title: Increased platelet microvesicle formation is associated with mortality in a porcine model of endotoxemia.
abstract: BACKGROUND
  Gram-negative sepsis in humans and endotoxemia in pigs induce the formation of platelet microvesicles. These microvesicles are active in homeostasis and may thus contribute to the outcome in patients with activated coagulation and fibrinolysis. We decided to prospectively evaluate the effects of endotoxemia on microvesicle formation and some common physiologic variables against survival in a porcine model.
  
  
  METHODS
  Nineteen included pigs were anesthetized, monitored and subjected to an infusion of E. coli endotoxin. Microvesicle formation was determined by flow cytometry.
  
  
  RESULTS
  The formation of microvesicles was significantly increased in the 6 pigs that died during endotoxin exposure. This increased formation became significant from the 3rd hour of endotoxemia. Microvesicle formation did not increase in surviving endotoxemic pigs. Cardiac index, mean arterial blood pressure, base excess and systemic vascular resistance index were distinctly reduced in the animals that died as compared to those surviving the endotoxemic period.
  
  
  CONCLUSIONS
  The increased formation of platelet microvesicles seems to be associated with poor prognosis in porcine endotoxemia. Since microvesicles are active in coagulation, they may contribute to the derangement of the coagulation system caused by endotoxemia. Different degrees of microvesicle formation may reflect inter-individual responses to a given challenge.
authors.affiliation: Department of Anesthesiology & Intensive Care, University Hospital, Uppsala, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Eriksson
authors.forename: D
authors.initials: D
authors.lastname: Nelson
authors.forename: A
authors.initials: A
authors.lastname: Nordgren
authors.forename: A
authors.initials: A
authors.lastname: Larsson
mesh_terms: D000138:Acidosis / Q000503:physiopathology; D000471:Alkalosis / Q000503:physiopathology; D000818:Animals; D001777:Blood Coagulation / Q000502:physiology; D001792:Blood Platelets / Q000502:physiology / Q000648:ultrastructure*; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D004195:Disease Models, Animal; D019446:Endotoxemia / Q000097:blood* / Q000503:physiopathology; D004927:Escherichia coli Infections / Q000097:blood* / Q000503:physiopathology; D005260:Female; D005342:Fibrinolysis / Q000502:physiology; D005434:Flow Cytometry; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D008297:Male; D015539:Platelet Activation / Q000502:physiology*; D011379:Prognosis; D011446:Prospective Studies; D012772:Shock, Septic / Q000097:blood* / Q000503:physiopathology; D015996:Survival Rate; D013552:Swine; D013997:Time Factors; D014617:Vacuoles / Q000502:physiology / Q000648:ultrastructure; D014655:Vascular Resistance / Q000502:physiology