AJP - Heart and Circulatory Physiology, Vol 253, Issue 6 1349-H1357, Copyright © 1987 by American Physiological Society
Decreased lymphatic pumping after intravenous endotoxin administration in sheep
R. M. Elias, M. G. Johnston, A. Hayashi and W. Nelson
Department of Pathology, University of Toronto, Ontario, Canada.
The effects of endotoxin on the ability of lymphatic vessels to pump fluid
in vivo have been assessed with the use of a sheep model system that
permits analysis of lymph pumping in sheep without the complication of
variable lymph inputs. This involved the isolation of intestinal lymphatic
vessels from all lymph input, with saline or lymph provided from a
reservoir. The blood and nerve supplies to the vessel were left intact.
With no net driving pressure, but with a transmural pressure applied to the
vessel to initiate spontaneous contractions and fluid pumping, the
intravenous administration of endotoxin (3.3 micrograms/kg in anesthetized
sheep and 33 micrograms/kg in nonanesthetized animals) reduced fluid
propulsion in both groups of animals (P less than 0.02 and P less than
0.03, respectively). Comparisons with animals that did not receive
endotoxin revealed maximum inhibition greater than 90% in anesthetized and
50% in nonanesthetized sheep. Normal pulsatile lymphatic pressures
(produced from lymphatic contractions) were reduced in frequency and
amplitude after endotoxin administration. Endotoxin itself had no effect on
the vessels when added to the fluid in the reservoir, suggesting that the
inhibition of the "lymph pump" was mediated through the interaction of
endotoxin with cellular or humoral elements in the host. In addition to
suppression of lymphatic contractile activity, the intravenous injection of
endotoxin enhanced lymph formation as indicated by the 3- to 10-fold
increases in lymph flow rates in the two groups. We conclude that, for a
given transmural pressure, the systemic administration of endotoxin reduces
lymphatic pumping activity. We speculate that this effect may be important
in the pathogenesis of the edema associated with sepsis.
