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Inhibition of thromboxane biosynthesis in splanchnic ischemia shock
Circulatory Shock
|January 1, 1986
Summary
Dazoxiben administration reduced shock in dogs after splanchnic artery occlusion by modulating thromboxane and prostacyclin levels. This treatment also mitigated tissue damage and hemodynamic deterioration, suggesting a protective effect.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
- Gastrointestinal Surgery
Background:
- Splanchnic artery occlusion (SAO) leads to shock and tissue damage.
- Eicosanoids play a critical role in the response to ischemia and reperfusion injury.
Purpose of the Study:
- To investigate the effects of dazoxiben on eicosanoid levels and outcomes following SAO in dogs.
- To explore the relationship between eicosanoid metabolism, tissue damage, and hemodynamic changes after SAO.
Main Methods:
- Dogs were subjected to a 3-hour splanchnic artery occlusion (SAO).
- Dazoxiben was administered (5 mg/kg, i.v.) prior to SAO.
- Plasma concentrations of thromboxane, prostacyclin, prostaglandin E2, and beta-glucuronidase were measured.
- Hemodynamic parameters were monitored throughout the study.
Main Results:
- Dazoxiben suppressed plasma thromboxane concentrations and reduced the incidence of shock post-SAO.
- Pretreatment with dazoxiben moderated increases in plasma prostacyclin but augmented prostaglandin E2 after SAO release.
- Alterations in eicosanoid metabolism correlated with moderated increases in plasma beta-glucuronidase activity, indicating reduced tissue damage.
- Dazoxiben mitigated progressive hemodynamic deterioration following SAO.
Conclusions:
- Dazoxiben demonstrates a protective effect against shock and tissue damage induced by SAO in dogs.
- Modulation of eicosanoid metabolism by dazoxiben is linked to improved outcomes after splanchnic ischemia.
- Findings suggest a causal relationship between eicosanoid levels, splanchnic tissue injury, and circulatory failure.