Effect of granulocyte depletion in a ventilated surfactant-depleted lung

Abstract

In a previous paper Cutz, Bryan et al. showed that in rabbits after repetitive lung lavage high-frequency oscillatory ventilation maintained excellent gas exchange and did not cause hyaline membrane formation (J. Appl. Physiol. 55: 131-138, 1983). In contrast, conventional mechanical ventilation had poor gas exchange and extensive hyaline membrane formation and we attributed these differences to mechanical barotrauma. However, we completely overlooked the large number of granulocytes in the damaged lung. To investigate this using the same model we have used mechanical ventilation on two groups of rabbits, one with normal granulocytes, the other depleted of granulocytes by pretreatment with nitrogen mustard. The nondepleted rabbits had poor gas exchange, a substantial protein leak into the lung and extensive hyaline membranes. The depleted animals had good gas exchange, a very small protein leak and no hyaline membranes. Repletion of granulocytes from donor rabbits lead to poor gas exchange and hyaline membrane formation. It is concluded that lung lavage causes prompt margination of granulocytes which become activated by the ongoing epithelial barotrauma of conventional ventilation.

Ventilation with high tidal volume induces inflammatory lung injury

“…More recently, experimental studies suggested that mechanical ventilation increases pulmonary levels of inflammatory mediators and induces neutrophil accumulation (14)(15)(16). These studies suggest the hypothesis that ventilator-induced lung injury has an inflammatory component.…”

Suppressive oligonucleotides inhibit inflammation in a murine model of mechanical ventilator induced lung injury

“…Thus, the use of isoflurane might have delayed the onset or reduced the magnitude of MV-elicited changes in inflammatory cell activation/migration in the lungs. Previous in vitro and in vivo studies demonstrated that mechanical deformation rapidly alter the phosphorylation of proteins in pulmonary parenchyma and immune cells, and that these changes could persist after MV was discontinued (37,38). In clinical settings, VILI can contribute to organ failure and increased mortality in patients with pre-existing lung disease (39,40).…”

The Effect of Caffeic Acid in the Prevention of Lung Damage Due to Mechanical Ventilation in Rats

“…VILI'nın muhtemel mekanizmaları 9 hava boşluklarının tekrarlayan kollapsı ve yeniden açılması, 15 inflamasyon ve nötrofil artışı, 16 hemodinamik basınç değişiklikleri, 17 sür-faktan inaktivasyonu, akciğerde hücresel deformasyondur. 18 Şiddetli VILI'nın göstergelerinden biri alveoler ödemdir.…”