scholarly journals Lung capillaries raise the hypoxia alarm

2012 ◽  
Vol 122 (11) ◽  
pp. 3845-3847 ◽  
Author(s):  
Jahar Bhattacharya
Keyword(s):  
1978 ◽  
Vol 45 (5) ◽  
pp. 666-673 ◽  
Author(s):  
A. Bidani ◽  
E. D. Crandall

A quantitative analysis of the reaction and transport processes that occur in blood during and after gas exchange has been used to investigate mechanisms that might account for positive alveolar-mixed venous (A-V) and alveolar-arterial (Aa) PCO2 differences during rebreathing. The analysis was used to determine PCO2 changes that take place in blood as it travels from veins to arteries under conditions in which no CO2 is exchanged in the lung. The predicted A-V and Aa PCO2 differences are all positive and lie within the range of reported measured values. The differences are due to disequilibrium of [H+] between plasma and red blood cells, and to disequilibrium of the reactions CO2 in equilibrium HCO3- + H+ in plasma, as blood leaves the tissue and/or lung capillaries. The differences are increased with exercise and with continued O2 uptake in the lung, the latter due to the Haldane shift. We conclude that the two disequilibria and the Haldane shift contribute to the reported PCO2 differences in rebreathing animals but may not fully account for them. These mechanisms cannot explain any PCO2 differences that might exist during net CO2 elimination from blood in the lung.


1931 ◽  
Vol 31 (2) ◽  
pp. 247-256 ◽  
Author(s):  
Leonard S. Dudgeon ◽  
H. K. Goadby

1. The tissue reactions in rabbits from intravenous injections of live and dead Staphylococcus aureus and massive doses of indian ink and colloidal silver have been studied.2. Any particles injected into the circulation cause the accumulation of polymorphs in the lung capillaries.3. Inert colloidal particles such as indian ink are clumped in the capillaries of the lungs, liver, spleen and kidneys, and are phagocytosed by the endothelial cells.4. Staphylococci (S. aureus), live or dead, are nearly all held up in the lungs, where they are actively phagocytosed by the polymorphs within 5 minutes of an intravenous injection.5. Subsequently the cocci are distributed to the other organs, where phagocytosis continues mainly by polymorphs, but in the liver also by the Kupfer cells.6. Special attention is drawn to the localisation of the cocci in certain areas in the kidneys.7. Platelet counting on animals injected with various substances showed that there is an agglomeration of the particles with the platelets, which are consequently removed from the circulation.8. In the case of the inert particles the platelets are then restored to the circulation. With organisms (S. aureus) some of the platelets appear to be completely removed from the blood together with the bacteria.


1989 ◽  
Vol 76 (3) ◽  
pp. 269-276 ◽  
Author(s):  
D. Tighe ◽  
R. Moss ◽  
S. Boghossian ◽  
M. F. Heath ◽  
B. Chessum ◽  
...  

1. Using specific-pathogen-free New Zealand White rabbits, we have compared the effects of faecal peritonitis over a period of 5 h in eight test animals with eight controls in which a sham operation was performed. 2. There was morphological damage to lungs, liver and spleen of test animals. Lung capillaries and sinusoids of the liver showed occlusion by cell debris and leucocytes, with endothelial damage. The lungs also showed alveolar epithelial disruption, basement membrane exposure and type II pneumocytes lacking lamellar bodies. In the liver there was fibrin deposition and swollen Kupffer cells. The spleen showed degranulating neutrophils, fibrin deposits, platelet aggregates and activated macrophages, with no damage to the endothelium. 3. There was no morphological damage to the kidney or heart of test animals or to any organs of sham-operated animals. 4. There were mixed anaerobes and aerobes in faecal material used to induce peritonitis. Cultures of liver, spleen and kidney isolated four different types of micro-organisms. Blood cultures showed two types of micro-organisms. Cultures of lung and heart showed one type of micro-organism. 5. The presence of micro-organisms in an organ could not be correlated with the degree of histological damage to that organ. 6. In test animals an early significant reduction in circulating leucocytes and platelets was sustained for the duration of the experiment with significant diffuse intravascular coagulation. 7. There was no change in test animal neutrophil adhesiveness until 120 min, when significant reduction was observed. 8. Serum phospholipase A2 (EC 3.1.1.4) activity in the test group showed a threefold increase at 300 min.


1971 ◽  
Vol 219 (2) ◽  
pp. 303-330 ◽  
Author(s):  
I. C. S. Normand ◽  
R. E. Olver ◽  
E. O. R. Reynolds ◽  
L. B. Strang ◽  
Keasley Welch
Keyword(s):  

Science News ◽  
1989 ◽  
Vol 136 (3) ◽  
pp. 39
Author(s):  
S. Hart
Keyword(s):  

2015 ◽  
Vol 308 (5) ◽  
pp. L464-L478 ◽  
Author(s):  
Anne Hilgendorff ◽  
Kakoli Parai ◽  
Robert Ertsey ◽  
Edwin Navarro ◽  
Noopur Jain ◽  
...  

Elastin plays a pivotal role in lung development. We therefore queried if elastin haploinsufficient newborn mice ( Eln+/−) would exhibit abnormal lung structure and function related to modified extracellular matrix (ECM) composition. Because mechanical ventilation (MV) has been linked to dysregulated elastic fiber formation in the newborn lung, we also asked if elastin haploinsufficiency would accentuate lung growth arrest seen after prolonged MV of neonatal mice. We studied 5-day-old wild-type ( Eln+/+) and Eln+/− littermates at baseline and after MV with air for 8–24 h. Lungs of unventilated Eln+/− mice contained ∼50% less elastin and ∼100% more collagen-1 and lysyl oxidase compared with Eln+/+ pups. Eln+/− lungs contained fewer capillaries than Eln+/+ lungs, without discernible differences in alveolar structure. In response to MV, lung tropoelastin and elastase activity increased in Eln+/+ neonates, whereas tropoelastin decreased and elastase activity was unchanged in Eln+/− mice. Fibrillin-1 protein increased in lungs of both groups during MV, more in Eln+/− than in Eln+/+ pups. In both groups, MV caused capillary loss, with larger and fewer alveoli compared with unventilated controls. Respiratory system elastance, which was less in unventilated Eln+/− compared with Eln+/+ mice, was similar in both groups after MV. These results suggest that elastin haploinsufficiency adversely impacts pulmonary angiogenesis and that MV dysregulates elastic fiber integrity, with further loss of lung capillaries, lung growth arrest, and impaired respiratory function in both Eln+/+ and Eln+/− mice. Paucity of lung capillaries in Eln+/− newborns might help explain subsequent development of pulmonary hypertension previously reported in adult Eln+/− mice.


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