TY - JOUR
T1 - Cardiopulmonary responses to continuous administration of endotoxin
AU - Traber, D. L.
AU - Redl, H.
AU - Schlag, G.
AU - Herndon, D. N.
AU - Kimura, R.
AU - Prien, T.
AU - Traber, L. D.
PY - 1988
Y1 - 1988
N2 - The cardiopulmonary response to continuous administration of lipopolysaccharide (LPS) was studied in chronically instrumented sheep. LPS was administered in doses of 0 (sham), 6, 9, 12, and 24 ng·kg-1·h-1 for 24 h. No significant changes in the measured variables occurred in the sham group and in the 6 ng·kg-1·h-1-LPS group. With 9, 12, and 24 ng·kg-1·h-1-LPS, cardiac index rose and peripheral resistance fell to the same extent in all three groups. Lung lymph flow (Q(L)) increased with increasing concentration of LPS. These elevations in Q(L) occurred in the presence of only minor increases in the pulmonary artery pressure, which rose to the same extent in the 9, 12, and 24 ng·kg-1·h-1 groups. Consequently, the changes in Q(L) were attributable to changes in fluid conductance of the pulmonary microvasculature rather than variations in hydrostatic pressure. The increase in Q(L) correlated with a decrease in prekallikrein levels (r = 0.97), indicating that the changes in fluid conductance might have been kinin mediated.
AB - The cardiopulmonary response to continuous administration of lipopolysaccharide (LPS) was studied in chronically instrumented sheep. LPS was administered in doses of 0 (sham), 6, 9, 12, and 24 ng·kg-1·h-1 for 24 h. No significant changes in the measured variables occurred in the sham group and in the 6 ng·kg-1·h-1-LPS group. With 9, 12, and 24 ng·kg-1·h-1-LPS, cardiac index rose and peripheral resistance fell to the same extent in all three groups. Lung lymph flow (Q(L)) increased with increasing concentration of LPS. These elevations in Q(L) occurred in the presence of only minor increases in the pulmonary artery pressure, which rose to the same extent in the 9, 12, and 24 ng·kg-1·h-1 groups. Consequently, the changes in Q(L) were attributable to changes in fluid conductance of the pulmonary microvasculature rather than variations in hydrostatic pressure. The increase in Q(L) correlated with a decrease in prekallikrein levels (r = 0.97), indicating that the changes in fluid conductance might have been kinin mediated.
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M3 - Article
C2 - 3364588
AN - SCOPUS:0023951186
SN - 0002-9513
VL - 254
SP - 23/5
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 5
ER -