[Effect of changes in airway pressure and the inspiratory volume on the fluid filtration rate and pulmonary artery pressure in isolated rabbit lungs perfused with blood and acellular solution].
It has been reported that ventilation with large tidal volumes causes pulmonary edema in rats by the stimulation and release of proinflammatory mediators. Our objective was to determine the level at which volutrauma induced by changes in Airway Pressure (PAW) and Inspiratory Volume (VI) produce significant changes on the Fluid Filtration Rate (FFR) and Pulmonary Artery Pressure (PAP) in lungs perfused with blood (cellular groups) or with a buffer-albumin solution (acellular groups), with a Positive End Expiratory Pressure (PEEP) 0 or 2 cmH2O and to study the effect of a vasodilator with antiinflammatory properties (fenoterol) in blood-perfused groups. Three experimental groups were used: the cellular groups studied the effect of increased PAW and IV in isolated lungs perfused with blood and PEEP 0 and 2; the acellular groups studied the increased PAW and IV in isolated lungs perfused with a buffer-albumin solution and PEEP 0 and 2; The fenoterol group studied the effect of increased PAW and IV in isolated lungs perfused with blood + fenoterol and PEEP 2. The results show that an increase of FFR is produced earlier in acellular groups than in cellular ones and that the damage in cellular groups is microscopically and macroscopically inferior when compared to acellular groups. Fenoterol did not inhibit edema formation, and that PEEP 2, both in the cellular and the acellular groups, has a protective effect. We propose the possible existence of mediators with protective effects against the formation of pulmonary edema in the blood. These data suggest that volutrauma induced pulmonary edema has a predominantly traumatic origin when the lungs are perfused with blood.
Crespo
Astrid
A
Laboratorio de Fisiología Respiratoria, Escuela de Medicina Luis Razctti, Facultad de Medicina, Universidad Central de Venezuela, Caracas, Venezuela.
Novoa
Eva
E
Urich
Daniela
D
Trejo
Humberto
H
Pezzulo
Alejandro
A
Sznajder
Jacob I
JI
Livia
Fernández
F
Sánchez-de León
Roberto
R
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D003627:Data Interpretation, Statistical; D004195:Disease Models, Animal; D005280:Fenoterol / Q000494:pharmacology; D005374:Filtration; D008168:Lung / Q000187:drug effects / Q000473:pathology; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors; D011175:Positive-Pressure Respiration / Q000009:adverse effects; D011651:Pulmonary Artery / Q000502:physiology*; D001261:Pulmonary Atelectasis / Q000209:etiology; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D011817:Rabbits; D015656:Respiratory Mechanics; D013990:Tidal Volume
D000318:Adrenergic beta-Agonists; D010972:Platelet Activating Factor; D005280:Fenoterol