Tuberc Respir Dis.  2003 May;54(5):522-531. 10.4046/trd.2003.54.5.522.

Aspirin Reduces Acute Lung Injury in Rats Subjected to Severe Hemorrhage

Affiliations
  • 1Department of Internal Medicine, Catholic University of Daegu, Daegu, Korea.
  • 2Department of Physiology, Catholic University of Daegu, Daegu, Korea. yypark@cataegu.ac.kr

Abstract

BACKGROUND: Hemorrhagic shock and trauma are two of the most common causes of acute lung injury. The activation of cyclooxygenase is one of the important causes of acute lung injury. This study investigated the effect of aspirin, a well-known cyclooxygenase inhibitor, on severe hemorrhage-induced acute lung injury in rats.
METHODS
The hemorrhagic shock was induced by withdrawing blood; 20ml/kg of B.W., through the femoral artery in 5 min. The mean arterial pressure was recorded through the femoral artery on a polygraph.
RESULTS
In the present investigation, the lung tissue myeloperoxidase activity, protein contents and leukocyte counts, in bronchoalveolar lavage fluid, increased significantly 2 and 24 h after the hemorrhage induction. Although the decreased mean arterial pressure spontaneously recovered, acute lung injury occurred after severe hemorrhage. These changes were effectively prevented by a single intravenous injection of aspirin (10 mg/kg of B.W.) 30 min before the hemorrhage.
CONCLUSION
These results suggest that severe hemorrhage-induced acute lung injury is mediated, in part, by the activation of cyclooxygenase. Furthermore, pretreatment of aspirin in acute lung injury-prone patients, or prophylactic treatment of aspirin to the patients with precipitating conditions, could be helpful in the prevention of acute lung injury.

Keyword

Hemorrhage; Acute lung injury; Aspirin; Cyclooxygenase

MeSH Terms

Acute Lung Injury*
Animals
Arterial Pressure
Aspirin*
Bronchoalveolar Lavage Fluid
Femoral Artery
Hemorrhage*
Humans
Injections, Intravenous
Leukocyte Count
Lung
Peroxidase
Prostaglandin-Endoperoxide Synthases
Rats*
Shock, Hemorrhagic
Aspirin
Peroxidase
Prostaglandin-Endoperoxide Synthases
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