title: Endotoxin-induced heart dysfunction in rats: assessment of myocardial perfusion and permeability and the role of fluid resuscitation.
abstract: OBJECTIVE
  The pathophysiology of sepsis-induced myocardial dysfunction is still controversial. Whether microcirculatory hypoperfusion together with capillary leakage can occur in the heart wall also remains a matter of debate. The objective was to evaluate the impact of fluid resuscitation on endotoxin-induced myocardial dysfunction.
  
  
  METHODS
  Adult rats were given intraperitoneal injection of endotoxin (lipopolysaccharide, Escherichia coli, 10 mg/kg) or phosphate-buffered solution, followed up by echocardiography and acetate micro-positron emission tomography scan imaging, together with final hemodynamic, biochemical, and pathologic evaluations up to 48 hrs.
  
  
  METHODS
  University laboratory.
  
  
  METHODS
  Pathogen-free male Wistar rats (350 g).
  
  
  METHODS
  Influence of isovolumic fluid infusion type (saline vs. pentastarch) on these variables was assessed in 11 groups of six animals including an unchallenged control one.
  
  
  RESULTS
  Endotoxin injection induced a) myocardial dysfunction (decrease of approximately 15-20% in left ventricular ejection fraction); b) ventricular enlargement (approximately 1.5- to 1.7-fold increase in left ventricular systolic volume); c) cardiac output increase (10-15%); d) myocardial hypoperfusion ( approximately 1.5- to 2-fold decrease in acetate k1 constant rate); e) increased oxygen consumption (k2); and f) interstitial wall increase. Endotoxin injection also enhanced levels of arterial lactates and troponin I. Colloid (pentastarch) over crystalloid (saline) fluid resuscitation significantly reversed echocardiographic changes, some positron emission tomography imaging alterations, and lactate and troponin I levels without further enhancing interstitial spaces.
  
  
  CONCLUSIONS
  Endotoxin can induce reversible myocardial alterations with evidence of coronary hypoperfusion and heart wall enlargement/damage, some of which can be prevented by fluid resuscitation. The use of crystalloids is less beneficial than pentastarch.
authors.affiliation: Groupe de Recherche en Physiopathologie Respiratoire, Université de Sherbrooke, PQ, Canada.
authors.forename: Frederic
authors.initials: F
authors.lastname: Chagnon
authors.forename: M'hamed
authors.initials: M
authors.lastname: Bentourkia
authors.forename: Roger
authors.initials: R
authors.lastname: Lecomte
authors.forename: Michel
authors.initials: M
authors.lastname: Lessard
authors.forename: Olivier
authors.initials: O
authors.lastname: Lesur
mesh_terms: D000818:Animals; D009202:Cardiomyopathies / Q000473:pathology* / Q000628:therapy*; D004195:Disease Models, Animal; D004731:Endotoxins; D005440:Fluid Therapy / Q000379:methods*; D006334:Heart Function Tests; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D010477:Perfusion; D010539:Permeability; D049268:Positron-Emission Tomography; D011336:Probability; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values; D012151:Resuscitation / Q000379:methods; D012680:Sensitivity and Specificity; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000503:physiopathology
chemical_list: D004731:Endotoxins