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Pulmonary artery endothelial cell function in swine pseudomonas sepsis
M Kadletz1, R J Dignan, P G Mullen
1Department of Surgery, Medical College of Virginia-Virginia Commonwealth University, Richmond 23298-0645, USA.
The Journal of Surgical Research
|January 1, 1996
Summary
Sepsis significantly impairs pulmonary artery endothelial cells' response to acetylcholine, independent of pulmonary hypertension. This study reveals sepsis-induced endothelial cell injury affecting vasoreactivity in pulmonary arteries.
Area of Science:
- Pulmonary Medicine
- Sepsis Research
- Vascular Biology
Background:
- Sepsis substantially increases pulmonary vascular resistance.
- This increase may stem from endothelial cell injury or altered vasoreactivity due to pulmonary hypertension.
Purpose of the Study:
- To test if sepsis causes endothelial cell injury.
- To determine if increased pulmonary pressure alters vascular reactivity.
Main Methods:
- Young swine underwent Pseudomonas aeruginosa sepsis or saline control infusion.
- Pulmonary artery segments were tested in a myograph at varying pressures.
- Vessel responses to acetylcholine, bradykinin, and sodium nitroprusside were measured.
Main Results:
- Sepsis decreased maximal contraction to potassium but not prostaglandin.
- Bradykinin-induced nitric oxide production was unaffected by sepsis.
- Acetylcholine-induced relaxation was significantly reduced in septic animals.
- Vessel reactivity was not altered by simulated pulmonary hypertension.
Conclusions:
- Sepsis induces endothelial cell dysfunction in pulmonary arteries.
- This dysfunction involves altered receptor sensitivity to acetylcholine.
- Pulmonary hypertension does not appear to drive this sepsis-induced endothelial cell alteration.