The Pulmonary Effect of Nitric Oxide Synthase Inhibition Following Endotoxemia in a Swine Model.
Abstract
Sepsis results in a systemic inflammatory response that is mediated by various cytokines and activated leukocytes. Systemic vasodilation and hypotension characteristic of sepsis have been hypothesized to occur secondarily to endogenous overproduction of nitric oxide (NO). In contrast to the systemic vasodilatory response, pulmonary vasoconstriction and pulmonary arterial hypertension caused by the release of potent vasoconstrictors usually occurs. Despite this pulmonary vasoconstrictive response, we and others have found that hypoxic pulmonary vasoconstriction (HPv) is blunted and blood flow to poorly and unventilated lung areas is maintained. This loss of the hypoxic vasoconstrictive response adversely affects pulmonary oxygenation by increasing the ventilation perfusion ratio (VA/Q) mismatching. Because respiratory failure following sepsis is a significant comorbid factor, therapy aimed at attenuating this deleterious process may exert a beneficial effect on outcome.
Document Details
- Document Type
- Technical Report
- Publication Date
- Dec 01, 1994
- Accession Number
- ADA297086
Entities
People
- Avery A. Johnson
- Bryan S. Jordan
- Datzo Saitoh
- Hiroshi Ogura
- Patrick J. Offner
Organizations
- United States Army Institute of Surgical Research