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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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Immunohistochemical staining for SP-C (original magnification 400×).(A) Sham group. (B) CTRL group. (C) SURF group. The amount of SP-C-positive cells in the CTRL and SURF groups was significantly lower than that in the Sham group, however, that in the SURF group was significantly higher than that in the CTRL group (D). All values are expressed as the mean ± SD.
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pone-0072574-g009: Immunohistochemical staining for SP-C (original magnification 400×).(A) Sham group. (B) CTRL group. (C) SURF group. The amount of SP-C-positive cells in the CTRL and SURF groups was significantly lower than that in the Sham group, however, that in the SURF group was significantly higher than that in the CTRL group (D). All values are expressed as the mean ± SD.

Mentions: The staining of type II cells was sporadic in the CTRL group (Figure 9B), but homogeneous and clear in the Sham and SURF groups (Figure 9A and C). The amount of SP-C-positive cells in the CTRL and SURF groups was significantly lower than that in the Sham group, however, that in the SURF group was significantly higher than that in the CTRL group (Figure 9D).


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)

Immunohistochemical staining for SP-C (original magnification 400×).(A) Sham group. (B) CTRL group. (C) SURF group. The amount of SP-C-positive cells in the CTRL and SURF groups was significantly lower than that in the Sham group, however, that in the SURF group was significantly higher than that in the CTRL group (D). All values are expressed as the mean ± SD.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3757025&req=5

pone-0072574-g009: Immunohistochemical staining for SP-C (original magnification 400×).(A) Sham group. (B) CTRL group. (C) SURF group. The amount of SP-C-positive cells in the CTRL and SURF groups was significantly lower than that in the Sham group, however, that in the SURF group was significantly higher than that in the CTRL group (D). All values are expressed as the mean ± SD.
Mentions: The staining of type II cells was sporadic in the CTRL group (Figure 9B), but homogeneous and clear in the Sham and SURF groups (Figure 9A and C). The amount of SP-C-positive cells in the CTRL and SURF groups was significantly lower than that in the Sham group, however, that in the SURF group was significantly higher than that in the CTRL group (Figure 9D).

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