Re. Drake et al., LYMPH-FLOW IN SHEEP WITH RAPID CARDIAC VENTRICULAR PACING, American journal of physiology. Regulatory, integrative and comparative physiology, 41(5), 1997, pp. 1595-1598
Increases in systemic venous pressure (P-V) associated with heart fail
ure cause an increase in microvascular fluid filtration into the tissu
e spaces. By removing this excess filtrate from the tissues, lymphatic
vessels help to prevent edema. However, the lymphatics drain into sys
temic veins and an increase in P-V may interfere with lymphatic flow.
To test this, we cannulated caudal mediastinal node efferent lymphatic
s in sheep. We used rapid cardiac ventricular pacing (240-275 beats/mi
n) to cause heart failure for 4-7 days. Each day we determined the lym
ph flow rate two ways. First, we adjusted the lymph cannula height so
that the pressure at the outflow end of the lymphatic was zero. After
we determined the lymph flow with zero outflow pressure, we raised the
cannula so that outflow pressure was equal to the actual venous press
ure. We quantitated the effect of venous pressure on lymph flow rate b
y comparing the flow rate with outflow pressure=P-V to the flow rate w
ith zero outflow pressure. At baseline, P-V=5.0+/-2.5 (SD) cmH(2)O and
we found no difference in the two lymph flow rates. Pacing caused P-V
and both lymph flow rates to increase significantly. However for P-V
<15 cmH(2)O, we found little difference in the two lymph flow rates. T
hus increases in P-V to 15 cmH(2)O at the outflow to the lymphatics ha
d little effect on lymph flow. By comparison, P-V >15 cmH(2)O slowed l
ymph flow by 55+/-29% relative to the lymph flow rate with zero outflo
w pressure. Thus P-V values >15 cmH(2)O interfere with lymph flow from
the sheep caudal mediastinal lymph node.