 days than in controls of mice exposed for 60 days. These results suggest that elastin degradation took place during development of pulmonary changes in mice exposed to CS, and activation of MMPs specific for elastin may be a determining factor for susceptibility to emphysema.

Animals↗
PubMed2002

Reproducibility of scoring emphysema by HRCT.

PURPOSE: We evaluated the reproducibility of three visual scoring methods of emphysema and compared these methods with pulmonary function tests (VC, DLCO, FEV1 and FEV%) among farmer's lung patients and farmers. MATERIAL AND METHODS: Three radiologists examined high-resolution CT images of farmer's lung patients and their matched controls (n=70) for chronic interstitial lung diseases. Intraobserver reproducibility and interobserver variability were assessed for three methods: severity, Sanders' (extent) and Sakai. Pulmonary function tests as spirometry and diffusing capacity were measured. RESULTS: Intraobserver kappa-values for all three methods were good (0.51-0.74). Interobserver kappa varied from 0.35 to 0.72. The Sanders' and the severity methods correlated strongly with pulmonary function tests, especially DLCO and FEV1. CONCLUSION: The Sanders' method proved to be reliable in evaluating emphysema, in terms of good consistency of interpretation and good correlation with pulmonary function tests.

Aged↗