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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2-3
|
| pubmed:dateCreated |
1981-4-21
|
| pubmed:abstractText |
Experimental results suggested that in normovolaemia 0.5% of the total pulmonary circulation flows through the bronchial arteries. In haemorrhagic shock bronchial flow dropped to 0.04% of the total pulmonary circulation and ceased completely below 40 mmHg. The authors claim that a hypoperfusion of both circulatory systems (pulmonary and bronchial) is an important pathogenetic factor in the first step of the development of the shock lung. A two-hour abolishment of the nutritive circulation of the lung caused already hypotension, hypoxaemia and metabolic acidosis. Tissue hypoxia was confirmed by the rise in the enzymatic activity of the lung tissue. An abolishment of bronchial circulation in the described manner was enough to induce the development of the shock lung, as confirmed by the visible changes (changed colour, greater weight, development of congestive atelectasis and oedema) of the lung and by the haemodynamic and respiratory changes. Here too the increase in pulmonary vascular resistance is attributed an important role due perhaps in the beginning to an enhancement of the sympathetic tone and later to hypoxia and metabolic acidosis. If the effect of haemorrhage alone is compared to the effect of simultaneous haemorrhage and elimination of the bronchial artery, it appears that the functional lesion of the lung becomes considerably more pronounced with the abolishment of the nutritive circulation. Severe hypoxia and metabolic acidosis cause an extreme rise of the pulmonary vascular resistance. The severity of metabolic acidosis, the degree to which pulmonary vascular resistance has increased and its duration seem decisive from the aspect of both the development and outcome of the shock lung.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:status |
MEDLINE
|
| pubmed:issn |
0001-5431
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
20
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
115-30
|
| pubmed:dateRevised |
2003-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:555174-Animals,
pubmed-meshheading:555174-Blood Pressure,
pubmed-meshheading:555174-Bronchi,
pubmed-meshheading:555174-Dogs,
pubmed-meshheading:555174-Female,
pubmed-meshheading:555174-Lung Compliance,
pubmed-meshheading:555174-Male,
pubmed-meshheading:555174-Pulmonary Artery,
pubmed-meshheading:555174-Pulmonary Circulation,
pubmed-meshheading:555174-Regional Blood Flow,
pubmed-meshheading:555174-Respiratory Distress Syndrome, Adult,
pubmed-meshheading:555174-Shock, Hemorrhagic,
pubmed-meshheading:555174-Vascular Resistance
|
| pubmed:year |
1979
|
| pubmed:articleTitle |
Role of the arterial bronchial system in the pathomechanism of the shock lung.
|
| pubmed:publicationType |
Journal Article
|