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Protective effect of surfactant inhalation against warm ischemic injury in an isolated rat lung ventilation model.

Ohsumi A, Chen F, Sakamoto J, Nakajima D, Kobayashi M, Bando T, Date H - PLoS ONE (2013)

Bottom Line: Surfactant inhalation significantly improved dynamic compliance and airway resistance.Moreover, surfactant inhalation significantly decreased inducible nitric oxide synthase and caspase-3 transcript levels, and increased those of Bcl-2 and surfactant protein-C.The reduction in oxidative damage and the inhibition of apoptosis might contribute to the protection of the warm ischemic lungs.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

ABSTRACT
Warm ischemia-reperfusion injury remains a crucial issue in transplantation following the cardiac death of donors. Previously, we showed that surfactant inhalation during warm ischemia mitigated ischemia-reperfusion injury. This study investigated the mechanisms of surfactant inhalation protection of the warm ischemic lung after reoxygenation with ventilation alone. In an isolated rat lung ventilation model, cardiac arrest was induced in the CTRL (control) and SURF (surfactant treatment) groups by ventricular fibrillation. Ventilation was restarted 110 min later; the lungs were flushed, and a heart and lung block was procured. In the SURF group, a natural bovine surfactant (Surfacten®) was inhaled for 3 min at the end of warm ischemia. In the Sham (no ischemia) group, lungs were flushed, procured, and ventilated in the same way. Afterwards, the lungs were ventilated with room air without reperfusion for 60 min. Surfactant inhalation significantly improved dynamic compliance and airway resistance. Moreover, surfactant inhalation significantly decreased inducible nitric oxide synthase and caspase-3 transcript levels, and increased those of Bcl-2 and surfactant protein-C. Immunohistochemically, lungs in the SURF group showed weaker staining for 8-hydroxy-2'-deoxyguanosine, inducible nitric oxide synthase, and apoptosis, and stronger staining for Bcl-2 and surfactant protein-C. Our results indicate that surfactant inhalation in the last phase of warm ischemia mitigated the injury resulting from reoxygenation after warm ischemia. The reduction in oxidative damage and the inhibition of apoptosis might contribute to the protection of the warm ischemic lungs.

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Physiological lung functions during ventilation.(A) Airway resistance. (B) Dynamic compliance. **p<0.01 or ***p<0.001 between the Sham (open circles) and CTRL groups (boxes). †p<0.05 or ††p<0.01 or †††p<0.001 between the CTRL and SURF groups (solid circles). §p<0.05 between the Sham and SURF groups. Data are expressed as mean values ± SD (BL = baseline).
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pone-0072574-g001: Physiological lung functions during ventilation.(A) Airway resistance. (B) Dynamic compliance. **p<0.01 or ***p<0.001 between the Sham (open circles) and CTRL groups (boxes). †p<0.05 or ††p<0.01 or †††p<0.001 between the CTRL and SURF groups (solid circles). §p<0.05 between the Sham and SURF groups. Data are expressed as mean values ± SD (BL = baseline).

Mentions: In the CTRL group, airway resistance increased and dynamic compliance decreased during the latter half of the evaluation period, and were significantly higher and lower than those in the Sham group (p<0.001 and p<0.01 at 60 minutes after evaluation period). However, in the SURF group, the airway resistance and dynamic compliance were maintained at almost the same levels as those at the initiation of the evaluation, and were significantly lower and higher, respectively, than those in the CTRL group (p<0.001 and p<0.05 at 60 minutes, respectively; Figure 1A and B).


Protective effect of surfactant inhalation against warm ischemic injury in an isolated rat lung ventilation model.

Ohsumi A, Chen F, Sakamoto J, Nakajima D, Kobayashi M, Bando T, Date H - PLoS ONE (2013)

Physiological lung functions during ventilation.(A) Airway resistance. (B) Dynamic compliance. **p<0.01 or ***p<0.001 between the Sham (open circles) and CTRL groups (boxes). †p<0.05 or ††p<0.01 or †††p<0.001 between the CTRL and SURF groups (solid circles). §p<0.05 between the Sham and SURF groups. Data are expressed as mean values ± SD (BL = baseline).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3757025&req=5

pone-0072574-g001: Physiological lung functions during ventilation.(A) Airway resistance. (B) Dynamic compliance. **p<0.01 or ***p<0.001 between the Sham (open circles) and CTRL groups (boxes). †p<0.05 or ††p<0.01 or †††p<0.001 between the CTRL and SURF groups (solid circles). §p<0.05 between the Sham and SURF groups. Data are expressed as mean values ± SD (BL = baseline).
Mentions: In the CTRL group, airway resistance increased and dynamic compliance decreased during the latter half of the evaluation period, and were significantly higher and lower than those in the Sham group (p<0.001 and p<0.01 at 60 minutes after evaluation period). However, in the SURF group, the airway resistance and dynamic compliance were maintained at almost the same levels as those at the initiation of the evaluation, and were significantly lower and higher, respectively, than those in the CTRL group (p<0.001 and p<0.05 at 60 minutes, respectively; Figure 1A and B).

Bottom Line: Surfactant inhalation significantly improved dynamic compliance and airway resistance.Moreover, surfactant inhalation significantly decreased inducible nitric oxide synthase and caspase-3 transcript levels, and increased those of Bcl-2 and surfactant protein-C.The reduction in oxidative damage and the inhibition of apoptosis might contribute to the protection of the warm ischemic lungs.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

ABSTRACT
Warm ischemia-reperfusion injury remains a crucial issue in transplantation following the cardiac death of donors. Previously, we showed that surfactant inhalation during warm ischemia mitigated ischemia-reperfusion injury. This study investigated the mechanisms of surfactant inhalation protection of the warm ischemic lung after reoxygenation with ventilation alone. In an isolated rat lung ventilation model, cardiac arrest was induced in the CTRL (control) and SURF (surfactant treatment) groups by ventricular fibrillation. Ventilation was restarted 110 min later; the lungs were flushed, and a heart and lung block was procured. In the SURF group, a natural bovine surfactant (Surfacten®) was inhaled for 3 min at the end of warm ischemia. In the Sham (no ischemia) group, lungs were flushed, procured, and ventilated in the same way. Afterwards, the lungs were ventilated with room air without reperfusion for 60 min. Surfactant inhalation significantly improved dynamic compliance and airway resistance. Moreover, surfactant inhalation significantly decreased inducible nitric oxide synthase and caspase-3 transcript levels, and increased those of Bcl-2 and surfactant protein-C. Immunohistochemically, lungs in the SURF group showed weaker staining for 8-hydroxy-2'-deoxyguanosine, inducible nitric oxide synthase, and apoptosis, and stronger staining for Bcl-2 and surfactant protein-C. Our results indicate that surfactant inhalation in the last phase of warm ischemia mitigated the injury resulting from reoxygenation after warm ischemia. The reduction in oxidative damage and the inhibition of apoptosis might contribute to the protection of the warm ischemic lungs.

Show MeSH
Related in: MedlinePlus