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  • 1
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Physiology 55 (1993), S. 503-525 
    ISSN: 0066-4278
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Biology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Physiology 61 (1999), S. 543-572 
    ISSN: 0066-4278
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Biology
    Notes: Abstract The pulmonary blood-gas barrier needs to satisfy two conflicting requirements. It must be extremely thin for efficient gas exchange, but also immensely strong to withstand the extremely high stresses in the capillary wall when capillary pressure rises during exercise. The strength of the blood-gas barrier on the thin side is attributable to the type IV collagen in the basement membranes. However, when the wall stresses rise to very high levels, ultrastructural changes in the barrier occur, a condition known as stress failure. Physiological conditions that alter the properties of the barrier include intense exercise in elite human athletes. Some animals, such as Thoroughbred racehorses, consistently break their alveolar capillaries during galloping, causing hemorrhage. Pathophysiological conditions causing stress failure include neurogenic pulmonary edema, high-altitude pulmonary edema, left heart failure, and overinflation of the lung. Remodeling of the capillary wall occurs in response to increased wall stress, a good example being the thickening of the capillary basement membrane in diseases such as mitral stenosis. The blood-gas barrier is able to maintain its extreme thinness with sufficient strength only through continual regulation of its wall structure. Recent experimental work suggests that rapid changes in gene expression for extracellular matrix proteins and growth factors occur in response to increases in capillary wall stress. How the blood-gas barrier is regulated to be extremely thin but sufficiently strong is a central issue in lung biology.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Ultrasructure Research 91 (1985), S. 1-12 
    ISSN: 0022-5320
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-136X
    Keywords: Key words Cheetah ; Fiber type ; Mitochondrial volume density ; Skeletal muscle ; Sprinting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract To establish a skeletal muscle profile for elite sprinters, we obtained muscle biopsy samples from the vastus lateralis, gastrocnemius and soleus of African cheetahs (Acinonyx jubatus). Muscle ultrastructure was characterized by the fiber type composition and mitochondrial volume density of each sample. Maximum enzyme activity, myoglobin content and mixed fiber metabolite content were used to assess the major biochemical pathways. The results demonstrate a preponderance of fast-twitch fibers in the locomotor muscles of cheetahs; 83% of the total number of fibers examined in the vastus lateralis and nearly 61% of the gastrocnemius were comprised of fast-twitch fibers. The total mitochondrial volume density of the limb muscles ranged from 2.0 to 3.9% for two wild cheetahs. Enzyme activities reflected the sprinting capability of the cheetah. Maximum activities for pyruvate kinase and lactate dehydrogenase in the vastus lateralis were 1519.00 ± 203.60 and 1929.25±482.35 μmol min−1 · g wet wt−1, respectively, and indicated a high capacity for glycolysis. This study demonstrates that the locomotor muscles of cheetahs are poised for anaerobically based exercise. Fiber type composition, mitochondrial content and glycolytic enzyme capacities in the locomotor muscles of these sprinting cats are at the extreme range of values for other sprinters bred or trained for this activity including greyhounds, thoroughbred horses and elite human athletes.
    Type of Medium: Electronic Resource
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  • 5
    Publication Date: 1991-06-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 6
    Publication Date: 2019-06-28
    Description: There are no previous studies investigating the effect of microgravity exposure during spaceflight on lung tissue. We examined the ultrastructure of the left lungs of 5 Czechoslovakian Wistar rats flown on the 13 day, 19+ hr. Cosmos 2044 mission, and compared them to 5 vivarium and 5 synchronous controls at 1-g conditions, and 5 rats exposed to 14 days of tail-suspension. Within 10 minutes of sacrifice by decapitation, the lungs were removed and immersed in 3% glutaraldehyde in 0.1M phosphate buffer (total osmolarity of the fixative: 560 mOsm; pH = 7.4). The tissue stored at 5 C was transported to our laboratory where it was processed for light and electron microscopy. No significant perivascular cuffing caused by interstitial edema was present in the tissue samples. Some of the flight, tail-suspended, and synchronous control rats showed alveolar edema, while vivarium controls did not. The pulmonary capillaries appeared to be more congested in the flight animals than in the other groups. This could be related to the increased hematocrit due to the microgravity exposure. In all 5 flight, 4 tail-suspended, and 3 synchronous rats, red blood cells (RBC) were present in the alveolar spaces. The RBC were either suspended free in the alveoli or observed lining the alveolar wall. The frequency of RBC lining the alveolar walls appeared greater in the dorsal (gravity non-dependent) than in ventral (gravity dependent) regions of the lung in these three animal groups. In 3 of the vivarium controls, a few RBC were found in the alveolar spaces. Intra-capillary fluid-filled vesicles were observed in the flight, tail-suspended and synchronous animals, but not in the vivarium controls. The formation of intra-capillary fluid-filled vesicles has been previously associated with pulmonary hypertension induced by high altitude exposure and mitral stenosis. In conclusion, pulmonary hemorrhage and alveolar edema of unknown origin occurred to a greater extent in the flight, tail-suspended, and synchronous control animals, and in the dorsal regions of the lung when compared to the vivarium controls. The etiology of these changes, which are possibly due to an increase in pulmonary vascular pressure, requires further investigation.
    Keywords: Life Sciences (General)
    Type: US Experiments Flown on the Soviet Biosatellite Cosmos 2044; 221-231; NASA-TM-108802
    Format: text
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  • 7
    Publication Date: 2019-07-13
    Description: We previously showed that when pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to test whether stress failure occurred more frequently at high than at low lung volumes for the same Ptm. Lungs of anesthetized rabbits were inflated to a transpulmonary pressure of 20 cmH2O, perfused with autologous blood at 32.5 or 2.5 cmH2O Ptm, and fixed by intravascular perfusion. Samples were examined by both transmission and scanning electron microscopy. The results were compared with those of a previous study in which the lung was inflated to a transpulmonary pressure of 5 cmH2O. There was a large increase in the frequency of stress failure of the capillary walls at the higher lung volume. For example, at 32.5 cmH2O Ptm, the number of endothelial breaks per millimeter cell lining was 7.1 +/- 2.2 at the high lung volume compared with 0.7 +/- 0.4 at the low lung volume. The corresponding values for epithelium were 8.5 +/- 1.6 and 0.9 +/- 0.6. Both differences were significant (P less than 0.05). At 52.5 cmH2O Ptm, the results for endothelium were 20.7 +/- 7.6 (high volume) and 7.1 +/- 2.1 (low volume), and the corresponding results for epithelium were 32.8 +/- 11.9 and 11.4 +/- 3.7. At 32.5 cmH2O Ptm, the thickness of the blood-gas barrier was greater at the higher lung volume, consistent with the development of more interstitial edema. Ballooning of the epithelium caused by accumulation of edema fluid between the epithelial cell and its basement membrane was seen at 32.5 and 52.5 cmH2O Ptm. At high lung volume, the breaks tended to be narrower and fewer were oriented perpendicular to the axis of the pulmonary capillaries than at low lung volumes. Transmission and scanning electron microscopy measurements agreed well. Our findings provide a physiological mechanism for other studies showing increased capillary permeability at high states of lung inflation.
    Keywords: Aerospace Medicine
    Type: Journal of applied physiology (Bethesda, Md. : 1985) (ISSN 8750-7587); 73; 1; 123-33
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  • 8
    Publication Date: 2019-07-13
    Description: 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.
    Keywords: Life Sciences (General)
    Type: Lancet (ISSN 0140-6736); 340; 8822; 762-7
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  • 9
    Publication Date: 2019-07-13
    Description: We previously showed that when the pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to determine whether some of the ultrastructural changes are rapidly reversible when the capillary pressure is reduced. To test this, the Ptm was raised to 52.5 cmH2O for 1 min of blood perfusion and then reduced to 12.5 cmH2O for 3 min of saline-dextran perfusion, followed by intravascular fixation at the same pressure. In another group of animals, the pressure was elevated for 1 min of blood and 3 min of saline-dextran before being reduced. The results were compared with previous studies in which the capillary pressures were maintained elevated at 52.5 cmH2O during the entire procedure. Control studies were also done at sustained low pressures. The results showed that the number of endothelial and epithelial breaks per millimeter and the total fraction area of the breaks were reduced when the pressure was lowered. For example, the number of endothelial breaks per millimeter decreased from 7.1 +/- 2.1 to 2.4 +/- 0.7, and the number of epithelial breaks per millimeter fell from 11.4 +/- 3.7 to 3.4 +/- 0.7. There was evidence that the breaks that closed were those that were initially small and were associated with an intact basement membrane. The results suggest that cells can move along their underlying matrix by rapid disengagement and reattachment of cell adhesion molecules, causing breaks to open or close within minutes.(ABSTRACT TRUNCATED AT 250 WORDS).
    Keywords: Life Sciences (General)
    Type: Journal of applied physiology (Bethesda, Md. : 1985) (ISSN 8750-7587); 73; 3; 1150-8
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  • 10
    Publication Date: 1999-03-01
    Description: ▪ Abstract  The pulmonary blood-gas barrier needs to satisfy two conflicting requirements. It must be extremely thin for efficient gas exchange, but also immensely strong to withstand the extremely high stresses in the capillary wall when capillary pressure rises during exercise. The strength of the blood-gas barrier on the thin side is attributable to the type IV collagen in the basement membranes. However, when the wall stresses rise to very high levels, ultrastructural changes in the barrier occur, a condition known as stress failure. Physiological conditions that alter the properties of the barrier include intense exercise in elite human athletes. Some animals, such as Thoroughbred racehorses, consistently break their alveolar capillaries during galloping, causing hemorrhage. Pathophysiological conditions causing stress failure include neurogenic pulmonary edema, high-altitude pulmonary edema, left heart failure, and overinflation of the lung. Remodeling of the capillary wall occurs in response to increased wall stress, a good example being the thickening of the capillary basement membrane in diseases such as mitral stenosis. The blood-gas barrier is able to maintain its extreme thinness with sufficient strength only through continual regulation of its wall structure. Recent experimental work suggests that rapid changes in gene expression for extracellular matrix proteins and growth factors occur in response to increases in capillary wall stress. How the blood-gas barrier is regulated to be extremely thin but sufficiently strong is a central issue in lung biology.
    Print ISSN: 0066-4278
    Electronic ISSN: 1545-1585
    Topics: Biology , Medicine
    Published by Annual Reviews
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