ArticleAmerican journal of physiology. Lung cellular and molecular physiology2023
The hemodynamic interplay between pulmonary ischemia-reperfusion injury and right ventricular function in lung transplantation: a translational porcine model.
Article in American journal of physiology. Lung cellular and molecular physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Passive versus active right ventricular support during lung transplantation: Insights from a porcine pulmonary ischemia-reperfusion injury model.JTCVS techniques · 2026Article
- Right Ventricular Pressure-Volume Loop Analysis in Large Animal Research: A Scoping Review of Current Practices Using Conductance and Admittance Catheters.Pulmonary circulation · 2026Review
- Right ventricular mechanical support as a bridge to lung transplantation: A literature review of current practices.JHLT open · 2025Review
- Complications related to extracorporeal life support in lung transplantation: single-center analysis.Journal of thoracic disease · 2023Article
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
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Abstract
Lung transplantation (LTx) is a challenging procedure. Following the process of ischemia-reperfusion injury, the transplanted pulmonary graft might become severely damaged, resulting in primary graft dysfunction. In addition, during the intraoperative window, the right ventricle (RV) is at risk of acute failure. The interaction of right ventricular function with lung injury is, however, poorly understood. We aimed to address this interaction in a translational porcine model of pulmonary ischemia-reperfusion injury. Advanced pulmonary and hemodynamic assessment was used, including right ventricular pressure-volume loop analysis. The acute model was based on clamping and unclamping of the left lung hilus, respecting the different hemodynamic phases of a clinical lung transplantation. We found that forcing entire right ventricular cardiac output through a lung suffering from ischemia-reperfusion injury increased afterload (pulmonary vascular resistance from baseline to end experiment
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