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PubMed1997

Thoracoscopic lung volume reduction surgery reduces dyspnea and improves exercise capacity in patients with emphysema.

Improved ventilation and exercise capacity follows thoracoscopic lung volume reduction surgery (TLVRS) in patients with severe emphysema. This improvement could be related to changes in inspiratory and expiratory flows following surgery, with consequent improvement in dyspnea indices. Changes in inspiratory/expiratory flows at rest and exercise and their relation to subjective improvement in dyspnea after TLVRS are not well known. We studied 25 patients with severe emphysema who underwent unilateral TLVRS performed in well-defined zones with decreased perfusion in nuclear medicine lung scans. Early follow-up after surgery (4.2 +/- 0.8 mo) showed significant improvements in exercise tolerance: The distance covered over a 6 min walk test increased from 934 +/- 297 to 1,071 +/- 241 ft (p = 0.01). Exercise tolerance using a bicycle ergometer showed increased exercise endurance from 4.43 +/- 1.7 to 5.71 +/- 1.8 min (p < 0.001). The maximum workload tolerated increased from 37 +/- 19 to 52 +/- 21 W (p < 0.01) and VO2 max changed from 9.7 +/- 2 to 11.8 +/- 3 (ml.kg)/min (p < 0.01). This increment was achieved by generating significantly larger minute ventilation (VE), from 24 +/- 11 to 29 +/- 10 L/min, reached through larger tidal volumes (increasing from 951 +/- 330 to 1,145 +/- 367 ml), while maintaining the same maximum respiratory rates. Increased VE was also accompanied by significant increases in both average inspiratory and expiratory flows measured during exercise: from 0.89 +/- 0.41 L/s to 1.06 +/- 0.08 L/s, and from 0.77 +/- 0.37 to 0.90 +/- 0.32 L/s respectively (p < 0.01). The parallel increment in flows resulted in constant T1/Ttot relationship. These functional changes correlated with increased inspiratory flows at rest measured with pulmonary function tests (forced inspiratory volume in one s [FIV1], expiratory flows [FVC, FEV1], and increased maximum voluntary ventilation [MVV]) following the surgically induced reduction in residual volume (RV). These objective changes occurred parallel to improved dyspnea indices. The Baseline Focal Score was 3.36 +/- 1.47 and the Transition Focal Score was 6.12 +/- 0.7. The objectively measured variables at rest that best correlated with subjective improvement in dyspnea were the change in MVV, change in resting arterial PaO2, and change in FEV1 following TLVRS. Exercise variables did not have significant correlation with subjective markers indicating improvement in dyspnea, with the exception of the change in Dyspneic Index [(VE/MVV)100] at maximum exercise.

Adult↗
PubMed1997

Effect of surgical lung volume reduction on breathing patterns in severe pulmonary emphysema.

Surgical lung volume reduction may improve pulmonary function and dyspnea in advanced pulmonary emphysema. To investigate mechanisms of these beneficial effects we studied breathing patterns before and after surgery. Nineteen patients with diffuse pulmonary emphysema (FEV1 < 35% of predicted, total lung capacity > 130% predicted) were studied within 1 mo before, and 1.5 to 7 mo after thoracoscopic volume reduction. Changes of rib cage and abdominal volumes were monitored with calibrated respiratory inductive plethysmography for 20 to 60 min during natural breathing at rest. Pulmonary function and dyspnea were also assessed. Postoperative tidal volumes, respiratory cycle times, and minute ventilation were not significantly different from preoperative values. The contribution of abdominal volume changes to tidal volumes increased from a mean +/- SD of 43 +/- 17% preoperatively to 58 +/- 14% postoperatively (p = 0.03). The fraction of inspiratory time with abdominal paradoxical motion decreased from 12.3 +/- 8.3% preoperatively to 5.1 +/- 5.1% postoperatively (p = 0.02). The phase shift between rib cage and abdominal motion was reduced postoperatively. Hyperinflation, airway obstruction, and subjective ratings of dyspnea were significantly improved. The better synchronization of rib cage-abdominal motion and the greater contribution of abdominal volume changes to tidal volumes are consistent with a reduction of inspiratory loading and a greater force-generating capacity of the diaphragm after surgery.

Adult↗
PubMed1998

Intrapulmonary gas mixing in panacinar- and centriacinar-induced emphysema in rats.

We studied ventilation distribution using the single-breath washout technique in rats with two types of induced emphysema: panacinar-like (by instilled elastase) and centriacinar-like (by inhaled CdCl2 combined with oral intake of beta-aminopropionitrile). Morphologically, panacinar and centriacinar groups presented a similar degree of airspace enlargement, which was irregularly distributed and also accompanied by fibrosis only in the centriacinar group. In terms of mechanical properties, the centriacinar group presented lower end-expiratory flows and lower compliance than the panacinar group. The ventilation distribution patterns were also different between both groups. Single-breath washout phase III slopes, reflecting mainly diffusion-convection-dependent inhomogeneities in rat lungs, were largest in the centriacinar group. The SF6-He slope difference, which was reversed in both emphysema groups with respect to the control group, could be attributed mainly to He slope changes in the panacinar group and to SF6 slope changes in the centriacinar group. In addition, the respective He and SF6 slope decrease as a function of end-inspiratory breath-hold time, was only different from the control group in the centriacinar group. The observed ventilation distribution patterns can be explained by interacinar elastic changes in the panacinar group and severe interacinar structural alterations in the centriacinar group.

Administration, Inhalation↗
PubMed1999

Volume of graft and native lung after single-lung transplantation for emphysema.

To assess how the presence of the hyperinflated native lung influences the volume of the graft after single-lung transplantation (SLT) for emphysema, we used chest computed tomography to measure the TLC of each lung at a mean of 326 d before and 239, 588, and 932 d after SLT in nine patients. In addition, we obtained measurements of TLC and FRC in these nine patients plus one additional recipient at 697 d after surgery, and in 10 nonsmoking normal subjects matched for age, sex, height, and weight. On the nontransplanted side, TLC averaged 3.57 L before and 3.73 L, 3.70 L, and 3.73 L after SLT (NS). Corresponding values on the transplanted side were 3.42 L before and 2.06 L, 1.96 L, and 1.90 L after surgery, respectively (p < 0. 0002). Compared with the values obtained on the ipsilateral side in the control subjects, the FRC of the graft amounted to 100%, but its TLC was decreased to 79% (p < 0.005). We conclude that (1) the TLC of the graft and of the native lung do not change over time after SLT for emphysema, and (2) compared with the ipsilateral lung in normal control subjects, the TLC of the graft is substantially reduced, but its FRC is within normal limits.

Female↗
PubMed1999

A quantification of the lung surface area in emphysema using computed tomography.

Quantitative analysis of computed tomography (CT) has been combined with a stereologically based histologic analysis of lung structure to assess regional lung inflation and the structural features of the lung parenchyma. In this study, CT measurements of lung inflation were compared with histologic estimates of surface area in order to develop prediction equations that allow lung surface to volume ratio and surface area to be predicted from an analysis of the CT scan. The results show that mild emphysema is associated with an increase in lung volume and a reduction in surface to volume ratio, whereas surface area and tissue weight were only decreased in severe disease. The CT predicted surface to volume ratio correlated with histology, and both predicted and measured surface areas correlated with the diffusing capacity. We conclude that this CT analysis can be used to monitor the progression of emphysematous lung destruction in individual patients, and to assess the impact of both surgical and medical treatments for emphysema.

Aged↗
PubMed1999

Diaphragm dimensions after single-lung transplantation for emphysema.

We used three-dimensional reconstructions obtained with spiral computed tomography to measure total diaphragm surface area (Adi), and the surface area of the dome (Ado) and of the zone of apposition (Aap) of the diaphragm in nine patients with single-lung transplantation (SLT) for emphysema and nine normal subjects matched for age, sex, height, and weight. Measurements were obtained at supine FRC, midinspiratory capacity, and TLC. In the normal subjects, Ado and Adi were greater on the right than on the left side, and the right dome was positioned more cranially than the left one, presumably because of the presence of the liver. Compared with either the ipsilateral side in the controls or the native side in the patients, Ado was smaller on the transplanted side because the mediastinum was shifted toward the graft. Adi showed a similar trend. On the other hand, the radius of curvature of the dome in the coronal and sagittal planes was similar on the side of the graft and on the ipsilateral side in the controls. In conclusion, we found that after SLT for emphysema, diaphragm configuration comes back to normal but Ado, and with it Adi, remain smaller than in normal subjects because the mediastinum is displaced toward the graft.

Adult↗
PubMed2001

Bronchoscopic volume reduction: a safe and effective alternative to surgical therapy for emphysema.

Lung volume reduction surgery (LVRS), the removal of damaged, hyperexpanded lung, has been shown to improve respiratory function in many patients with end-stage emphysema. We report the results of an animal study using a new transbronchoscopic alternative to LVRS in which a washout solution and fibrin-based glue are used to collapse, seal, and scar target regions of abnormal lung. Twelve sheep had static and dynamic lung functions measured at baseline. Emphysema was produced by inhaled papain (7,000 U/wk x 4 wk), resulting in a significant increase of lung volumes, compliance, and airway resistance. The animals were then divided into three treatment groups of four animals, and underwent surgical volume reduction (SVR), bronchoscopic volume reduction (BVR), or bronchoscopy alone (Sham-BVR). Response to each intervention was assessed 8 to 12 wk after treatment by measuring lung function and examining lung tissue. BVR and SVR groups responded with significant and similar decreases in TLC and residual volume (RV). Tissue examination demonstrated that BVR caused collapse of the lung with focal scarring in 11 of 20 target territories (55% success rate). Three of the 11 target zones developed sterile abscesses. Postprocedure complications were less frequent with BVR than with SVR. This pilot study suggests that lung volume reduction can be achieved in animals without surgery using a bronchoscopic approach and a novel fibrin-based glue system. BVR has the potential for simplifying volume reduction, extending indications, and reducing morbidity, mortality, and costs in humans.

Animals↗
PubMed1987

Lysophosphatidylcholine augments elastase-induced alveolar epithelial permeability and emphysema in the hamster.

We administered low dose porcine pancreatic elastase (PPE) with and without lysophosphatidylcholine (lysoPC), a naturally occurring constituent of lung lipids with known membrane-perturbing properties, to test the hypothesis that alveolar epithelial solute permeability is a determinant of the severity of elastase-induced emphysema in experimental animals. Four age- and weight-matched groups of hamsters received intratracheal injections of one of the following in a total volume of 0.5 ml TRIS buffered saline: (1) no additions, (2) 4 units PPE, (3) 135 micrograms lysoPC, or (4) 4 units PPE plus 135 micrograms lysoPC. Thirty minutes later the permeability surface area products (PS) of the alveolar epithelium to 14C-sucrose and 125I-dextran 70 were measured in excised, perfused lungs from some animals from each group. The remaining animals were killed at 6 wk, at which time pressure-volume relationships were measured in excised lungs, and the mean linear intercept was determined from sections of fixed lung tissue. Neither PPE nor lysoPC alone caused statistically significant increases in PS for either tracer. The PPE plus lysoPC caused statistically insignificant increases in sucrose PS but approximate tenfold increases in dextran 70 PS, which were highly significant (p less than 0.001). Although focal air-space enlargement was observed in some lungs 6 wk after exposure to PPE, pressure-volume relationships and mean linear intercepts were not significantly different from control values. Lungs previously exposed to lysoPC were indistinguishable from control lungs for all measurements. Severe emphysema was uniformly observed in animals that received PPE in combination with lysoPC; lysoPC had no demonstrable effect upon PPE-induced hydrolysis of native elastin in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Cadmium-chloride-induced air-space enlargement with interstitial pulmonary fibrosis is not associated with destruction of lung elastin. Implications for the pathogenesis of human emphysema.

To determine whether lung elastin is lost during the evolution of cadmium-induced air-space enlargement with pulmonary fibrosis, the lung elastin of 5- to 7-day-old golden Syrian hamster pups was radiolabeled by giving [3H]valine. At maturity, a single intratracheal instillation of 0.5 ml of 0.025% CdCl2 solution was given. Lung mechanics, histologic examination, and biochemistry were studied 5, 10, 21, 42, 105, and 180 days after the cadmium treatment. The animals developed fibrosis and air-space enlargement with decreased lung volumes, compliance, and forced expiratory flow; their functional residual capacity was increased. The total lung collagen and total lung elastin were increased, but there was no loss of radiolabel in lung elastin. We conclude that CdCl2-induced air-space enlargement with pulmonary fibrosis is not accompanied by loss of neonatally formed lung elastic fibers. We hypothesize that air-space enlargement with fibrosis represents a stereotyped response of the lung to fibrosing injuries, which we hypothesize is due to forces from more fibrotic and atelectatic areas causing overdistension of less abnormal air spaces. The air-space enlargement of fibrosing human diseases such as sarcoidosis and eosinophilic granuloma may have a similar basis. Evidence is reviewed that human centrilobular emphysema may be a form of focal air-space enlargement with interstitial fibrosis; there may be mechanisms in addition to elastase-antielastase imbalance that cause human emphysema.

Animals↗
PubMed1988

Augmentation of elastase-induced emphysema by cigarette smoke. Effects of reduced nicotine content.

To examine the role of nicotine in the augmentation of elastase-induced emphysema by cigarette smoke, animals that had been pretreated with porcine pancreatic elastase (PPE) were exposed to cigarette smokes that had a five-fold difference in their nicotine concentrations. Young adult female Long-Evans rats were divided into seven groups: (1) untreated controls; (2) low nicotine cigarette smoke exposure (Kentucky 2A1 reference cigarettes; 35.0 mg total particulate matter, 0.42 mg nicotine, and 0.38 mg nitrogen oxides per cigarette); (3) high nicotine cigarette smoke exposure (Kentucky 2R1 reference cigarettes; 38.8 mg total particulate matter, 2.2 mg nicotine, and 0.34 mg nitrogen oxides per cigarette; (4) PPE alone; (5) PPE + sham smoke exposure; (6) PPE + 2A1 smoke exposure; and (7) PPE + 2R1 smoke exposure. Three days after intratracheal administration of PPE (400 IU/kg), animals in the smoke-treated groups were exposed to 10 puffs of cigarette smoke daily, 7 days/wk for 14 wk. Sham-treated animals received room air in place of cigarette smoke. After the exposures, pulmonary function tests were performed under general anesthesia. Whole lungs were examined for gross pathologic changes, and samples of lung tissue were harvested for quantitative morphometry. Cigarette smoke exposure alone did not produce significant changes in pulmonary function or structure. On the other hand, treatment with elastase alone produced a constellation of pulmonary functional and structural changes that were pathognomonic of emphysema. Exposure to 2R1 but not 2A1 cigarette smoke significantly augmented the emphysematous changes produced by PPE.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

A 16-month study of the development of genetic emphysema in tight-skin mice.

The tight-skin (tsk) mouse has been recently proposed as a model of genetically determined emphysema. In the present study, the development of this lung lesion was investigated morphometrically in both male and female tsk mice from 4 days to 16 months of age. "Pallid" (pa) mice with a closely related genetic background served as controls. Despite small differences in the mean linear intercept seen at 1 and at 16 months, both male and female tsk mice were found to be similarly susceptible to the development of the emphysematous lesion. Three main phases were observed in the evolution of the emphysema. The first phase, from 4 days to 2 months after birth, included enlargement of the peripheral lung units, already evident at 4 and at 15 days, and destruction of the lung parenchyma, which occurred between 15 days and 1 month and rapidly progressed for as long as 2 months. A second phase of stabilization or of mild progression of the emphysematous lesion occurred between 2 and 8 months of age. A third phase, in the advanced age between 8 and 16 months, included a further exacerbation of the parenchymal destruction. At 16 months of age, the lungs of the pa mice also showed some patchy areas of air-space enlargement with destruction of the alveolar septa.

Animals↗
PubMed1990

Cigarette smoke causes physiologic and morphologic changes of emphysema in the guinea pig.

To investigate the long-term effect of cigarette smoke on pulmonary structure and function, we exposed groups of guinea pigs to the smoke of 10 cigarettes each day, 5 days per week, for 1, 3, 6, and 12 months. We found that the guinea pigs developed progressive lung destruction (emphysema) and alterations in their pulmonary function tests similar to that seen in humans with cigarette smoke-induced chronic obstructive lung disease. This method of smoke-induced lung destruction should provide a good model for the study of the early changes of emphysema.

Animals↗
PubMed1991

Evidence that genetic emphysema in tight-skin mice is not caused by neutrophil elastase.

Mutant tight-skin mice that had severe pulmonary emphysema were crossed with beige mice that contained neutrophils deficient in elastase activity. The resultant tight skin-beige cross mice were deficient in neutrophil elastase activity, yet they were still afflicted with the same degree of severe emphysema as the tight-skin mice. The results indicate that neutrophil elastase does not cause the emphysematous lesions found in tight-skin mice.

Animals↗
PubMed1976

Diaphragmatic changes in emphysema.

The diaphragms and lungs of 95 men were quantitatively examined at autopsy, and the following observations were made. The area of the whole diaphragm had a significant inverse correlation (r= -0.412, P less than 0.001) with the percentage of the lung occupied by emphysematous lesions. Most of the reduction in the area of the whole diaphragm associated with advanced emphysema occured in the muscular portion; in contrast, the thickness of the diaphragm was not affected by percentage of the lung occupied by emphysematous lesions. Neither body height nor postmortem lung volume had as close a relation to area of the whole diaphragm as did percentage of the lung occupied by emphysematous lesions. The conclusion drawn from these observations is that the diaphragm area reduction associated with emphysema is related to altered thoracic shape, probably diaphragm flattening in particular, and is better described as contracture than as atrophy. It is speculated that these morphologic changes contribute to the altered diaphragmatic function characteristic of chronic obstructive pulmonary disease, and thereby to the ventilatory abnormalities seen in patients with this disorder.

Adult↗
PubMed1976

Emphysema and its relation to age.

To establish whether a correlation existed between emphysema and age, 24 lungs were used to measure the alveolar membrane fenestrations; the average area of 100 fenestrae was then plotted against age. Eighteen of these lungs were from patients 17 to 86 years of age with no history of respiratory ailments, whereas 6 lungs were from patients in whom an antemortem diagnosis of emphysema had been made. A significant, positive correlation between age and the area of fenestrae (t=2.4;p greater than 0.05) was found in the group of 18 lungs from patients with no respiratory ailements. The same could not be said categorically about the lungs from the emphysematous group, because the number of lungs examined was too small. We postulate that the pores of Kohn are part of the degenerating emphysematous process and are the first stage in the formation of fenestrae. A possible mechanism for the formation of fenestrae and their classification into 4 grades is presented.

Adolescent↗
PubMed1977

Experimental emphysema induced with purified human neutrophil elastase: tissue localization of the instilled protease.

Human neutrophilic polymorphonuclear leukocyte (PMN) elastase was purified by affinity chromatography to greater than 95% homogeneity as judged by disc-gel electrophoresis. Dog lung elastin was prepared from alveolar-enriched tissue by prior extraction of soluble and collagenous lung proteins with 0.1 M NaOH at 98 degrees C. Digestion of the remaining insoluble residue by the purified PMN enzyme was monitored by Lowry assay of acid-soluble peptides released. The PMN enzyme possessed 60% of the digestive activity of crystallized porcine pancreatic elastase (weight:weight comparison) when tested in vitro against this substrate in phosphate-NaCl buffer at pH 7.5. Whole tissue studies were then performed in lungs of laboratory animals. One-ml samples containing purified PMN elastase were instilled into lavaged and saline-perfused isolated dog lung at the level of the sixth to seventh generation bronchus. Treatment with 384 mug of the PMN enzyme produced anatomic emphysema after a 90-min incubation at room temperature, which was comparable to that produced by 100 mug of porcine pancreatic elastase. Frozen sections of treated and control lungs were examined for the presence of PMN elastase by the indirect immunoperoxidase method using a monospecific rabbit antiserum against PMN elastase as the primary stain. Light microscopy revealed elastase bound to connective tissue in the treated lungs, in close proximity to aldehyde-fuchsin-counterstained elastic fibers. A similar experiment was tn of enzyme solutions containing 1;0 mg of elastase per ml produced discrete lesions within 90 min, as before. Light microscopic studies in conjunction with the indirect immunoperoxidase staining method again demonstrated elastase in association with connective tissue elements in the lesion area. In addition, part of the instilled protease could be demonstrated within alveolar macrophages. Electron microscopy combined with immunoperoxidase staining revealed direct attachment of th einstilled enzyme to elastic fibers within alveolar septa. In enzyme-treated tissue, some septa showed severe depletion of intercellular structures with the exception of colalgen, which was generally preserved. These results show that human leukocyte elastase penetrated dog alveolar septal connective tissue after airway instillation and that the enzyme attaches to elastic fibers, inducing histologic changes comparable to thos seen in human emphysema.

Animals↗
PubMed1977

Possible mechanisms of emphysema in smokers: cigarette smoke condensate suppresses protease inhibition in vitro.

To study the possible role of suppression of antiproteases by cigarette smoke in the pathogenesis of pulmonary emphysema in smokers, the following experiments were carried out. Elastin-agarose gels were impregnated with cigarette smoke condensate dissolved in dimethyl sulfoxide or with the solvent alone. This procedure affected neither local pH of the gel nor subsequent physical behavior (diffusion) of antiprotease. Elastases from various sources were then allowed to diffuse through the impregnated gels toward a counter-diffusing sample of antiprotease. The effectiveness of the antiprotease in blocking the enzyme was determined from the extent of elastolysis. The elastin substrates used included beef ligament elastin and dog lung elastin. The enzymes used were porcine pancreatic elastase and pure human leukocyte elastase. The antiproteases tested included human serum, pure human a1-antitrypsin, human bronchopulmonary lavage fluid, and a synthetic chloromethyl ketone inactivator of elastase. The results showed that whole, unfractionated cigarette smoke condensate suppressed all of the antiproteases tested, except for the chloromethyl ketone. These observations are discussed in terms of the protease-pathogenesis model of pulmonary emphysema.

Humans↗
PubMed1980

Morphologic changes in the muscular pulmonary arteries: relationship to cigarette smoking, airway disease, and emphysema.

The muscular pulmonary arteries were studied by morphometric methods in 25 long-term cigarette smokers and were compared with those of 14 lifelong nonsmokers. Muscular pulmonary arteries < 500 microns in external diameter were identified and counted. The external diameter, medial thickness, and intimal thickness were measured in each of these arteries. Smokers had an increased number of transected muscular arteries < 200 microns in diameter (p < 0.03), increased medial smooth muscle (p < 0.02), and more intimal thickening (p < 0.04). Among smokers, these vascular changes correlated significantly with the severity of small airway disease and with the degree of emphysema, but not with bronchial mucous gland enlargement. We conclude that regular cigarette smoking is associated with morphologic changes in the muscular pulmonary arteries that evolve in parallel with small airway disease and emphysema. Although the functional significance of these findings is unknown, they may be important in the eventual development of pulmonary hypertension and cor pulmonale.

Adult↗