title: Beneficial effects of hydrocortisone and papaverine on a model of pulmonary embolism induced by autologous blood clots in isolated and perfused rabbit lungs.
abstract: OBJECTIVE
  Mechanical obstruction has been considered the prime determinant of haemodynamic changes after pulmonary embolism (PE); however, the function of vasoconstrictive and inflammatory mediators in the physiopathology of this disease is unclear. The aim of this investigation was to study the effect of an anti-inflammatory and a vasodilator in a setting of induced PE.
  
  
  METHODS
  A prospective, laboratory study was undertaken using 30 New Zealand white rabbits. A model of isolated and perfused rabbit lungs was used; PE was induced using autologous blood clots. Six study groups were established (each n = 5): PE without any drug (PG); PE + papaverine (PpG); PE + hydrocortisone (HG); PE in West's Zone III (ZIIIG); PE using acellular perfusate (AG) and PE using acellular perfusate + papaverine (APpG). The pulmonary artery pressure (PAP) and fluid filtration rate (FFR) were continuously measured during the experiments.
  
  
  RESULTS
  Increases in PAP and oedema formation were observed in the PG after embolization. The PpG and the APpG showed neither oedema nor significant PAP increases. The HG group developed less oedema and less increase in PAP compared with the PG. The ZIIIG developed oedema the fastest. The AG developed less oedema and increases in PAP compared with the PG.
  
  
  CONCLUSIONS
  These findings suggest that vasoconstriction and inflammatory mediators play an important role in the physiopathology of PE, as neither PAP increases nor oedema were observed in the PpG and a reduction of oedema and PAP was seen in the HG group. The decrease in oedema and PAP in the acellular group strongly suggests a key role of circulating blood cells.
authors.affiliation: Section of Respiratory Physiology, Experimental Medicine Institute, Central University of Venezuela, Caracas, Venezuela.
authors.forename: Humberto E
authors.initials: HE
authors.lastname: Trejo
authors.forename: Daniela
authors.initials: D
authors.lastname: Urich
authors.forename: Alejandro A
authors.initials: AA
authors.lastname: Pezzulo
authors.forename: Juan C
authors.initials: JC
authors.lastname: Caraballo
authors.forename: Jeydith
authors.initials: J
authors.lastname: Gutiérrez
authors.forename: Ignacio J
authors.initials: IJ
authors.lastname: Castro
authors.forename: Greenmy R
authors.initials: GR
authors.lastname: Centeno
authors.forename: Roberto
authors.initials: R
authors.lastname: Sánchez de León
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D004195:Disease Models, Animal; D006439:Hemodynamics; D006854:Hydrocortisone / Q000494:pharmacology*; D066298:In Vitro Techniques; D010208:Papaverine / Q000494:pharmacology*; D011446:Prospective Studies; D011654:Pulmonary Edema / Q000503:physiopathology; D011655:Pulmonary Embolism / Q000503:physiopathology*; D011817:Rabbits; D015656:Respiratory Mechanics; D014661:Vasoconstriction / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D000893:Anti-Inflammatory Agents; D014665:Vasodilator Agents; D010208:Papaverine; D006854:Hydrocortisone