Inhaled nitric oxide affects endogenous surfactant in experimental lung transplantation

• Published in: Transplantation Vol. 77; no. 6; p. 812
• Main Authors: Valiño, Fernando, Casals, Cristina, Guerrero, Rosa, Alvarez, Lourdes, Santos, Martín, Sáenz, Alejandra, Varela, Andrés, Claro, Miguel A, Tendillo, Francisco, Castillo-Olivares, José L
• Format: Journal Article
• Language: English
• Published: United States 27.03.2004
• Subjects: Adenosine; Administration, Inhalation; Allopurinol; Animals; Bronchoalveolar Lavage Fluid - chemistry; Glutathione; Insulin; Lung; Lung Transplantation - physiology; Nitric Oxide - administration & dosage; Nitric Oxide - pharmacology; Organ Preservation; Organ Preservation Solutions; Oxygen - blood; Pulmonary Surfactants - isolation & purification; Raffinose; Respiratory Function Tests; Swine; Transplantation, Homologous
• ISSN: 0041-1337
• DOI: 10.1097/01.TP.0000116421.57232.81

Inhalation of nitric oxide (NO) has been proposed as a therapy to improve lung transplantation outcome. We investigated the effect that inhaled NO has on the surfactant system in the context of ischemia-reperfusion injury. Single left-lung transplantation was performed in weight-matched pairs of Landrace pigs. A double-lung block from the donor animal was flushed with University of Wisconsin solution at 4 degrees C followed by immersion in cold University of Wisconsin solution for 22 hr. The left donor lung was transplanted into the recipient. Recipients were divided into two groups: (1) treated with inhaled NO (40 ppm) (n=6) immediately after initiating lung reperfusion and (2) without treatment (n=6). Lung function was measured during 2 hr of reperfusion. Surfactant components in small and large aggregates, isolated from cell-free bronchoalveolar lavages, and surfactant function were measured. NO inhalation significantly decreased arterial oxygenation. With respect to the surfactant system, NO inhalation worsened the surfactant adsorption rate to an air-liquid interface and affected levels of hydrophobic surfactant proteins (SPs), SP-B and SP-C, and phospholipids, which decreased in large surfactant aggregates but not in small surfactant aggregates. SP-A was reduced in large surfactant aggregates of transplanted lungs from both untreated and NO-treated groups. A decreased level of SP-A, SP-B, and SP-C in large surfactant aggregates of transplanted lungs treated with NO is a marker of lung injury. We conclude that treatment with inhaled NO after lung transplantation is deleterious for the surfactant system and causes a parallel worsening of arterial oxygenation.