Journal of Applied Physiology, Vol 62, Issue 3 863-869, Copyright © 1987 by American Physiological Society
CVF-induced decomplementation: effect on lung transvascular protein flux after thrombin
A. Johnson, S. K. Lo, F. B. Blumenstock and A. B. Malik
We examined the effects of cobra venom factor (CVF) on the changes in
pulmonary hemodynamics and transvascular fluid and protein exchange
following thrombin-induced pulmonary microembolism. Studies were made in
unanesthetized sheep prepared with lung lymph fistulas. The animals
received tranexamic acid (100 mg) to suppress fibrinolysis and were then
challenged with an intravenous infusion of alpha-thrombin (80 U/kg).
Control-thrombin challenged sheep were compared with the CVF-treated sheep
challenged with the same thrombin dosage. CVF treatment (187 U X kg-1 X
day-1 for 4 days) decreased the total hemolytic complement activity by 45%
of control. Thrombin infusion in control sheep increased the mean pulmonary
arterial pressure (Ppa), pulmonary vascular resistance (PVR), and lymph
protein clearance (pulmonary lymph flow X lymph-to-plasma protein
concentration ratio, Clym). Thrombin infusion in CVF-treated sheep produced
smaller increments in Ppa, PVR, and Clym. Pulmonary lymph obtained from
control-thrombin and CVF-thrombin sheep induced migration of granulocytes
obtained from normal unchallenged sheep. The granulocytes obtained from
CVF-treated sheep responded relatively less to the migratory and
O-2-generating stimuli (i.e., zymosan-treated serum, pulmonary lymph from
sheep after thrombin challenge, and plasma from sheep after CVF treatment)
compared with normal granulocytes. The attenuation of the thrombin-induced
increases in Ppa, PVR, and lung transvascular fluid and protein exchange by
CVF treatment may be the result of impaired function of granulocytes.
