Effect of heparin or fibrinogen depletion on lung fluid balance in sheep after emboli.
Investigators have proposed that fibrinogen, fibrin, or their degradation products are essential for the increased lung vascular permeability to fluid and protein that may occur after microemboli. To test this hypothesis, we used 20 anesthetized ventilated sheep in which we measured lung lymph flow, pulmonary artery and left atrial pressures, thermodilution cardiac output, and lymph/plasma protein concentrations. We injected glass bead microemboli (200 micrometers diam) sufficient to raise pulmonary vascular resistance to three times base-line values and cause increased lung lymph flow with a parallel increase in protein clearance, which is characteristic of increased lung vascular permeability. Neither large doses of heparin (3,000 U/kg) nor fibrinogen depletion with viper venom (ancrod, 2 U/kg), by themselves, affected steady-state pulmonary hemodynamics or lung fluid balance. These treatments prior to giving sufficient amounts of emboli to triple the pulmonary vascular resistance did not prevent the increased lung vascular permeability. We conclude that neither fibrin deposition nor degradation are essential to microembolic lung vascular injury in sheep.
D000721:Ancrod; D000818:Animals; D002199:Capillary Permeability; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism*; D006493:Heparin / Q000627:therapeutic use*; D008168:Lung / Q000098:blood supply; D011655:Pulmonary Embolism / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D012756:Sheep
D005338:Fibrin Fibrinogen Degradation Products; D005340:Fibrinogen; D006493:Heparin; D000721:Ancrod