Isoflurane Inhalation After Circulatory Arrest Protects Against Warm Ischemia Reperfusion Injury of the Lungs

Fujinaga, Takuji; Nakamura, Takayuki; Fukuse, Tatsuo; Chen, Fengshi; Zhang, Jitian; Ueda, Shugo; Hamakawa, Hiroshi; Omasa, Mitsugu; Sakai, Hiroaki; Hanaoka, Nobuharu; Wada, Hiromi; Bando, Toru

doi:10.1097/01.tp.0000237207.73439.2e

Cited by 47 publications

(25 citation statements)

References 40 publications

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“…Bnip3 is induced by hypoxia [19] and can overcome Bcl2 suppression and induce autophagy [20], and possibly increases as a response to hypoxia and secondary to the Bcl2 increase. Others have reported increased apoptosis after hypoxic/ischemic insults in the lungs [10,11,21], while one study reported no increase in apoptosis [22]. …”

Section: Discussionmentioning

confidence: 99%

Temporal Patterns of Gene Expression Profiles in the Neonatal Mouse Lung after Hypoxia-Reoxygenation

Rognlien

Wollen²,

Atneosen-Åsegg³

et al. 2016

Neonatology

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Background: One out of four children with neonatal asphyxia has lung involvement. Still, there has been little research on injury mechanisms of hypoxia-reoxygenation in the neonatal lung. Objectives: To make a temporal profile of the gene expression changes of 44 a priori selected genes after hypoxia-reoxygenation in the newborn mouse lung, and to compare the changes after hyperoxic and normoxic reoxygenation. Methods: Postnatal day 7 mice were randomized to 2-hour hypoxia (8% O₂) and 30-min reoxygenation in either 60% O₂ or air. After 0-72 h of observation, gene expression changes and protein concentrations in whole lung homogenates were examined. Results: Immediately after completed reoxygenation, 7 genes of mediators of inflammation were downregulated, and there was an antiapoptotic gene expression pattern. Three DNA glycosylases were downregulated, while genes involved in cell cycle renewal indicated both increased and decreased cell cycle arrest. Sod1 (T2.5h median H60: 1.01, H21: 0.88, p = 0.005; T5h median H60: 1.04, H21: 0.85, p = 0.038) and Il1b (T0h median H60: 0.86, H21: 1.08, p = 0.021) were significantly differentially expressed when comparing hyperoxic and normoxic reoxygenation. Conclusion: In this newborn mouse lung hypoxia-reoxygenation model, we found downregulation of genes of mediators of inflammation, an antiapoptotic gene expression pattern, and downregulation of DNA glycosylases. Sod1 and Il1b were significantly differentially expressed when comparing reoxygenation using 60% O₂ with air.

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Section: Discussionmentioning

confidence: 99%

Temporal Patterns of Gene Expression Profiles in the Neonatal Mouse Lung after Hypoxia-Reoxygenation

Rognlien

Wollen²,

Atneosen-Åsegg³

et al. 2016

Neonatology

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show abstract

“…Perfusion was driven by a roller pump, as previously reported. 4,5 Rats were anesthetized with an intraperitoneal injection of sodium pentobarbital (50 mg/kg). After tracheotomy and intubation, ventilation was initiated.…”

Section: Isolated Rat Lung Perfusion Modelmentioning

confidence: 99%

“…It has been reported previously that inhalation of several drugs during warm ischemia can ameliorate pulmonary warm I-R injury. 4,5 Milrinone is a phosphodiesterase 3 (PDE3) inhibitor that inhibits the breakdown of cyclic adenosine monophosphate (cAMP) and maintains intracellular cAMP levels, resulting in a potent positive inotropic effect and selective relaxation of smooth muscle. In the current study, it was hypothesized that nebulized milrinone would inhibit the breakdown of cAMP and maintain lung tissue cAMP levels during warm ischemia, resulting in the attenuation of pulmonary warm I-R injury.…”

mentioning

confidence: 99%

Nebulized Phosphodiesterase III Inhibitor During Warm Ischemia Attenuates Pulmonary Ischemia–Reperfusion Injury

Zhang

Chen

Zhao

et al. 2009

The Journal of Heart and Lung Transplantation

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“…16,17 The perfusate consisted of heparinized rat blood obtained from 2 donor rats and saline with 4% of bovine serum albumin, and the pH was adjusted to between 7.25 and 7.35 with sodium bicarbonate. No leukocyte filter was used.…”

Section: Reperfusionmentioning

confidence: 99%

Successful Sub-zero Non-freezing Preservation of Rat Lungs at −2°C Utilizing a New Supercooling Technology

Okamoto

Nakamura

Zhang

et al. 2008

The Journal of Heart and Lung Transplantation

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Isoflurane Inhalation After Circulatory Arrest Protects Against Warm Ischemia Reperfusion Injury of the Lungs

Abstract: Isoflurane inhalation attenuates warm IRI with the protection of mitochondria. Our results suggest that isoflurane inhalation after circulatory arrest can be a simple and effective method to protect the lung against warm ischemia.

Cited by 47 publications

References 40 publications

Temporal Patterns of Gene Expression Profiles in the Neonatal Mouse Lung after Hypoxia-Reoxygenation

Temporal Patterns of Gene Expression Profiles in the Neonatal Mouse Lung after Hypoxia-Reoxygenation

Nebulized Phosphodiesterase III Inhibitor During Warm Ischemia Attenuates Pulmonary Ischemia–Reperfusion Injury

Successful Sub-zero Non-freezing Preservation of Rat Lungs at −2°C Utilizing a New Supercooling Technology

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