The role of fibrin formation in the pathogenesis of bacteremic shock in the primate.
In this study, an attempt was made to elucidate further the role of intravascular fibrin formation in the pathogenesis of sepsis in the primate. It was found that injected live Escherichia coli caused death in primates within four to 11 hours as a result of microcirculatory failure and acidosis. Pretreatment with Arvin did not prolong the survival rate, probably because of an overloading of the reticuloendothelial system with fibrin degradation products. This study does not support an obligatory role for intravascular coagulation or fibrin formation in primate sepsis and coincides with an earlier report (6) from this laboratory on cats. Vascular damage and malfunction, secondary to mediators released by platelets, leukocytes, red cells or Hageman factor, are not ruled out.
D000721:Ancrod / Q000494:pharmacology; D000818:Animals; D001769:Blood; D001777:Blood Coagulation; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D004195:Disease Models, Animal; D004927:Escherichia coli Infections / Q000503:physiopathology; D005260:Female; D005337:Fibrin / Q000096:biosynthesis*; D000882:Haplorhini; D006339:Heart Rate; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000097:blood; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D010215:Papio; D012772:Shock, Septic / Q000097:blood / Q000209:etiology* / Q000503:physiopathology
D007773:Lactates; D002245:Carbon Dioxide; D005337:Fibrin; D000721:Ancrod; D010100:Oxygen