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PubMed2001

Core to rind distribution of severe emphysema predicts outcome of lung volume reduction surgery.

Computed tomography (CT) has shown that emphysema is more extensive in the inner (core) region than in the outer (rind) region of the lung. It has been suggested that the concentration of emphysematous lesions in the outer rind leads to a better outcome following lung volume reduction surgery (LVRS) because these regions tend to be more surgically accessible. The present study used a recently described, computer-based CT scan analysis to quantify severe emphysema (lung inflation > 10.2 ml gas/g tissue), mild/moderate emphysema (lung inflation = 10.2 to 6.0 ml gas/g tissue), and normal lung tissue (lung inflation < 6.0 ml gas/g tissue) present in the core and rind of the lung in 21 LVRS patients. The results show that the quantification of severe emphysema independently predicts change in maximal exercise response and FEV(1). We conclude that a greater extent of severe emphysema in the rind of the upper lung predicts greater benefit from LVRS because it identifies the lesions most accessible to removal by LVRS.

Female↗

PubMed1987

Mild emphysema is associated with reduced elastic recoil and increased lung size but not with air-flow limitation.

Thirty-nine excised human lungs were examined to identify early changes in the small airways, their size distribution, and their elastic recoil in relation to mild degrees of emphysema. Elastic recoil measurement, single-breath nitrogen (SBN2) tests, and FEV1 were obtained from 18 lungs with no emphysema and 21 emphysematous lungs with no greater than Grade 5 emphysema score. The mean number of alveolar attachments per brochiole was determined from all the bronchioles cut in cross section. When the 2 groups of lungs were compared, the percentage of predicted elastic recoil of the nonemphysematous lungs was significantly greater at 50, 70, 80, and 90% of TLC than in the mildly emphysematous lungs. The TLC of the emphysematous lungs (% of predicted) was also significantly greater than in the nonemphysematous lungs. Pigment of the small airways was the only pathologic feature that was significantly greater in the emphysematous lungs than in the nonemphysematous lungs. Size distribution in the small airways was similar except for the airways zero to 0.2 mm, which were more frequent in the emphysematous lungs. When data from both groups were combined, elastic recoil was shown to be related to both the number of alveolar attachments (p less than 0.03) and the mean diameter of the small airways (p less than 0.01). We conclude that structural and functional changes in lungs with mild emphysema include reduced elastic recoil, increased lung size, and some size distribution changes in the small airways. Mild emphysema is not associated with air-flow limitation.

Airway Resistance↗

PubMed1988

Nitrogen-dioxide-induced emphysema in rats. Lack of worsening by beta-aminopropionitrile treatment.

We evaluated the effect of beta-aminopropionitrile (beta APN) on the nitrogen dioxide (NO2) animal model of emphysema. Rats maintained on a beta APN-supplemented or a regular diet were exposed to 30 ppm NO2 for intervals ranging from 1 to 8 wk. Emphysema development was assessed by histologic evaluation and by changes in lung volume and mean linear intercept values. Evidence of pathologic changes were also documented by clinical and radiographic findings of osteolathyrism. The induction of centriacinar emphysema was attributed specifically to NO2 exposure. Neither the severity of the emphysema nor the time course of its development was altered by the beta APN-supplemented diet. These findings are in marked contrast to those observed with the exogenous elastase model of the disease, and they suggest that elastin synthesis and repair may not modulate elastin destruction in the NO2 model of emphysema.

Aminopropionitrile↗

PubMed1988

Exponential analysis of the pressure-volume curve. Correlation with mean linear intercept and emphysema in human lungs.

We investigated the effect of obvious emphysematous lesions and the mean airspace size in the lung surrounding these lesions on the exponential constant K of the lung pressure-volume curve. The severity of the centrilobular emphysematous (CLE) lesions was determined in resected lung specimens, and the mean linear intercept (Lm) was measured on random histologic sections taken from regions without obvious emphysema. The exponential constant K was determined by fitting lung pressure-volume data obtained from the patient just prior to resection to the equation V = A - Be-KP. This allowed us to compare patients with little or no emphysema that had either normal (0.16 +/- 0.03 SD; n = 12) or increased (0.27 +/- 0.04 SD; n = 12) K to other patients that had severe emphysema but either normal (0.17 +/- 0.01 SD; n = 10) or increased (0.25 +/- 0.03 SD; n = 10) K. In subjects without emphysema, K was significantly related to Lm, suggesting that K is a measure of mean alveolar size. In the subjects with emphysema, a lower value for K was associated with more severe airway dysfunction and gas trapping. We conclude that K reflects airspace size except when airway closure subtracts the contribution of lung units from the deflation pressure-volume curve.

Aged↗

PubMed1988

Nitrogen and energy relationships in malnourished patients with emphysema.

The purpose of this study was to examine the impact of nutritional support on nitrogen-energy relationships and functional parameters in malnourished patients with emphysema. Malnourished patients without lung disease served as the control group. Ten ambulatory, stable patients with emphysema and six patients without lung disease received an infusion of 5% dextrose (baseline) plus electrolytes (D5W) for two days, which was followed by an enteral or a parenteral infusion of either a carbohydrate-based (CB, 53% carbohydrate) or a fat-based diet (FB, 55% fat) for 1 wk each, in a randomized cross-over design. All patients had greater than 10% weight loss. Caloric intake was set at 1.7 times the resting energy expenditure (REE) as measured during the baseline period. The REE of patients with emphysema was 23 and 27% above that of the control group during baseline and refeeding periods, respectively. The increased REE was met primarily by an increased carbohydrate oxidation. During the infusion of D5W, N balance was lower in patients with emphysema, but during repletion N balance was similar in both groups of patients. Two weeks of nutritional support with either a CB or a FB diet increased body weight, N balance, and arm muscle area and improved maximal inspiratory pressure, skeletal muscle strength, and endurance-strength (using quadriceps, hamstring, and handgrip) to a similar degree in malnourished patients with and without lung disease. In other stress states, such as infection, it has been shown that hypermetabolism, hypercatabolism, and preferential fat oxidation occur concomitantly. Patients with emphysema are unusual because, although they are hypermetabolic, they are not hypercatabolic and do not demonstrate preferential fat oxidation.

Aged↗

PubMed1989

Limitations of computed tomography in the assessment of emphysema.

Thirty-eight patients undergoing lobectomy or pneumonectomy for carcinoma had preoperative computed tomography (CT) of the chest. Twenty-seven had both 1.5 mm and 10 mm collimation scans, and eleven had 10 mm collimation images only. These images were analyzed for the extent and severity of emphysema, and the analysis compared to the pathologic findings in the corresponding transverse slice of lung. The latter was graded by a modification of a panel of standards and by a grid system numerically expressing extent and severity. The grid system is theoretically superior to the panel of standards because it allows better quantitation of early emphysema and, contrary to the set of standards, is designed to analyze transverse CT images and corresponding pathologic slices. There was good correlation between the CT score and the pathologic score using the panel of standards (r = 0.81, p less than 0.001) but a lower correlation with the grid system (r = 0.70, p less than 0.001). The correlation improved slightly with 1.5 as compared to 10 mm collimation scans. Close comparison between the CT and grid scores showed that CT was sensitive in demonstrating early distal acinar and irregular emphysema. However, CT consistently underestimated the extent of centriacinar and panacinar emphysema because most lesions less than 0.5 cm in diameter were missed. We conclude that CT is insensitive in detecting the earliest lesions of emphysema.

Humans↗

PubMed1990

The nutritional status in advanced emphysema associated with chronic bronchitis. A study of amino acid and catecholamine levels.

Advanced emphysema with bronchitis is associated with significant weight loss and malnutrition, the true cause of which has not been clearly identified. The purpose of this exploratory study was to compare plasma amino acids and related compounds and catecholamines in a group of patients with advanced end-stage emphysema with a control group of similar age and sex in an effort to further understand this malnourished state. Fasting blood samples were obtained by venipuncture after a rest period. Plasma amino acid levels were determined by ion exchange high pressure liquid chromatography with fluorometric detection. Plasma catecholamines were determined by radioenzymatic analysis. Anthropometric measurements, the usually accepted biochemical markers of nutrition, dietary analysis, pulmonary function tests, and a historical analysis of the state of health including drug use and smoking history in each subject were analyzed. Ages and heights were comparable, whereas weights were significantly decreased in the patients with emphysema. Total serum protein and serum albumin values were significantly lower in the patient group. Significant respiratory muscle weakness was indicated by reduced negative inspiratory force in these end-stage patients, contrasting with well-preserved muscle strength usually found in obstructive lung disease. The dietary caloric intake of the patients was comparable to that of the control subjects. We conclude that the fine balance of the amino acid pool in patients with bronchitis and emphysema is well preserved, except for significant elevations of aspartic acid, glutamine, and cystine, and a decreased level of leucine. In addition, norepinephrine levels were significantly increased. Weight loss in patients with emphysema and bronchitis is likely due to increased energy demands related to hypermetabolism.

Aged↗

PubMed1990

Influence of preexisting pulmonary emphysema on susceptibility of rats to inhaled diesel exhaust.

The susceptibilities of normal rats and rats with preexisting pulmonary emphysema to chronically inhaled diesel exhaust were compared. Rats were exposed 7 h/day, 5 days/wk for 24 months to diesel exhaust at 3.5 mg soot/m3, or to clean air as controls. Emphysema was induced in one-half of the rats by intratracheal instillation of elastase 6 wk before exhaust exposure. Measurements included lung burdens of diesel soot, respiratory function, bronchoalveolar lavage, clearance of radiolabeled particles, pulmonary immune responses, lung collagen, excised lung weight and volume, histopathology, and mean linear intercept of terminal air spaces. Parameters indicated by analysis of variance to exhibit significant interactions between the influences of emphysema and exhaust were examined to determine if the effects were more than additive (indicating increased susceptibility). Although 14 of 63 parameters demonstrated emphysema-exhaust interactions, none indicated increased susceptibility. Less soot accumulated in lungs of emphysematous rats than in those of nonemphysematous rats, and the reduced accumulation had a sparing effect in the emphysematous rats. The results did not support the hypothesis that emphysematous lungs are more susceptible than are normal lungs to chronic exposure to high levels of diesel exhaust. The superimposition of effects of emphysema and exhaust, however, might still warrant special concern for heavy exposures of emphysematous subjects.

Animals↗

PubMed1990

Tsk mice with genetic emphysema. Right ventricular hypertrophy occurs without hypertrophy of muscular pulmonary arteries or muscularization of arterioles.

The causes for the development of right ventricular hypertrophy (RVH) in emphysema are not fully understood. In the 1960s, studies of RVH in association with emphysema found no correlation between the extent of tissue damage in the lung and the RV weight. This was thought to disprove the theory that the RVH was due to an increase in pulmonary vascular resistance secondary to capillary destruction. In the present study, the development of RVH was investigated in tight-skin (tsk) mice with genetic emphysema. RVH started to develop in mature to senescent animals between 8 and 16 months of age and progressed thereafter. At 24 months of age, RV weight and the ratios RV/body weight and RV/LV + S weight were, respectively, 52, 96, and 60% greater than in control (pa) mice. At this time blood gas analysis revealed hypoxemia in tsk but not in pa mice. The mean linear intercept of tsk mice was 83% larger and the surface area of the walls of distal air spaces per unit lung volume was 40% smaller than in pa mice. There was a strong correlation between the severity of emphysema, assessed by both techniques, and the RV/LV + S ratio (p less than 0.001 for both). No muscularized arterioles were seen in the tsk mice, and the medial thickness of muscular arteries was almost identical in the two groups. This demonstrates that in emphysema, RVH can develop in the absence of pulmonary vascular changes and is probably due to tissue (and thus capillary) destruction.

Animals↗

PubMed1991

Alveolar attachments in emphysema of human lungs.

We have studied alveolar attachments to membranous bronchioles in 41 patients enrolled in the National Institutes of Health Intermittent Positive Pressure Breathing Trial who died, came to autopsy, and provided adequate tissue for examination. The patients had moderate to severe chronic airflow obstruction and, on the average, severe emphysema. We measured the number of normal attachments per membranous bronchiole per case (N), the number of normal attachments per mm of circumference per bronchiole per case (Nunit), and the ratio of abnormal to all attachments (R). All measurements correlated closely to all measurements of emphysema and to irregular shape of bronchioles (deformity index). Measurement of abnormal attachments correlated with abnormal tests of pulmonary function, including evidence of airflow obstruction and diffusing capacity for carbon monoxide (DLCO). Nunit showed the most frequent correlations, but both N and Nunit were only related independently of emphysema for Phase III of the single-breath nitrogen test. R was related to loss of DLCO. We conclude that loss of attachments is not itself a cause of airflow obstruction but rather a correlate of emphysema, which is the proximate cause of the obstruction. Loss of alveolar attachments has an effect only on the single-breath nitrogen tests independent of emphysema.

Bronchi↗

PubMed1993

Effect on single-breath washout and lung function of elastase-induced emphysema in rats.

Lung volumes, diffusing capacity (DLCO), quasi-static pressure-volume curves (P-V), forced expiration (FE) and He-SF6 single-breath washout (SBW) were performed in Wistar rats with emphysema induced by different doses of pancreatic elastase in saline, instilled intratracheally 6 wk prior to the tests. Emphysema was quantitatively assessed by mean linear intercept (Lm) measurements on 5-microns lung sections. Lung volume, P-V curve, and FE dependence on Lm, as well as the nonsignificant dependence of DLCO on Lm, are generally similar to results reported by others. The most interesting observation concerns the SBW: N2 slopes of the alveolar plateau, compared for identical lung volumes, did not change with the degree of emphysema. By contrast, the He-SF6 slope difference did depend significantly on the degree of emphysema. Based on the diffusion front theory, the present work suggests that in rats with elastase-induced emphysema, the phase III slope modifications relate mainly to elastic and not to structural alterations.

Analysis of Variance↗

PubMed1977

The induction of pulmonary emphysema with human leukocyte elastase.

Purified human leukocyte elastase was injected into the tracheas of 46 hamsters. Thirteen animals died spontaneously within 1 week, with extensive lung hemorrhage. The elastin content of the lungs was only slightly less than control values 3 hours after injection. At 2 months, the lungs of the remaining animals showed mild, patchy emphysema and morphometric changes consistent with emphysema. These results contrasted with the effects of a similar elastolytic dose of pancreatic elastase administered to 26 other hamsters in that only one animal died spontaneously, the lung elastin content 3 hours after injection was substantially decreased, and severe emphysema was present 2 months later. Leukocyte elastase appears to be capable of causing emphysema; but unlike pancreatic elastase, leukocyte elastase produces emphysema that is mild, even at a dose sufficient to produce intense lung hemorrhage and a high mortality.

Animals↗

PubMed1985

Nutritional emphysema in the rat. Influence of protein depletion and impaired lung growth.

Emphysema is produced by severe food restriction in rats and is postulated to result from depletion of lung connective tissue. We studied (1) whether total dietary protein depletion worsens nutritional emphysema, and (2) whether the reduced content of lung connective tissue in nutritional emphysema results from lack of accumulation caused by impaired lung growth or by a net loss from the lung. Lewis rats weighing 200 g were restricted to one third food intake with or without protein for 6 wk. Lungs were assessed by morphometry, pressure-volume (P-V) measurements, and content of collagen and elastin. Emphysema was found by morphometry (but not by P-V measurements) in food-restricted rats, and contrary to expectation, emphysema was less severe in those depleted of protein. Collagen and elastin content were reduced in emphysematous lungs; however, the levels were not below those found prior to nutritional intervention, suggesting that lack of growth, not depletion, accounts for the reduced content.

Animals↗

PubMed1987

Pulmonary emphysema in a nonsmoking patient with Salla disease.

Severe emphysema is reported in a patient with Salla disease, a recessively inherited disorder of sialic acid metabolism that leads to intralysosomal accumulation of free sialic acid in cells of various tissues. The disease is among the rare genetically determined diseases typical of the Finnish population. The patient was 41 yr old at the time of his death. He had been a nonsmoker with no evidence of alpha-1-antitrypsin deficiency. Chest radiographs suggested that severe emphysema had developed during the last 4.5 yr of his life. Emphysema was also documented by postmortem radiography, which showed it to be located mainly in the lower lobes. The uneven distribution of tissue destruction within individual lobules, as shown in histologic sections, indicated a centrilobular type of emphysema, which was probably related to the basic storage disease. Thus, some involvement of storage lysosomes in altering the functioning of pulmonary macrophages is suspected. The serum proteinase inhibitory capacity as well as the alpha-1-antitrypsin phenotypes were normal among 5 brothers and sisters of the patient, 1 of whom was affected by the disease. The exact pathogenetic mechanism(s) for the rapid development of severe emphysema in this rare case of Salla disease remains unclear.

Adult↗

PubMed2004

The development of emphysema in cigarette smoke-exposed mice is strain dependent.

Only 20% of smokers develop chronic obstructive pulmonary disease. An important determinant of susceptibility is genomic variation. We undertook this study to define strains of mice with different susceptibilities for the development of smoking-induced emphysema because they could help identify genetic factors of susceptibility. NZWLac/J, C57BL6/J, A/J, SJ/L, and AKR/J strains were exposed to cigarette smoke for 6 months. Elastance (Htis), the extent of emphysema (mean linear intercept [Lm]), and the inflammatory cell and cytokine response were measured. NZWLac/J had no change in Lm or Htis (resistant). C57BL6/J, A/J, and SJ/L increased Lm, but not Htis (mildly susceptible). AKR/J increased Lm and Htis (super-susceptible). Only AKR/J had significant inflammation comprising macrophages, neutrophils, and T cells. The AKR/J showed an upregulation of Th1 cytokines whereas in the C57BL/6/J and NZWlac/J, cytokines did not change or were downregulated. We conclude that Lm, elastance, and inflammation are features that are needed to phenotype emphysema in mice. The inflammatory cell and cytokine profile may be an important determinant of the phenotype in response to cigarette smoke exposure. The identification of resistant and susceptible strains for the development of emphysema could be useful for genomic studies of emphysema susceptibility in mice and eventually in humans.

Animals↗

PubMed2004

Recurrence of pulmonary emphysema in an alpha-1 proteinase inhibitor-deficient lung transplant recipient.

Several types of primary disease may recur after lung transplantation, but recurrence of pulmonary emphysema has so far never been published. We report the case of a 49-year-old white male who underwent single lung transplantation for emphysema related to alpha-1 antitrypsin deficiency and to superimposed smoking. The postoperative course was complicated by several rejection episodes. Subsequently, the patient remained stable without evidence of graft dysfunction for more than 10 years, but he resumed light smoking at 8 years after transplant. At 11 years after transplant, although the patient was still asymptomatic and had a stable lung function, recurrence of emphysema on the grafted side was diagnosed on computerized tomography of the thorax. One year later, the patient began to experience a moderate decline in lung function. Two separate bronchoalveolar lavages performed after the onset of the recurrence disclosed a significant elastolytic activity related to neutrophil serine-elastase in lavage fluid. In summary, we describe a case of recurrence of pulmonary emphysema in a patient with alpha-1 antitrypsin deficiency. The resumption of smoking has probably played a central role in the presence of elastolytic activity in lavage fluid and in the recurrence of emphysema.

Acute Disease↗

PubMed2004

Early emphysema in patients with anorexia nervosa.

Postmortem studies of patients who died in the Warsaw Ghetto during World War II suggested that death from starvation was associated with pulmonary emphysema. This study re-examines this hypothesis in patients who are chronically malnourished because of anorexia nervosa. Age, smoking history, body mass index, and pulmonary function were measured in 21 subjects with anorexia nervosa and 16 control subjects. Computed tomography (CT) scans were obtained from three regions of the lung (at the level of the aortic arch, the carina, and the posterior position of the eighth rib) using a multislice scanner. The CT measurements of lung density, emphysema, and surface area-to-volume ratio were obtained using the X-ray attenuation values. CT measurements of emphysema were greater in the group that was anorexic than in historical control subjects (p < 0.001). Furthermore, there were significant correlations between the body mass index and the CT measures of emphysema for all the patients and between diffusing capacity and the CT measurements in the patients who were anorexic. A multiple linear regression analysis showed the diffusing capacity was predicted best by the percentage of lung voxels within the large emphysematous changes category. These data demonstrate that emphysema-like changes are present in the lungs of patients who are chronically malnourished.

Adult↗

PubMed2004

An animal model of autoimmune emphysema.

Although cigarette smoking is implicated in the pathogenesis of emphysema, the precise mechanisms of chronic progressive alveolar septal destruction are not well understood. We show, in a novel animal model, that immunocompetent, but not athymic, nude rats injected intraperitoneally with xenogeneic endothelial cells (ECs) produce antibodies against ECs and develop emphysema. Immunization with ECs also leads to alveolar septal cell apoptosis and activation of matrix metalloproteases MMP-9 and MMP-2. Anti-EC antibodies cause EC apoptosis in vitro and emphysema in passively immunized mice. Moreover, immunization also causes accumulation of CD4+ T cells in the lung. Adoptive transfer of pathogenic, spleen-derived CD4+ cells into naive immunocompetent animal also results in emphysema. This study shows for the first time that humoral- and CD4+ cell-dependent mechanisms are sufficient to trigger the development of emphysema, suggesting that alveolar septal cell destruction might result from immune mechanisms.

Animals↗