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Vol. 23. Issue 5.
Pages 234-237 (September - October 1987)
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Vol. 23. Issue 5.
Pages 234-237 (September - October 1987)
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Enfermedad pulmonar experimental por diisocianato de tolueno
Experimental pulmonary disease induced by toluene diisocyanate
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A. Martinez-Berganza Asensio, F. Escolar Castellon
Servicio de Neumología. Departamento de Medicina. Facultad de Medicina. Universidad de Zaragoza
J.D. Escolar Castellon*, P. Roche Roche*
* Departamento de Anatomía. Facultad de Medicina. Universidad de Zaragoza.
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A pesar de que la enfermedad profesional por diisocianato de tulueno (DIT) es conocida desde hace años, todavía se discuten los mecanismos patógenos que intervienen en su desencadenamiento. Para aportar datos al conocimiento de la etiopatogenia, se ha establecido un modelo experimental en ratas.

Se sometió a 8 ratas a una atmósfera de vapores de DIT, de forma ininterrumpida durante 30 días, posteriormente las ratas fueron sacrificadas, se les realizó lavado broncoalveolar (LBA) y estudio histológico que incluía inmunohistioquimia para la detección de IgG.

El LBA mostró un incremento de los linfodtos (38%), lo que coincidía con la infiltración de linfodtos peribronquial y, en menor grado, de los tabiques alveolares. Asimismo, se detectaron depósitos de IgG en las paredes de los capilares alveolares. Todos estos hechos sugieren: la participación de mecanismos de hipersensibilidad retardada tipo III, mediada por IgG; así como, la implicación tanto de las vías aéreas como del parénquima pulmonar. Quedando por aclarar las posibilidades evolutivas de los depósitos de IgG, encontrados en las paredes alveolares.

Even though the occupational disease induced by toluene diisocyanate (DIT) has been known for years, the pathogenetic mechanisms that trigger this condition remain unclear. An experimental model has been developed in the rat in order to provide some insight on the etiopathogenesis of the disease.

Eight rats were mantained on an DIT atmosphere continuosly for 30 days and then killed. Bronchoalveolar lavage (LBA) and histological exam including immunohistochemical assessment for IgG detection were performed in all the animals.

An increased proportion of lymphocytes (39%) was found in the bronchoalveolar lavage, together with a peribronchial lymphocytic infiltration of the alveolar septa. IgG deposits on the alveolar capillary walls were also found. These findings suggest that IgG-mediated type III delayed hypersensitivity mechanisms are involved, and that both airway and pulmonary parenchyma are affected. The final outcome of the IgG deposits found on the alveolar walls is still confuse.

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Bibliografía
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Copyright © 1987. Sociedad Española de Neumología y Cirugía Torácica
Archivos de Bronconeumología
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