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 (mitoKATP) 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 mitoKATP, an important mediator of ischemic preconditioning induced cardiac protection.
Highlights
Myocardial infarction as a result of coronary heart disease is a serious health concern, accounting for more deaths each year than any other individual disease [1]
Our data indicate a cardiac protective role of dodecafluoropentane emulsion (DDFPe) that persists beyond its retention time in the body and is dependent on mitoKATP, an important mediator of ischemic preconditioning induced cardiac protection
The effect of DDFPe on infarct size was quantified from tetrazolium chloride (TTC) stained transverse cross sections of hearts from mice undergoing left anterior descending (LAD) occlusion
Summary
Myocardial infarction as a result of coronary heart disease is a serious health concern, accounting for more deaths each year than any other individual disease [1]. Myocardial infarction occurs due to occlusion of one or more arteries, typically a coronary or branching artery, supplying the myocardium. Arterial occlusion results in ischemia of the downstream tissue, which cause myocardial damage and necrosis. It is imperative that myocardial damage is limited, and the most effective therapy is the reperfusion of the ischemic tissue. Myocardial damage begins within 20 to 30 min of the ischemic period, with irreversible myocyte necrosis occurring over the course of several hours. Percutaneous coronary intervention (PCI) is a mainstay for reperfusion therapy. Reports indicate that the average door-to-balloon time for patients arriving at a facility capable of PCI is 60 min. In cases where interhospital transfer is required for PCI only 33 % have a door-
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