Journal ArticleDOI
The effect of ibuprofen on endotoxin-induced injury in sheep
Robert A. Balk,A. Francine Tryka,Roger C. Bone,Gerald H. Mazurek,Lorin G. Holst,James W. Townsend +5 more
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Thromboxane may be involved in the pathogenesis of the early hemodynamic derangements of endotoxemia, which was associated with histologic and ultrastructural evidence of lung injury in awake sheep.About:
This article is published in Journal of Critical Care.The article was published on 1986-12-01. It has received 11 citations till now. The article focuses on the topics: Lung injury & Cyclooxygenase.read more
Citations
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Journal ArticleDOI
Prostaglandins, cyclo-oxygenase inhibitors, and thromboxane synthetase inhibitors in the pathogenesis of multiple systems organ failure.
TL;DR: The available evidence does suggest that there is some role played by TXA2 and PGI2 in the physiologic and hemodynamic manifestations of sepsis, but the exact role remains undetermined.
Journal ArticleDOI
Anti-inflammatory Therapy for Acute Lung Injury: A Review of Animal and Clinical Studies
Craig A. Metz,William J. Sibbald +1 more
TL;DR: In this article, the authors compare and contrast published research on the use of anti-inflammatory agents, steroidal and non-steroidal, in animal models of acute lung injury.
BookDOI
Acute renal failure in the intensive therapy unit
TL;DR: Interestingly, acute renal failure in the intensive therapy unit that you really wait for now is coming and it's significant to wait for the representative and beneficial books to read.
Journal ArticleDOI
The role of cyclooxygenase products in lung injury induced by tumor necrosis factor in sheep.
TL;DR: It is hypothesized that the inflammatory effects of TNFalpha are due at least in part to cyclooxygenase products, and therefore cyclo oxygengenase inhibition would have similar effects on TNF alpha-induced lung injury as has previously been demonstrated for LPS- induced lung damage.
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Decreased left ventricular contractility during porcine endotoxemia is not prevented by ibuprofen.
TL;DR: It is concluded that products of the cyclooxygenase pathway do not play a major role in the early decrease in left ventricular contractility after endotoxin, and ibuprofen may have a role in reducing the other cardiovascular effects of sepsis.
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Journal ArticleDOI
Intravascular activation of complement and acute lung injury. Dependency on neutrophils and toxic oxygen metabolites.
TL;DR: These studies suggest that intravascular activation of the complement system leads to neutrophil aggregation and activation, intrapulmonary capillary sequestration of neutrophils, and vascular injury, which may be related to production of toxic oxygen metabolites by complement-activated neutrophILS.
Journal Article
Acute effects of Escherichia coli endotoxin on the pulmonary microcirculation of anesthetized sheep structure:function relationships.
Meyrick B,Brigham Kl +1 more
TL;DR: Correlation of the structural with the physiologic changes shows that the initial accumulation of leukocytes in the microcirculation occurs when pulmonary hypertension develops, which is similar to the alterations that occur early in the development of the syndrome in man.
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Respiratory failure after endotoxin infusion in sheep: lung mechanics and lung fluid balance
TL;DR: The response to high-dose endotoxin in sheep closely resembles acute respiratory failure in humans following gram-negative septicemia and increased with increasing survival time after endotoxin infusion, suggesting that pulmonary edema accumulated at the same rate in all fatally injured sheep, regardless of other variables.
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Pulmonary injury and prostaglandin production during endotoxemia in conscious sheep
TL;DR: It is concluded that prostaglandins, particularly PGF2 alpha and prostacyclin, are released from the lung after endotoxemia and appear in lung lymph as sensitive indicators of pulmonary microvascular injury.
Journal ArticleDOI
Effects of cyclooxygenase inhibitors on the alterations in lung mechanics caused by endotoxemia in the unanesthetized sheep.
TL;DR: Both the pulmonary hypertension and changes in lung mechanics observed after endotoxemia may be mediated, at least in part, by constrictor prostaglandins or thromboxanes and that gas exchange may be improved by preventing endogenous synthesis of these mediators.