Ancrod prevents vascular occlusion in thermally injured rats.
Predictable vascular responses to burn injury can occur where blood vessels are occluded in and just beneath the site of trauma. The loss of vascular patency is linked to the development of ischemia in the surrounding skin. Several mechanisms may be responsible for this occlusion, and their identification will provide a logical means for prevention or reversal of the occlusion. The role of fibrin deposition was investigated here using a rat burn model. If an intravascular fibrin clot is a primary cause of early occlusion, the depletion of circulating fibrinogen should prevent its deposition. Ancrod, a pit viper venom trypsin-like proteinase, when given systemically, converts fibrinogen into a soluble product which does not clot. In studies here, the host is depleted of fibrinogen by intravenous injections of ancrod for 3 days before standard burn trauma. Burn injury in defibrinogenized rats resulted in greatly reduced local vascular occlusion. These results support the idea that vascular occlusion caused by burn injury is dependent on the deposition of fibrin. It is conjectured that the vascular occlusion of burn injury can be reversed by preventing or breaking down intravascular fibrin clots.
D000721:Ancrod / Q000627:therapeutic use*; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000517:prevention & control*; D002056:Burns / Q000473:pathology / Q000503:physiopathology*; D005337:Fibrin / Q000032:analysis; D007511:Ischemia / Q000517:prevention & control; D008297:Male; D008955:Models, Cardiovascular; D051381:Rats; D011919:Rats, Inbred Strains; D012867:Skin / Q000098:blood supply / Q000293:injuries* / Q000473:pathology; D014654:Vascular Patency / Q000187:drug effects
D005337:Fibrin; D000721:Ancrod