Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary capillaries have extremely thin walls to allow rapid exchange of respiratory gases across them. Recently it has been shown that the wall stresses become very large when the capillary pressure is raised, and in anaesthetised rabbits, ultrastructural damage to the walls is seen at pressures of 40 mm Hg and above. The changes include breaks in the capillary endothelial layer, alveolar epithelial layer, and sometimes all layers of the wall. The strength of the thin part of the capillary wall can be attributed to the type IV collagen in the extracellular matrix. Stress failure of pulmonary capillaries results in a high-permeability form of oedema, or even frank haemorrhage, and is apparently the mechanism of neurogenic pulmonary oedema and high-altitude pulmonary oedema. It also explains the exercise-induced pulmonary haemorrhage that occurs in all racehorses. Several features of mitral stenosis are consistent with stress failure. Overinflation of the lung also leads to stress failure, a common cause of increased capillary permeability in the intensive care environment. Stress failure also occurs if the type IV collagen of the capillary wall is weakened by autoantibodies as in Goodpasture's syndrome. Neutrophil elastase degrades type IV collagen and this may be the starting point of the breakdown of alveolar walls that is characteristic of emphysema. Stress failure of pulmonary capillaries is a hitherto overlooked and potentially important factor in lung and heart disease.
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PMID:Stress failure of pulmonary capillaries: role in lung and heart disease. 809 42

The mammalian pulmonary blood-gas barrier is well known to be extremely thin. For example, in the human lung, half of the area of the barrier (the 'bulging' part) has a thickness of only 0.2-0.4 micron. We show here that the barrier is also immensely strong. This is an essential requirement because the capillary wall stresses during heavy exercise become very large (about 7 x 10(4) N/m2 = 70 kPa) when capillary pressure increases to 30 mmHg. Stress failure of the pulmonary capillary wall consistently occurs in experimental rabbit preparations at abnormally high pressures exceeding 40 mmHg and may be the cause of bleeding into the lung in galloping racehorses. The great strength of the thin side of the blood-gas barrier can be attributed to the extracellular matrix, especially the type IV collagen which is predominantly located in the very thin lamina densa. The alveolar wall is therefore particularly vulnerable to injurious agents which attack type IV collagen such as autoantibodies in Goodpasture's Syndrome and perhaps neutrophil elastase in emphysema. The combination of extreme thinness and great strength of the blood-gas barrier poses a unique design requirement.
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PMID:Strength of the pulmonary blood-gas barrier. 162 33

The following hypothesis is proposed: Experimental lung disease in old rats is different from this disease in adult rats. In order to demonstrate this, we performed a morphometrical evaluation of the pulmonary state of two groups of rats at different ages and to which Goodpasture's syndrome had been induced. 115 Wistar rats were used. They were divided into four different groups as follows: 1) Healthy adult rats which had not been subjected to treatment; 2) diseased adult rats to which antipulmonary serum had been administered; 3) healthy old rats; and 4) diseased old rats. With the help of a computerized system, the length of the alveolar chord, the thickness of the alveolar wall and the surface of the bronchial-associated lymphoid tissue in each group was calculated. We also counted the number of alveolar macrophages (AM) with haemosiderin, the percentage of goblet bronchial cells and that of AM, lymphocytes and polymorphonuclear leukocytes of the broncho-alveolar lavage (BAL). The following results were obtained. When related to the diseased adult rats, the diseased old rats showed an increase in the alveolar chord and a decrease in the thickness of the alveolar wall, as well as in the number of AM with haemosiderin, goblet cells and BAL lymphocytes. These results support the proposed hypotheses, since the diseased adult animals showed signs of alveolar inflammation with interstitial edema, while in the diseased old animals these results are compatible with emphysema.
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PMID:Goodpasture's syndrome in aging. An experimental study on the rat. I. 830 14