ArticleCardiovascular drugs and therapy2014
Dodecafluoropentane emulsion elicits cardiac protection against myocardial infarction through an ATP-Sensitive K+ channel dependent mechanism.
Article in Cardiovascular drugs and therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The impact of intravenous dodecafluoropentane on a murine model of acute lung injury.Intensive care medicine experimental · 2023Article
- Perfluorocarbon-based oxygen carriers: from physics to physiology.Pflugers Archiv : European journal of physiology · 2021Review
- Treatment of Swine Closed Head Injury with Perfluorocarbon NVX-428.Medical sciences (Basel, Switzerland) · 2020Article
- ATP-sensitive potassium channels gene polymorphism rs1799858 affects the risk of macro-/micro-vascular arteriosclerotic event in patients with increased low-density lipoprotein cholesterol levels.Lipids in health and disease · 2020Article
- Imaging assessment of cardioprotection mediated by a dodecafluoropentane oxygen-carrier administered during myocardial infarction.Nuclear medicine and biology · 2019Article
- Nanomedicines: A Potential Treatment for Blood Disorder Diseases.Frontiers in bioengineering and biotechnology · 2019Review
- Efficacy of the perfluorocarbon dodecafluoropentane as an adjunct to pre-hospital resuscitation.PloS one · 2018Article
- Development of Ultrasound Microbubbles and Phase Shift Microbubbles in Theranostics.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnologyReview
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Authors and funding
6 authors.
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Abstract
purposeDodecafluoropentane emulsion (DDFPe) is a perfluorocarbon with high oxygen dissolving, transport, and delivery capacity that may offer the potential to limit ischemic injury prior to clinical reperfusion. Here we investigated the cardiac protective potential of DDFPe in a mouse model of myocardial infarction.
methodsMyocardial infarction was initiated by permanent ligation of the left anterior descending (LAD) coronary artery. Mice were administered vehicle or 5-hydroxydecanoate (5-HD) intravenously 10 min before LAD occlusion followed by a single intravenous administration of vehicle or DDFPe immediately after occlusion. Heart tissue and serum samples were collected 24 after LAD occlusion for measurement of infarct size and cardiac troponin I (cTnI) levels, respectively.
resultsDDFPe treatment reduced infarct size by approximately 72% (36.9 ± 4.2% for vehicle vs 10.4 ± 2.3% for DDFPe; p < 0.01; n = 6-8) at 24 h. Serum cTnI levels were similarly reduced by DDFPe (35.0 ± 4.6 ng/ml for vehicle vs 15.8 ± 1.6 ng/ml for DDFPe; p < 0.01; n = 6-8). Pretreatment with 5-HD, a mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) inhibitor, blocked the reduction in infarct size (29.2 ± 4.4% for 5-HD vs 35.4 ± 7.4% for 5-HD+DDFPe; p = 0.48; n = 6-8) and serum cTnI levels (27.4 ± 5.1 ng/ml for 5-HD vs 34.6 ± 5.3 ng/ml for 5-HD+DDFPe; p = 0.86; n = 6-8) by DDFPe.
conclusionOur data indicate a cardiac protective role of DDFPe that persists beyond its retention time in the body and is dependent on mitoK(ATP), an important mediator of ischemic preconditioning induced cardiac protection.
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