Ischemia-reperfusion Injury of the Lung: Role of Surfactant

Surfactant pretreatment ameliorates ischemia-reperfusion injury of the lung

“…Surfactant therapy before ischemia is thought to be more beneficial than treatment at the time of reperfusion or after reperfusion [2]. This may be explained by the fact that surfactant given to the donor results in a more homogenous distribution in the lung as compared to treatment at reperfusion, when alveolar damage has already occurred [8]. In the latter case, intratracheally instilled surfactant will predominantly accumulate in open areas of the lung instead of atelectatic areas, where it is most needed.…”

“…The accumulation of fluid in the alveolus is predominantly due to the damaged surfactant system, illustrated by an increase in the SA/LA ratio. As a result surfactant cannot maintain its surface lowering function inside the alveolus causing further development of pulmonary edema and subsequently decreased lung compliance and gas exchange, contributing to early morbidity and mortality [1][2][3][4]8]. Although prolonged ventilation strategies could probably reduce mortality in this experimental setting, animals were ventilated postoperatively for as short periods as possible because of the confounding effect of ventilation on LIRI [17].…”

“…It is known that when serum proteins accumulate in the alveoli, they are able to further dose-dependently inhibit surfactant function, probably by competing with surfactant phospholipids for a place at the air-water interface, resulting in additional deterioration of the lung function [8,18]. Surfactant replacement therapy at the time of reperfusion interrupts this vicious circle by restoring the fluid homeostasis across the alveolocapillary membrane [18].…”

“…In 1998, Hohlfeld and colleagues demonstrated surfactant alterations in human lung transplant recipients, more than 1 year after transplantation [7]. Active pulmonary surfactant is composed of phospholipids and surfactant associated proteins and is essential for normal lung physiology, since it lowers the surface tension at the air-fluid interface inside the alveolus [8]. Surfactant hereby prevents alveoli from collapsing at the end of expiration and preserves the fluid homeostasis across the alveolo-capillary membrane.…”

“…Surfactant hereby prevents alveoli from collapsing at the end of expiration and preserves the fluid homeostasis across the alveolo-capillary membrane. Inactivation of surfactant occurs due to the formation of reactive oxygen species (ROS), proteolytic enzymes, eicosanoids and lipases after LIRI and leads to a disturbed fluid balance homeostasis, resulting in pulmonary edema, decreased lung compliance and impaired gas exchange [8,9]. Severe LIRI occurs in 15-30% of lung transplant recipients and contributes to morbidity and mortality after lung transplantation resulting in a one-year survival rate of less than 80% [10].…”