Journal of Applied Physiology, Vol 62, Issue 3 1068-1075, Copyright © 1987 by American Physiological Society
Role of lipids in bone marrow-induced pulmonary edema
W. M. Selig, K. E. Burhop and A. B. Malik
We examined the mechanism of the bone marrow-induced pulmonary edema in the
isolated Ringer-perfused rabbit lung. Bone marrow administration (0.2 ml/kg
body wt) increased pulmonary arterial pressure, capillary pressure,
arterial resistance, and venous resistance within 2-4 min. Bone marrow also
produced marked increases in lung wet weight and the capillary filtration
coefficient but at later time points (90-120 min) during the perfusion.
Only the triglyceride-containing lipid component of the bone marrow
produced increases in pulmonary hemodynamics, lung wet weight, and the
capillary filtration coefficient comparable to those observed after bone
marrow. Bone marrow and the lipid component of bone marrow both produced
increases in venous effluent lipoprotein lipase activity (the enzyme
responsible for hydrolysis of triglycerides to free fatty acids). Bone
marrow also stimulated the production of thromboxane B2 but not
6-ketoprostaglandin F1 alpha in the perfused lung. Both meclofenamate (1
microM), a cyclooxygenase inhibitor, and U-60,257 (10 microM), a
lipoxygenase inhibitor, attenuated the bone marrow-induced pulmonary
hemodynamic response, whereas only U-60,257 attenuated the increases in
lung wet weight and the capillary filtration coefficient. In conclusion,
pulmonary embolization induced by bone marrow results in increases in lung
weight and the capillary filtration coefficient in the isolated
Ringer-perfused rabbit lung. Pulmonary vasoconstriction is partially
dependent on arachidonic acid metabolites but appears to be independent of
circulating blood-formed elements. The lipid component of bone marrow or
products derived from this component (e.g., free fatty acids and
lipoxygenase products) may mediate the bone marrow-induced pulmonary edema.
