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Vol. 29. Issue 6.
Pages 264-269 (August - September 1993)
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Vol. 29. Issue 6.
Pages 264-269 (August - September 1993)
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Daño pulmonar difuso en la rata por la administración endovenosa del factor activador plaquetario
Diffuse pulmonary damage by intravenous administration of the platelet activator factor to the rat
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E. Novoa, G. Arenas
Departamentos de Medicina Experimental Norte, Facultad de Medicina, Universidad de Chile, Santiago, Chile
G. Varas*, M.E. Lathrop*, M.J. Oyarzún*
* Ciencias Preclínicas Oriente. Facultad de Medicina, Universidad de Chile, Santiago, Chile
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El factor activador plaquetario (PAF) ha sido propuesto como un posible intermediario en la patogénesis del síndrome de distrés respiratorio del adulto (SDRA).

Nuestro objetivo fue evaluar el papel del PAF como mediador de daño pulmonar y su efecto sobre el contenido de surfactante alveolar de ratas al ser administrado por vía endovenosa.

Se administró 8 μg de PAF/kg de peso corporal a 21 ratas Wistar de peso promedio 254±55 g (DS), sacrificadas al cabo de 1-4 y 24 horas. Como controles se utilizaron ratas sacrificadas en iguales tiempos, pero tratadas con NaCl 0,9% ev. En el lavado broncoalveolar (LBA) se determinó contenido de proteínas, fosfolípidos totales (PLT), fostatidilcolina disaturada (DSPC), recuento celular y actividad de las enzimas fosfatasa alcalina (F.Alc) y gama-glutamiltranspeptidasa (GGT). En cada serie se efectuó un estudio histológico y determinación de gases en sangre arterial antes y después de la administración de PAF.

La administración de PAF provocó una disminución del contenido de PLT y de DSPC que fue significativa (p < 0,05) al cabo de 1 y 4 horas. A las 4 horas hubo aumento del recuento celular del LBA, hiperventilación y lesiones histológicas leves. No se observaron cambios en el contenido de proteínas, ni en la actividad enzimática en ninguna de las series tratadas con PAF.

El PAF administrado por vía endovenosa en la rata, produce una disminución del contenido de surfactante alveolar, hecho que se acompaña de lesiones pulmonares leves aunque difusas.

The platelet activator factor (PAF) has been postulated as a likely mediator in the pathogenesis of adult respiratory distress syndrome (ARDS).

The aim of the present study was to assess the role of PAF as a mediator of pulmonary damage and its effect on alveolar surfactant content.

The effect of intravenous perfusion of PAF (8 μg/kg of body weight) was studied in 21 Wistar rats, with an average weight of 254±55g (SD). This serie was compared with control rats injected with NaCl 0.9% solution, at the end of 1-4 and 24 hours respectively. Total proteins, total phospholipid (TPL), disaturated phosphatidylcholine (DSPC), cell counting and enzymatic activity: alkaline phosphatase (P.alc) and gammaglutamyltranspeptidase (GGT) were analyzed in the bronchoalveolar lavage (BAL). In each experimental series an histologic study and determinations of arterial blood gases before and after the intravenous administration of PAF were carried out.

The administration of PAF caused a decrease of TPL and DSPC contents at the end of 1 and 4 hours (p < 0.05). An increase in cell counting, hyperventilation and slight histologic lesions of the lung 4 hours after administering PAF were also observed. However, none significant changes were found in these experiments in total proteins ñor in enzymatic activity from bronchoalveolar lavage.

It is concluded that the intravenous administration of PAF in rats produced a decrease in the alveolar surfactant content which was associated to slight but diffuse pulmonary lesions.

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Copyright © 1993. Sociedad Española de Neumología y Cirugía Torácica
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