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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The histopathology of hyperplasia of the carotid bodies was studied in 6 cases of hypoxaemia and right ventricular hypertrophy secondary to pan-acinar emphysema, and in five cases of systemic hypertension with left ventricular hypertrophy. The features of the hyperplasia were the same in the two groups. There was proliferation of sustentacular (type II) cells and compression of central cores of chief (type I) cells. It is speculated that the hyperplasia of sustentacular cells is associated in some way with the prevention of retention of sodium ions and water which characterises hypoxic cor pulmonale in "blue bloaters", systemic hypertension, and ascent to high altitude with the complications of acute mountain sickness, and pulmonary and cerebral oedema.
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PMID:Hyperplasia of the carotid body. 621 75

Right ventricular hypertrophy in elastase-induced emphysema in the System hamster was assessed by either the weight of the right ventricle as a fraction of body-weight or by the ratio of the weight of the right to the left ventricle. Right ventricular hypertrophy accompanies elastase-induced emphysema and is more severe in hamsters injected with elastase while fed a diet containing 0.5% beta-aminopropionitrile (BAPN), a combination that causes more severe emphysema. Measurements of arterial blood oxygen pressures showed that emphysematous animals were hypoxemic. Treatment of emphysematous animals with 35% O2 either during the development of right ventricular hypertrophy or after it had developed produced measurable amelioration of the hypertrophy in those groups with the more severe emphysema (elastase plus BAPN diet) but did not completely prevent it. The oxygen had no effect on the severity of the emphysema measured morphometrically. These results indicate that the cor pulmonale in elastase-induced emphysema is probably multifactorial, but hypoxia appears to be one of the major factors.
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PMID:The effect of oxygen on Cor pulmonale in experimental emphysema induced by elastase or elastase and beta-aminopropionitrile in hamsters. 621 38

The prevalence of right ventricular hypertrophy was studied in necropsy material from 215 coalworkers, a group which consisted of 115 men with simple or no pneumoconiosis and 100 with progressive massive fibrosis. Right ventricular hypertrophy was considered to be present if the ratio of the weight of the left ventricle plus septum to that of the right ventricle was less than 2:1. The prevalence of right ventricular hypertrophy was low (15%) in the absence of progressive massive fibrosis and appeared to be related to emphysema or airways disease or both, and not to simple pneumoconiosis. It was evident only in subjects who had smoked. In subjects with progressive massive fibrosis the prevalence of right ventricular hypertrophy was higher (34%) and it was occasionally seen in non-smokers. The prevalence increased with increasing size of lesion, and for any given size of lesion subjects with right ventricular hypertrophy had more panacinar emphysema than those without right ventricular hypertrophy. There was no relationship, however, between the extent of massive lesions or amount and type of emphysema and the degree of right ventricular hypertrophy.
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PMID:Right ventricular hypertrophy in a group of coalworkers. 622 8

The tight-skin (Tsk) mouse is a genetic model of pulmonary emphysema. In this mouse, right ventricular hypertrophy (RVH) starts to develop at approximately 8 months of age, probably as a consequence of the emphysema. The aim of the present study was to investigate cardiac collagen synthesis, content, and types both before and during the development of RVH. Collagen synthesis, assessed by the [3H]proline incorporation method, was significantly increased in the right ventricle of 3-month-old Tsk mice. This was accompanied by a marked increase in right ventricle collagen content. Collagen typing showed no difference from controls. At 8 months of age collagen synthesis had returned to control values, right ventricular collagen content was elevated but held lower values than at 3 months, and collagen typing showed a prevalence of the more compliant type III. By 16 months of age, right ventricular collagen content had returned to control values and there was a shift in collagen types due to a relative increase of the more rigid type I. At 24 months of age right ventricular collagen content was increased again and collagen type I continued to predominate. These results suggest a dynamic role for collagen both before and during the development of RVH secondary to emphysema.
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PMID:Cardiac collagen changes during the development of right ventricular hypertrophy in tight-skin mice with emphysema. 807 May 38

The weights of the individual carotid bodies and cardiac ventricles were obtained at necropsy in five series of subjects. The first comprised 10 cases free of cardiopulmonary disease to act as controls. The second consisted of 10 cases of pulmonary emphysema. The third was composed of 8 cases characterized by sustained alveolar hypoxia due to causes other than pulmonary emphysema. The fourth comprised 10 cases of systemic hypertension or severe left ventricular failure. The fifth was made up of 10 cases of diseases of the liver or alimentary canal. The study confirmed that enlargement of the carotid bodies is common in cases of pulmonary emphysema or sustained alveolar hypoxia with right ventricular hypertrophy. It is also common in cases of systemic hypertension with left ventricular hypertrophy. It was also revealed that enlargement of the carotid bodies may occur in cirrhosis of the liver. We believe this to be the first report of that association.
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PMID:The carotid bodies enlarge in some cases of cirrhosis of the liver. 820 96

Tl-201 myocardial scintigraphy was performed in 130 patients with chronic obstructive pulmonary disease (COPD) to evaluate right ventricular hypertrophy, and the clinical significance of this method was studied. Tl-201 uptake ratio of the right ventricle, which represents the ratio of total counts of the right ventricle to counts of the administered dose of Tl-201, was higher in COPD, especially in pulmonary emphysema and B type COPD by Burrows classification than in controls. The grade of visualization of the right ventricle by visual assessment (RVV) was marked (+3) in only a few cases and moderate (+2) in many cases (more than 80%) in all diseases except bronchial asthma. The incidences of right ventricular hypertrophy by electrocardiogram, right-sided heart failure and marked dyspnea (Hugh-Jones 4.5) were very low in cases with RVV grade +2 and very high in cases with +3. The grade of RVV was related to the severity of pulmonary perfusion impairment, although in diffuse panbronchiolitis the RVV was relatively slight compared with the impairment of perfusion. May parameters of pulmonary function such as %VC, FEV1.0%, RV/TLC, V25, %DLCO, Raw, delta N2 and PaO2 showed abnormal values in patients with RVV grade of (+2) or (+3) in all diseases except bronchial asthma. In COPD, Tl-201 myocardial scintigraphy seems to be useful for assessment of right ventricular overloading, and for follow-up observation and differentiation between cor pulmonale and right ventricular hypertrophy secondary to cardiac diseases by observing Tl-201 uptake of the lung and left ventricle.
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PMID:[Right ventricular visualization by Tl-201 myocardial scintigraphy in chronic obstructive pulmonary disease]. 851 19

Right ventricular cardiac function is altered by abnormalities affecting primarily the left-sided cardiac structures, the lungs, or the right-sided cardiac structures themselves. The most common cardiac causes for right ventricular dysfunction are chronic left ventricular ischemia and rheumatic mitral valvular disease. Pulmonary diseases that result in right ventricular dysfunction include pulmonary air-space disease, including emphysema, and pulmonary interstitial and parenchymal diseases, including idiopathic pulmonary fibrosis and cystic fibrosis. Chronic pulmonary vascular disease, including chronic thromboembolism and PPH have a significant effect on right ventricular performance. Common to all of these diseases is elevation of pulmonary vascular resistance with a commensurate increase in right ventricular pressure, resulting in right ventricular hypertrophy. The limited ability of right ventricular myocardium to function in the face of increased pulmonary resistance results in right ventricular dilatation, tricuspid regurgitation, and ultimately right ventricular failure. MR imaging provides direct, noninvasive visualization of the right ventricular chamber as well as the myocardium itself, allowing reliable demonstration of morphologic changes in the size and shape of the ventricle, thickness of the myocardium, and presence of abnormal infiltration by fat or edema. Furthermore, because MR imaging techniques do not depend upon geometric assumptions about the complex shape of the right ventricle, they may be used for accurate and reproducible quantitation of right ventricular volume and myocardial mass.
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PMID:MR imaging of pulmonary hypertension and right ventricular dysfunction. 872 68

Cor pulmonale is a significant cause of morbidity and mortality in patients with emphysema, but it is not known whether alveolar destruction is directly involved in the disease pathogenesis. The purpose of this study was to examine the relationship between susceptibility to smoking-induced cor pulmonale and alveolar destruction in eight inbred strains of mice: 129XI/SvJ, A/J, A/HeJ, BALB/cJ, C3H/HeJ, C57BL/6J, DBA/2J, and SWR/J. The mice were exposed to filtered air or mainstream cigarette smoke at a concentration of 250 mg/m(3) for 5.5 h/day, 5 days/wk for 5 mo, housed for 4 more months, and killed. The ratio of the weight of the right ventricle/left ventricle plus septum [RV/(LV + S)] was used to assess right ventricular hypertrophy. Alveolar mean linear intercept was used to quantify severity of alveolar destruction. Morphometric determination of blood vessel muscularization was done on sections from four mouse strains. Smoke exposure resulted in significant increases in RV/(LV + S) in the A/J and A/HeJ strains compared with air-exposed controls. The magnitude of the smoking-induced increase in RV/(LV + S) decreased as a function of the genetic distance of the other strains from the A/J and A/HeJ strains. Pulmonary vascular muscularization was significantly increased in smoke-exposed A/J and BALB/cJ mice but not in C3H/HeJ and C57BL/6 mice. Also, mouse strain susceptibility to smoking-induced pulmonary vascular muscularization did not correlate with changes in mean linear intercept. The data from this study suggest that alveolar destruction by itself is not sufficient to cause smoking-induced cor pulmonale in inbred mice.
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PMID:Susceptibility to pulmonary hypertension in inbred strains of mice exposed to cigarette smoke. 1727 9

Tumor necrosis factor (TNF)-alpha is a key pro-inflammatory cytokine, thought to be important in the pathogenesis of pulmonary emphysema. TNF-alpha overexpression in the lung leads to the phenotypic features of pulmonary emphysema, pulmonary hypertension, and right ventricular hypertrophy in mice bred in Denver, 5240 feet/1600 m of altitude. This study hypothesized that the altitude could affect the development of pulmonary emphysema as well as pulmonary hypertension. To investigate the effect of the altitude, TNF-alpha transgenic mice were bred at sea level, Fukuoka, Japan. The pulmonary physiology and histology demonstrated similar development of pulmonary emphysema, compared to the mice bred in Denver. With respect to pulmonary hypertension, right ventricular hypertrophy was attenuated. Interestingly, mortality rate was significant lower in the mice bred at sea level. In contrast with the results in Denver, a significant decrease of vascular endothelial growth factor (VEGF) and its receptors expression was not found. From these data, we consider that the altitude affects development of pulmonary hypertension through the expression of VEGF and its receptors. In contrast, the effect of altitude was not clear regarding the development of pulmonary emphysema.
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PMID:Attenuation of pulmonary hypertension, but not emphysematous change, by breeding emphysema model mice at sea level. 1820 85

In patients with chronic obstructive pulmonary disease (COPD), an inflammatory process is ongoing in the lungs, with concomitant damage of the alveolar structures and loss of airway function. In this inflammatory process, extracellular matrix degradation is observed. During this lung matrix degradation, small peptide fragments consisting of proline and glycine repeats generated from collagen fibers are liberated from the matrix by matrix metalloproteinases. Chemotactic activities of these collagen-derived peptides such as N-acetyl-proline-glycine-proline (PGP) via CXCR1 and CXCR2 have been reported. We show here that PGP induces neutrophil migration in vivo, which is dose dependent. Moreover, PGP is involved in the development of emphysema-like changes in the airways. The complementary peptide, L-arginine-threonine-arginine (RTR), has been shown to bind to PGP sequences and inhibit neutrophil infiltration. We show that RTR impedes both PGP- and interleukin-8-induced chemotaxis in vitro. In vivo, RTR prevents both migration and activation of neutrophils induced by PGP. Furthermore, RTR completely inhibits PGP-induced lung emphysema, assessed by changes in alveolar enlargement and right ventricular hypertrophy. In conclusion, these data indicate that collagen breakdown products, especially PGP, are important in the pathogenesis of COPD and that PGP antagonism via RTR ameliorates lung emphysema.
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PMID:Induction of lung emphysema is prevented by L-arginine-threonine-arginine. 1855 62


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