Bronchial blood flow and eicosanoid blockade following airway acid aspiration

Joseph C. Stothert, G. B. Gbaanador, Jessie Basadre, John Flynn, Lillian Traber, Daniel Traber

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

The systemic circulation to the lung is thought to be an important microvascular exchange region which may contribute to pulmonary edema resulting from airway injury. In a chronic sheep model, we have evaluated the flow through the bronchial artery after airway injury caused by the aspiration of 2.5 ml/kg of 0.1 N hydrochloric acid with and without inhibition of thromboxane synthetase and cyclooxygenase. Cyclooxygenase inhibition with ibuprofen resulted in no rise in bronchial artery blood flow associated with airway acid aspiration (9.8 ± 1.72 ml/min to 63.7 ± 8.9 ml/min in the control group versus 11.3 ± 2.5 ml/min to 10.3 ± 3.4 ml/min in the ibuprofen group). No difference in bronchial artery blood flow was noted between control acid aspiration and acid aspiration with thromboxane synthetase inhibition. Significant early reduction in lung lymph flow was noted in the cyclooxygenase inhibition group compared to control. These data suggest that inhibition of the cyclooxygenase pathway of eicosanoid production may lessen the injury caused by airway acid aspiration. The decrease in airway blood flow with associated reduction in lymph flow suggests that airway blood flow may be important in the generation of pulmonary edema in this model.

Original languageEnglish (US)
Pages (from-to)1483-1488
Number of pages6
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume30
Issue number12
DOIs
StatePublished - Dec 1990

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine

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