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AJP - Gastrointestinal and Liver Physiology, Vol 257, Issue 1 94-G98, Copyright © 1989 by American Physiological Society
ARTICLES |
B. S. Dunbar, J. R. Elk, R. E. Drake and G. A. Laine
Center for Microvascular and Lymphatic Studies, University of Texas Medical School, Houston 77030.
We used a circuit-model technique to analyze the flow from intestinal lymphatics. Postnodal lymph vessels from the small intestine were cannulated in five halothane-anesthetized dogs. We measured the flow rate from the cannula (QL) as we held the outflow end of the cannula at several heights above the site of cannulation. At each cannula height we calculated the pressure at the outflow end of the lymphatic (Po) as Po = QL X cannula resistance + height of the outflow end of the cannula above the cannulation site. Then we determined a best-fit regression line for QL vs. Po. The effective lymphatic resistance (RL) was estimated from the regression line as -delta Po/delta RL and the effective pressure driving lymph flow (PL) was taken as the Po at which QL = 0. At base line, RL = 0.039 +/- 0.018 (SD) cmH2O.min.microliters-1 and PL = 5.2 +/- 2.4 cmH2O. When we raised the portal venous pressure from 11.4 +/- 4.0 cmH2O (base line) to 34.4 +/- 9.0 cmH2O, RL decreased by only 26 +/- 11%, but PL rose by 160% to 13.6 +/- 8.7 cmH2O (P less than 0.05). Thus our data indicate that increases in portal venous pressure to 34.4 +/- 9.0 cmH2O cause intestinal lymph flow to increase primarily because of increases in the effective PL.
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