Prior exposure to endotoxin exacerbates lipopolysaccharide-induced hypoxemia and alveolitis in anesthetized swine

We sought to determine whether a standardized "priming" event, namely a small dose of LPS, would alter physiological responses to a subsequent larger "challenge" dose of endotoxin. Accordingly, four groups of pigs (N = 5-6) were studied. One group received neither priming nor cha...

Full description

Saved in:

Bibliographic Details
Published in:	Shock (Augusta, Ga.) Ga.), 1994-11, Vol.2 (5), p.362
Main Authors:	Wollert, P S, Menconi, M J, Wang, H, O'Sullivan, B P, Larkin, V, Allen, R C, Fink, M P
Format:	Article
Language:	eng
Subjects:	6-Ketoprostaglandin F1 alpha - blood Animals Blood Pressure Bronchoalveolar Lavage Fluid Cardiac Output Drug Administration Schedule Endotoxins - administration & dosage Endotoxins - toxicity Hypoxia - blood Hypoxia - chemically induced Hypoxia - physiopathology Lipopolysaccharides - administration & dosage Lipopolysaccharides - toxicity Male Oxygen - blood Partial Pressure Premedication Pulmonary Fibrosis - blood Pulmonary Fibrosis - physiopathology Shock, Septic - blood Shock, Septic - physiopathology Swine Thromboxane B2 - blood Time Factors Tumor Necrosis Factor-alpha - analysis Vascular Resistance
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	We sought to determine whether a standardized "priming" event, namely a small dose of LPS, would alter physiological responses to a subsequent larger "challenge" dose of endotoxin. Accordingly, four groups of pigs (N = 5-6) were studied. One group received neither priming nor challenge doses of LPS. A second group were not primed but were infused with a challenge dose (250 micrograms/kg) of LPS. A third group were pretreated 18 h before being studied with a priming dose of LPS (20 micrograms/kg), but were not infused with a second dose of LPS. A fourth group received both priming and challenge doses of LPS. Priming with LPS exacerbated endotoxin-induced arterial hypoxemia, and decreased animal-to-animal variability in the degree of hypoxemia induced by a challenge dose of endotoxin. Priming blunted the early phase (30 min) and exacerbated the delayed phase (120-210 min) of LPS-induced pulmonary hypertension. Priming blunted LPS-induced release of prostacyclin and thromboxane A2. The use of a priming dose of LPS increases the severity and reproducibility of LPS-induced acute lung injury in swine.
ISSN:	1073-2322 1540-0514