title: Inflammatory activation after experimental cardiac tamponade.
abstract: OBJECTIVE
  Cardiac tamponade is a medical emergency situation associated with a high rate of life-threatening complications, even after immediate interventions. Our aim was to characterize the acute inflammatory consequences of this event in a clinically relevant large animal model.
  
  
  METHODS
  Cardiac tamponade was induced for 60 min in anesthetized, ventilated and thoracotomized minipigs by intrapericardial fluid administration, the mean arterial pressure (MAP) being maintained in the interval of 40-45 mm Hg (n = 8). A further group (n = 7) served as sham-operated control. The global macrohemodynamics, including the right- and left-heart end-diastolic volumes (RHEDV and LHEDV), the pulmonary vascular resistance index (PVRI) and the superior mesenteric artery (SMA) flow, were monitored for 240 min, and the intestinal microcirculatory changes (pCO2 gap) were evaluated by indirect tonometry. Blood samples were taken for the determination of cardiac troponin T and vasoactive inflammatory mediators, including histamine, nitrite/nitrate, big-endothelin, superoxide and high-mobility group box protein-1 levels in association with intestinal leukocyte and complement activation.
  
  
  RESULTS
  The cardiac tamponade induced significant decreases in MAP, cardiac output, LHEDV and SMA flow, while the PVRI and the pCO2 gap increased significantly. After the removal of fluid from the pericardial sac, the MAP and the LHEDV were decreased, while the PVRI and the pCO2 gap remained elevated when compared with those in the sham-operated group. In the posttamponade period, the abrupt release of inflammatory mediators was accompanied by a significant splanchnic leukocyte accumulation and complement activation.
  
  
  CONCLUSIONS
  The macrocirculatory and splanchnic microcirculatory disturbances were accompanied by a significant proinflammatory reaction; endothelin and the complement system may be significant components of the inflammatory cascade that is activated in this porcine model of pericardial tamponade.
authors.affiliation: Institute of Surgical Research, University of Szeged, Szeged, Hungary.
authors.forename: A
authors.initials: A
authors.lastname: Vass
authors.forename: G
authors.initials: G
authors.lastname: Süveges
authors.forename: D
authors.initials: D
authors.lastname: Érces
authors.forename: M
authors.initials: M
authors.lastname: Nógrády
authors.forename: G
authors.initials: G
authors.lastname: Varga
authors.forename: I
authors.initials: I
authors.lastname: Földesi
authors.forename: M
authors.initials: M
authors.lastname: Futakuchi
authors.forename: M
authors.initials: M
authors.lastname: Imai
authors.forename: N
authors.initials: N
authors.lastname: Okada
authors.forename: H
authors.initials: H
authors.lastname: Okada
authors.forename: M
authors.initials: M
authors.lastname: Boros
authors.forename: J
authors.initials: J
authors.lastname: Kaszaki
mesh_terms: D000818:Animals; D002305:Cardiac Tamponade / Q000276:immunology* / Q000503:physiopathology; D003167:Complement Activation; D019332:Endothelin-1 / Q000097:blood; D005260:Female; D024243:HMGB1 Protein / Q000097:blood; D006439:Hemodynamics; D007249:Inflammation / Q000209:etiology*; D008297:Male; D009569:Nitric Oxide / Q000097:blood; D013552:Swine; D013556:Swine, Miniature
chemical_list: D019332:Endothelin-1; D024243:HMGB1 Protein; D009569:Nitric Oxide