Papel de los neumocitos II en un modelo experimental de lesión pulmonar aguda

  1. Ravelo Rodríguez, Raquel
  2. López Hernández, Milagros
  3. Gutiérrez García, Ricardo
  4. Valladares Parrilla, Francisco José
Revue:
Majorensis: Revista Electrónica de Ciencia y Tecnología

ISSN: 1697-5529

Année de publication: 2012

Número: 8

Pages: 21-31

Type: Article

D'autres publications dans: Majorensis: Revista Electrónica de Ciencia y Tecnología

Résumé

In the pulmonary alveoli, there are two remarkable types of cells: type I alveolar epithelial cells (AEC1) and type II alveolar epithelial cells (AEC2). They can be affected by the changes in the gas exchange, so the respiratory distress syndrome (ARDS) can change their cellular distribution and modify the tissue. This experimental work focus in the study of how a serious damage in the lung, the acute lung injury (ALI), caused by mechanical ventilation, produce an important change in the number and structure of type II alveolar epithelial cells. This study is based in three groups of male adults Sprague-Dawley rats for a prospective randomized and controlled experiment; group 1 breathes of spontaneous way and the rest of rats by means of a ventilator strategy during four hours: group 2 breathes high tidal volume and group 3 group has low tidal volume. Later, an histological evaluation of the lungs stained with Syrius red, HE and immunohistochemical stain for TTF1 (thyroid transcription factor 1 and a-actin of smooth muscle cells) were performed. The pulmonary samples of rats with normal breathing and to low volume did not show histological differences, and both had a similar disposition in cellular types. Nevertheless those that breathed to high volume they presented inflammatory infiltrates and perivascular edema and the type II alveolar epithelial cells displayed a marked hyperplasia. In conclusion the mechanical ventilation produces pulmonary damage, specially to AEC2 cells, which secrete surfactant making difficult the inflation and, therefore, the interchange of gases; the lung tries to repair this damage by proliferation of AEC2