Mechanical ventilation and lung infection in the genesis of air-space enlargement

Air-space enlargement may result from mechanical ventilation and/or lung infection. The aim of this study was to assess how mechanical ventilation and lung infection influence the genesis of bronchiolar and alveolar distention.

Four groups of piglets were studied: non-ventilated-non-inoculated (controls, n = 5), non-ventilated-inoculated (n = 6), ventilated-non-inoculated (n = 6), and ventilated-inoculated (n = 8) piglets. The respiratory tract of intubated piglets was inoculated with a highly concentrated solution of Escherichia coli. Mechanical ventilation was maintained during 60 hours with a tidal volume of 15 ml/kg and zero positive end-expiratory pressure. After sacrifice by exsanguination, lungs were fixed for histological and lung morphometry analyses.

Lung infection was present in all inoculated piglets and in five of the six ventilated-non-inoculated piglets. Mean alveolar and mean bronchiolar areas, measured using an analyzer computer system connected through a high-resolution color camera to an optical microscope, were significantly increased in non-ventilated-inoculated animals (+16% and +11%, respectively, compared to controls), in ventilated-non-inoculated animals (+49% and +49%, respectively, compared to controls), and in ventilated-inoculated animals (+95% and +118%, respectively, compared to controls). Mean alveolar and mean bronchiolar areas significantly correlated with the extension of lung infection (R = 0.50, p < 0.01 and R = 0.67, p < 0.001, respectively).

Lung infection induces bronchiolar and alveolar distention. Mechanical ventilation induces secondary lung infection and is associated with further air-space enlargement. The combination of primary lung infection and mechanical ventilation markedly increases air-space enlargement, the degree of which depends on the severity and extension of lung infection.