ArticleJACC. Basic to translational science2016
Intracoronary Poloxamer 188 Prevents Reperfusion Injury in a Porcine Model of ST-Segment Elevation Myocardial Infarction.
Article in JACC. Basic to translational science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 41 citations in OpenAlex.
- Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia-reperfusion injury.The Journal of physiology · 2026Review
- Article
- Cardioprotection by poloxamer 188 is mediated through increased endothelial nitric oxide production.Scientific reports · 2025Article
- Prkd1 regulates the formation and repair of plasma membrane disruptions (PMD) in osteocytes.Bone · 2024Article
- Effects of poloxamer 188 on traumatic brain injury.Brain, behavior, & immunity - health · 2024Review
- Hydrogels for Cardiac Restorative Support: Relevance of Gelation Mechanisms for Prospective Clinical Use.Current heart failure reports · 2023Review
- Article
- Rapid restitution of contractile dysfunction by synthetic copolymers in dystrophin-deficient single live skeletal muscle fibers.Skeletal muscle · 2023Article
- Article
- Consequences of poly(ethylene oxide) and poloxamer P188 on transcription in healthy and stressed myoblasts.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Molecular homing and retention of muscle membrane stabilizing copolymers by non-invasive optical imaging in vivo.Molecular therapy. Methods & clinical development · 2023Article
- P188 Therapy in In Vitro Models of Traumatic Brain Injury.International journal of molecular sciences · 2023Review
- Concentration Threshold for Membrane Protection by PEO-PPO Block Copolymers with Variable Molecular Architectures.ACS applied polymer materials · 2022Article
- Poloxamer-188 Exacerbates Brain Amyloidosis, Presynaptic Dystrophies, and Pathogenic Microglial Activation in 5XFAD Mice.Current Alzheimer research · 2022Article
- Differential Effects of Reperfusion on Cardiac Mitochondrial Subpopulations in a Preclinical Porcine Model of Acute Myocardial Infarction.Frontiers in cell and developmental biology · 2022Article
- Poloxamer 188 Exerts Direct Protective Effects on Mouse Brain Microvascular Endothelial Cells in an In Vitro Traumatic Brain Injury Model.Biomedicines · 2021Article
- No Direct Postconditioning Effect of Poloxamer 188 on Mitochondrial Function after Ischemia Reperfusion Injury in Rat Isolated Hearts.International journal of molecular sciences · 2021Article
- Evaluation of In Vitro Neuronal Protection by Postconditioning with Poloxamer 188 Following Simulated Traumatic Brain Injury.Life (Basel, Switzerland) · 2021Article
- Potential Effects of Poloxamer 188 on Rat Isolated Brain Mitochondria after Oxidative Stress In Vivo and In Vitro.Brain sciences · 2021Article
- Poloxamer 188 Attenuates Ischemia-Reperfusion-Induced Lung Injury by Maintaining Cell Membrane Integrity and Inhibiting Multiple Signaling Pathways.Frontiers in pharmacology · 2021Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPoloxamer 188 (P188) is a nonionic triblock copolymer believed to prevent cellular injury after ischemia and reperfusion.
objectivesThis study compared intracoronary infusion of P188 immediately after reperfusion with delayed infusion through a peripheral intravenous catheter in a porcine model of ST segment elevation myocardial infarction (STEMI). Cellular and mitochondrial injury were assessed.
methodsSTEMI was induced in 55 pigs using 45 minutes of endovascular coronary artery occlusion. Pigs were then randomized to four groups: control, immediate intracoronary (IC) P188, delayed peripheral P188, and polyethylene glycol (PEG) infusion. Heart tissue was collected after 4 hours of reperfusion. Assessment of mitochondrial function or infarct size was performed.
resultsMitochondrial yield improved significantly with IC P188 treatment compared to control animals (0.25% vs. 0.13%) suggesting improved mitochondrial morphology and survival. Mitochondrial respiration and calcium retention were also significantly improved with immediate IC P188 compared to controls (complex I RCI: 7.4 vs. 3.7 and calcium retention (nmol): 1152 vs. 386). This benefit was only observed with activation of complex I of the mitochondrial respiratory chain suggesting a specific impact of ischemia and reperfusion on this complex. Infarct size and serum troponin I were significantly reduced by immediate IC P188 infusion (infarct size: 13.9% vs. 41.1% and troponin I (μg/L): 19.2 vs. 77.4 μg/L). Delayed P188 and PEG infusion did not provide a significant benefit.
conclusionsIntracoronary infusion of P188 immediately upon reperfusion significantly reduces cellular and mitochondrial injury after ischemia and reperfusion in this clinically relevant porcine model of STEMI. The timing and route of delivery were critical to achieve the benefit.
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