The Journal of thoracic and cardiovascular surgery · 2024
Protective effects of 10 °C preservation on donor lungs with lipopolysaccharide-induced acute lung injury.
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Yamanashi Keiji, Wang Aizhou, Bellissimo Catherine A, Siebiger Gabriel, Oliveira Paolo, Zhang Yu, Montagne Juan, Garza Guillermo, Furie Nadav, Pal Prodipto, Liu Mingyao, Goligher Ewan C, Keshavjee Shaf, Cypel Marcelo
Аннотация
OBJECTIVES: Hypothermic lung preservation at 10 °C has been recently shown to enhance quality of healthy donor lungs during ischemia. This study aims to show generalizability of the 10 °C lung preservation using an endotoxin-induced lung injury with specific focus on the benefits of post-transplant lung function and mitochondrial preservation.
METHODS: Lipopolysaccharide (3 mg/kg) was injected intratracheally in rats to induce lung injury. Injured lungs were flushed with preservation solution and allocated to 3 groups (n = 6 each): minimum cold storage, 6-hour storage on ice (ice), and 6-hour storage at 10 °C (10 °C). Left lungs were transplanted and reperfused for 2 hours. After storage, lung tissue was used to evaluate the effects of hypothermic storage on the mitochondrial function: mitochondrial membrane potential was assessed by JC-1 staining; mitochondrial oxygen consumption was assessed using high-resolution respirometry.
RESULTS: Two hours after reperfusion, the oxygen tension/inspired oxygen fraction ratio from the graft was significantly greater in the 10 °C group than in the Ice group (P = .015), whereas the wet-to-dry weight ratio was significantly lower (P = .041). Levels of interleukin-8 in lung tissues were significantly lower in the 10 °C group than in the Ice group (P = .004). Mechanistically, we noted greater mitochondrial membrane potential and elevated state III respiration in the 10 °C group than in the Ice group (P = .015 and P = .002, respectively), implying higher metabolic activities may be maintained during 10 °C preservation.
CONCLUSIONS: Favorable metabolism during 10 °C preservation prevented ischemia-induced mitochondrial damages in injured lungs, leading to better post-transplant outcomes.
METHODS: Lipopolysaccharide (3 mg/kg) was injected intratracheally in rats to induce lung injury. Injured lungs were flushed with preservation solution and allocated to 3 groups (n = 6 each): minimum cold storage, 6-hour storage on ice (ice), and 6-hour storage at 10 °C (10 °C). Left lungs were transplanted and reperfused for 2 hours. After storage, lung tissue was used to evaluate the effects of hypothermic storage on the mitochondrial function: mitochondrial membrane potential was assessed by JC-1 staining; mitochondrial oxygen consumption was assessed using high-resolution respirometry.
RESULTS: Two hours after reperfusion, the oxygen tension/inspired oxygen fraction ratio from the graft was significantly greater in the 10 °C group than in the Ice group (P = .015), whereas the wet-to-dry weight ratio was significantly lower (P = .041). Levels of interleukin-8 in lung tissues were significantly lower in the 10 °C group than in the Ice group (P = .004). Mechanistically, we noted greater mitochondrial membrane potential and elevated state III respiration in the 10 °C group than in the Ice group (P = .015 and P = .002, respectively), implying higher metabolic activities may be maintained during 10 °C preservation.
CONCLUSIONS: Favorable metabolism during 10 °C preservation prevented ischemia-induced mitochondrial damages in injured lungs, leading to better post-transplant outcomes.