title: [Effect of hypocapnia/alkalosis on the fluid filtration rate in isolated and perfused rabbit lungs].
abstract: Hypocapnia/alkalosis is a consequence of several lung and metabolic pathologies. The aim of this study was to determine whether the increase of fluid filtration rate (FFR) that occurs during Hypocapnia/alkalosis circumstances is determined by hypocapnia, alkalosis or both. 7 groups were formed (N=36) using isolated rabbit lungs. Group 1: Control (PCO2 6%, pH: 7.35-7.45); Group 2 (n=6): Hypocapnia/Alkalosis (CO2 1%, pH: 7.9); Group 3 (n=6): Hypocapnia/Normo-pH (CO2 1% pH 7.35-7.45), Group 4 (n=6) Normocapnia/Alcalosis (CO2 6%, pH: 7.9). Fenoterol, papaverine and hydrocortisone were added to Groups 5, 6 and 7 (n=4) respectively, all under Normocapnia/Alkalosis. FFR and Pulmonary Arterial Pressure (Pap) were considerably higher in group 2 than in control (FFR: 1.92g/min +/- 0.6 vs 0.0 g/min +/- 0.006). A strong influence exerted by pH was observed when Group 3 and group 4 were compared (FFR: 0.02 g/min +/- 0.009 vs 2.3 g/min +/- 0.9) and (Pap: 13.5 cmH2O +/- 1.4 vs 90 cmH2O +/- 15). A reduced effect was observed in groups 5 and 6 (papaverine and hydrocorisone) and a totally abolished effect was observed in group 7 (fenoterol) (FFR: 0.001 +/- 0.0003 mL/min and Pap: 14 +/- 0.8 cmH2O). Pulmonary edema induced by Hypocapnia/alkalosis is a consequence of alkalosis and not of hypocapnia. This effect could be due to inflammatory damage in the lung parenchyma and alkalosis-mediated vasoconstriction.
authors: Sección de Fisiología Respiratoria, Facultad de Medicina, Escuela de Medicina Luis Razetti, Universidad Central de Venezuela, Caracas, Venezuela.
authors: Daniela
authors: D
authors: Urich
authors: Humberto
authors: H
authors: Trejo
authors: Alejandro
authors: A
authors: Pezzulo
authors: Juan Carlos
authors: JC
authors: Caraballo
authors: Jeydith
authors: J
authors: Gutiérrez
authors: Ignacio
authors: I
authors: Castro
authors: Roberto
authors: R
authors: Sánchez-de León
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000471:Alkalosis / Q000150:complications / Q000503:physiopathology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D005280:Fenoterol / Q000494:pharmacology; D018495:Fluid Shifts / Q000187:drug effects / Q000502:physiology*; D006854:Hydrocortisone / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D016857:Hypocapnia / Q000150:complications / Q000503:physiopathology*; D008168:Lung / Q000098:blood supply / Q000187:drug effects / Q000503:physiopathology*; D010208:Papaverine / Q000494:pharmacology; D010477:Perfusion; D011651:Pulmonary Artery; D011654:Pulmonary Edema / Q000209:etiology / Q000503:physiopathology*; D011817:Rabbits; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000318:Adrenergic beta-Agonists; D000893:Anti-Inflammatory Agents; D014665:Vasodilator Agents; D005280:Fenoterol; D010208:Papaverine; D006854:Hydrocortisone