Donor Treatment With a Hypoxia-Inducible Factor-1 Agonist Prevents Donation After Cardiac Death Liver Graft Injury in a Rat Isolated Perfusion Model

2017 ◽  
Vol 42 (3) ◽  
pp. 280-289 ◽  
Author(s):  
Xingjian Zhang ◽  
Zhongzhong Liu ◽  
Qi Xiao ◽  
Cheng Zeng ◽  
Chin-Hui Lai ◽  
...  
Keyword(s):  
Cardiac Death ◽  
Hypoxia Inducible Factor ◽  
Liver Graft ◽  
Donation After Cardiac Death ◽  
Hypoxia Inducible Factor 1 ◽  
Perfusion Model ◽  
Isolated Perfusion

Liver graft preservation using perfluorocarbon improves the outcomes of simulated donation after cardiac death liver transplantation in rats

2017 ◽  
Vol 23 (9) ◽  
pp. 1171-1185 ◽  
Author(s):  
Shinya Okumura ◽  
Tadahiro Uemura ◽  
Xiangdong Zhao ◽  
Yuki Masano ◽  
Tatsuaki Tsuruyama ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Cardiac Death ◽  
Liver Graft ◽  
Donation After Cardiac Death ◽  
Graft Preservation

Functional Recovery of Donation After Cardiac Death Liver Graft by Continuous Machine Perfusion Preservation in Pigs

2012 ◽  
Vol 44 (4) ◽  
pp. 946-947 ◽  
Author(s):  
T. Shigeta ◽  
N. Matsuno ◽  
H. Obara ◽  
H. Mizunuma ◽  
H. Kanazawa ◽  
...  
Keyword(s):  
Functional Recovery ◽  
Cardiac Death ◽  
Liver Graft ◽  
Donation After Cardiac Death ◽  
Machine Perfusion

Usefulness of Continuous Machine Perfusion Preservation with Rewarming Method for Donation after Cardiac Death Liver Graft

2012 ◽  
Vol 94 (10S) ◽  
pp. 527
Author(s):  
T. Shigeta ◽  
N. Matsuno ◽  
H. Obara ◽  
H. Mizunuma ◽  
T. Hirano ◽  
...  
Keyword(s):  
Cardiac Death ◽  
Liver Graft ◽  
Donation After Cardiac Death ◽  
Machine Perfusion

Effect of cold perfusion and perfluorocarbons on liver graft ischemia in a donation after cardiac death model

2014 ◽  
Vol 188 (2) ◽  
pp. 517-526 ◽  
Author(s):  
Dmitri Bezinover ◽  
Saravanan Ramamoorthy ◽  
Marek Postula ◽  
Gregory Weller ◽  
Saifeldin Mahmoud ◽  
...  
Keyword(s):  
Cardiac Death ◽  
Liver Graft ◽  
Donation After Cardiac Death

Usefulness of Continuous Machine Perfusion Preservation with Rewarming Method for Donation after Cardiac Death Liver Graft

2012 ◽  
Vol 94 (10S) ◽  
pp. 209
Author(s):  
T. Shigeta ◽  
N. Matsuno ◽  
H. Obara ◽  
H. Mizunuma ◽  
T. Hirano ◽  
...  
Keyword(s):  
Cardiac Death ◽  
Liver Graft ◽  
Donation After Cardiac Death ◽  
Machine Perfusion

Development of a Prolonged Warm Ex Vivo Perfusion Model for Kidneys Donated after Cardiac Death

2017 ◽  
Vol 40 (6) ◽  
pp. 265-271 ◽  
Author(s):  
Daniel Urcuyo ◽  
Matthew F. Blum ◽  
Qiang Liu ◽  
Ahmed Nassar ◽  
Laura D. Buccini ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Whole Blood ◽  
Cardiac Death ◽  
Ex Vivo ◽  
Donation After Cardiac Death ◽  
Donor Pool ◽  
Ex Vivo Perfusion ◽  
Perfusion Model ◽  
Renal Grafts ◽  
Kidney Perfusion

Purpose Ex vivo perfusion of marginal kidney grafts offers the chance to expand the donor pool, but there is no current clinical standard for the prolonged warm perfusion of renal grafts. This exploratory pilot study seeks to identify a stable ex vivo kidney perfusion model that can support low intravascular resistance and preserve histologic architecture in a porcine donation after cardiac death (DCD) model. Methods 15 kidneys were preserved in 1 of 3 settings: normothermic whole blood (NT-WB), normothermic Steen Solution™ (XVIVO Perfusion) with whole blood (NT-Steen/WB), or subnormothermic Steen Solution™ at 21°C (SNT-Steen). Kidneys were primarily assessed using hemodynamic parameters and histologic analysis. Results NT-WB perfusion resulted in high vascular resistance and glomerular necrosis. NT-Steen/WB and SNT-Steen resistance ranged between 0.18–0.45 mmHg/mL per minute and 0.25–0.53 mmHg/mL per minute, respectively, enabling stable perfusion for up to 24 hours. NT-Steen/WB demonstrated tubular and glomerular necrosis, while the histologic architecture of SNT-Steen was preserved with the exception of numerous proteinaceous casts. Conclusions Our results suggest that ex vivo kidney perfusion with Steen Solution™ at 21°C supports low and stable vascular resistance and provides adequate histologic preservation during 24-hour perfusion.

Vascular adaptations to hypoxia: molecular and cellular mechanisms regulating vascular tone

2007 ◽  
Vol 43 ◽  
pp. 105-120 ◽  
Author(s):  
Michael L. Paffett ◽  
Benjimen R. Walker
Keyword(s):  
Vascular Tone ◽  
Cellular Proliferation ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Hypoxia Inducible Factor ◽  
Systemic Circulation ◽  
Cellular Mechanisms ◽  
Hypoxia Inducible Factor 1 ◽  
Pulmonary Vasoconstriction ◽  
Adaptive Mechanisms ◽  
Adaptive Processes

Several molecular and cellular adaptive mechanisms to hypoxia exist within the vasculature. Many of these processes involve oxygen sensing which is transduced into mediators of vasoconstriction in the pulmonary circulation and vasodilation in the systemic circulation. A variety of oxygen-responsive pathways, such as HIF (hypoxia-inducible factor)-1 and HOs (haem oxygenases), contribute to the overall adaptive process during hypoxia and are currently an area of intense research. Generation of ROS (reactive oxygen species) may also differentially regulate vascular tone in these circulations. Potential candidates underlying the divergent responses between the systemic and pulmonary circulations may include Nox (NADPH oxidase)-derived ROS and mitochondrial-derived ROS. In addition to alterations in ROS production governing vascular tone in the hypoxic setting, other vascular adaptations are likely to be involved. HPV (hypoxic pulmonary vasoconstriction) and CH (chronic hypoxia)-induced alterations in cellular proliferation, ionic conductances and changes in the contractile apparatus sensitivity to calcium, all occur as adaptive processes within the vasculature.

TAp73 opposes tumor angiogenesis by promoting hypoxia-inducible factor 1α degradation

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Cancer Progression ◽  
Hypoxia Inducible Factor ◽  
Tumor Hypoxia ◽  
Human Lung Cancer ◽  
Regulatory Subunit ◽  
Patients With Cancer ◽  
Hypoxia Inducible Factor 1 ◽  
Chemically Induced ◽  
Induced Tumors ◽  
Patient Prognosis

Tumor hypoxia and hypoxia-inducible factor 1 (HIF-1) activationare associated with cancer progression. Here, we demonstrate thatthe transcription factor TAp73 opposes HIF-1 activity through anontranscriptional mechanism, thus affecting tumor angiogenesis.TAp73-deficient mice have an increased incidence of spontaneousand chemically induced tumors that also display enhanced vascularization.Mechanistically, TAp73 interacts with the regulatory subunit(α) of HIF-1 and recruits mouse double minute 2 homolog intothe protein complex, thus promoting HIF-1α polyubiquitination andconsequent proteasomal degradation in an oxygen-independentmanner. In human lung cancer datasets, TAp73 strongly predictsgood patient prognosis, and its expression is associated with lowHIF-1 activation and angiogenesis. Our findings, supported by invivo and clinical evidence, demonstrate a mechanism for oxygenindependentHIF-1 regulation, which has important implicationsfor individualizing therapies in patients with cancer.

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