Aerosolized perfluorocarbon suppresses early pulmonary inflammatory response in a surfactant-depleted piglet model.
The effect of new ventilation strategies on initial pulmonary inflammatory reaction was studied in a surfactant-depleted piglet model. Sixty minutes after induction of lung injury by bronchoalveolar lavage, piglets received either aerosolized FC77 (aerosol-PFC, 10 mL/kg/h, n = 5) or partial liquid ventilation (PLV) with FC77 at functional residual capacity volume (FRC-PLV, 30 mL/kg, n = 5), or at low volume (LV-PLV, 10 mL/kg per hour, n = 5), or intermittent mandatory ventilation (control, n = 5). After 2 h, perfluorocarbon application was stopped and intermittent mandatory ventilation continued for 6 h. After a total experimental period of 8 h, animals were killed and lung tissue obtained. mRNA expression of IL-1beta, IL-6, IL-8, and TGF-beta in porcine lung tissue was quantified using TaqMan real-time PCR and normalized to beta-actin (A) and hypoxanthine-guanine-phosphoribosyl-transferase (H). In the aerosol-PFC group, IL-1beta, IL-6, IL-8, and transforming growth factor (TGF)-beta mRNA expression in lung tissue was significantly lower than in the control group. Reduction was 95% for IL-1beta/H (p < 0.001), 73% for IL-6/H (p < 0.05), 87% for IL-8/H (p < 0.001), and 38% for TGF-beta/H (p < 0.01). A lower mRNA gene expression was also determined for IL-1beta and IL-8 when the aerosol-PFC group was compared with the LV-PLV group [91% for IL-1beta/H (p < 0.001), 75% for IL-8/H (p < 0.001)]. In the FRC-PLV group, mRNA expression of IL-1beta was significantly lower than in the control (p < 0.05) and LV-PLV (p < 0.01) group. In a surfactant-depleted piglet model, aerosol therapy with perfluorocarbon but not LV-PLV reduces the initial pulmonary inflammatory reaction at least as potently as PLV at FRC volume.
von der Hardt
Katharina
K
Klinik für Kinder und Jugendliche der Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054 Erlangen, Germany.
Schoof
Ellen
E
Kandler
Michael A
MA
Dötsch
Jörg
J
Rascher
Wolfgang
W
D000336:Aerosols; D000818:Animals; D001997:Bronchopulmonary Dysplasia / Q000503:physiopathology*; D004195:Disease Models, Animal; D005466:Fluorocarbons / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D007231:Infant, Newborn; D007375:Interleukin-1 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D008168:Lung / Q000503:physiopathology*; D011014:Pneumonia / Q000188:drug therapy* / Q000378:metabolism; D011663:Pulmonary Surfactants / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D013552:Swine; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D014691:Ventilation / Q000379:methods
D000336:Aerosols; D005466:Fluorocarbons; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D011663:Pulmonary Surfactants; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta