Intravascular and peritoneal coagulation and fibrinolysis in horses with acute gastrointestinal tract diseases.
Components of the coagulation and fibrinolytic cascades, prothrombin and activated partial thromboplastin times, endotoxin activity, and albumin concentration were measured in blood and peritoneal fluid from 20 healthy horses and from 153 horses with acute gastrointestinal tract diseases at admission. Overall, 77% (117/153) of affected horses survived to discharge from the hospital, and 85% (82/97) of horses discharged were reported to be normal 9 to 14 months later. Significant differences in hemostatic factors were more common in peritoneal fluid than in blood. Tissue plasminogen activator, plasminogen, protein C, antithrombin III, and alpha 2-antiplasmin activities and concentrations of fibrinogen and fibrin degradation products were significantly (P < 0.05) greater in peritoneal fluid from horses with colic, and, with the exception of fibrinogen concentration, were associated with detection of endotoxin. Higher values for these variables, except tissue plasminogen activator activity, were significantly (P < 0.05) associated with survival. Plasminogen, antithrombin III, and alpha 2-antiplasmin activities were significantly (P < 0.05) greater in peritoneal fluid from horses with inflammatory or strangulating lesions, compared with those in horses with simple colic. Plasminogen-activator inhibitor type 1 activity, fibrin degradation products concentration, and prothrombin time were significantly (P < 0.05) greater in the blood of horses with colic. Survival was inversely associated with significantly (P < 0.05) greater intravascular concentrations of fibrin degradation products and fibrinogen and prothrombin time. This study revealed marked contrasts between peritoneal and intravascular coagulation and fibrinolysis in horses with colic, indicating that inferences regarding the peritoneal environment, particularly with respect to fibrinolytic capacity, should not be made on the basis of factors measured in blood.
Collatos
C
C
Department of Large Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens 30602, USA.
Barton
M H
MH
Prasse
K W
KW
Moore
J N
JN
D000818:Animals; D000990:Antithrombin III / Q000032:analysis; D001202:Ascitic Fluid / Q000097:blood / Q000737:chemistry / Q000662:veterinary*; D001777:Blood Coagulation; D001780:Blood Coagulation Tests / Q000662:veterinary; D003085:Colic / Q000097:blood / Q000662:veterinary; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D005342:Fibrinolysis; D005500:Follow-Up Studies; D005767:Gastrointestinal Diseases / Q000097:blood / Q000662:veterinary*; D006487:Hemostasis; D006734:Horse Diseases / Q000097:blood*; D006736:Horses; D010958:Plasminogen / Q000032:analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D012189:Retrospective Studies; D010959:Tissue Plasminogen Activator / Q000032:analysis; D000979:alpha-2-Antiplasmin / Q000032:analysis
D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; D000979:alpha-2-Antiplasmin; D000990:Antithrombin III; D005340:Fibrinogen; D010958:Plasminogen; D010959:Tissue Plasminogen Activator