Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
1989-11-15
|
pubmed:abstractText |
We previously reported that pulmonary arterial occlusion for 48 h followed by 4 h of reperfusion in awake dogs results in marked edema and inflammatory infiltrates in both reperfused and contralateral lungs (Am. Rev. Respir. Dis. 134: 752-756, 1986; J. Appl. Physiol. 63: 942-950, 1987). In this experiment we study the effects of alveolar hypoxia on this injury. Anesthetized dogs underwent thoracotomy and occlusion of the left pulmonary artery. Twenty-four hours later the dogs were reanesthetized, and a double-lumen endotracheal tube was placed. The right lung was continuously ventilated with an inspiratory O2 fraction (FIO2) of 0.35. In seven study animals the left lung was ventilated with an FIO2 of 0 for 3 h after the left pulmonary artery occluder was removed. In six control animals the left lung was ventilated with an FIO2 of 0.35 during the same reperfusion period. Postmortem bloodless wet-to-dry weight ratios were 5.87 +/- 0.20 for the left lower lobe and 5.32 +/- 0.12 for the right lower lobe in the dogs with hypoxic ventilation (P less than 0.05 for right vs. left lobes). These values were not significantly different from the control dog lung values of 5.94 +/- 0.22 for the left lower lobe and 5.11 +/- 0.07 for the right lower lobe (P less than 0.05 for right vs. left lobes). All values were significantly higher than our laboratory normal of 4.71 +/- 0.06. We conclude that reperfusion injury is unaffected by alveolar hypoxia during the reperfusion phase.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
8750-7587
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
67
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
528-33
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:2793653-Animals,
pubmed-meshheading:2793653-Blood Pressure,
pubmed-meshheading:2793653-Cardiac Output,
pubmed-meshheading:2793653-Dogs,
pubmed-meshheading:2793653-Female,
pubmed-meshheading:2793653-Fixatives,
pubmed-meshheading:2793653-Heart Rate,
pubmed-meshheading:2793653-Hemodynamics,
pubmed-meshheading:2793653-Male,
pubmed-meshheading:2793653-Oxygen Consumption,
pubmed-meshheading:2793653-Pulmonary Alveoli,
pubmed-meshheading:2793653-Pulmonary Edema,
pubmed-meshheading:2793653-Pulmonary Gas Exchange,
pubmed-meshheading:2793653-Reperfusion Injury,
pubmed-meshheading:2793653-Time Factors
|
pubmed:year |
1989
|
pubmed:articleTitle |
Lack of alveolar O2 during lung reperfusion does not decrease edema formation.
|
pubmed:affiliation |
Department of Anesthesiology, University of Washington School of Medicine, Seattle 98195.
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.
|