Articles by Dirk J Duncker in JoVE
Surgical Placement of Catheters for Long-term Cardiovascular Exercise Testing in Swine Daphne P M De Wijs-Meijler*1, Kelly Stam*2, Richard W B van Duin1, Annemarie Verzijl2, Irwin K Reiss3, Dirk J Duncker2, Daphne Merkus2 1Experimental Cardiology and Neonatology, Erasmus MC, 2Experimental Cardiology, Erasmus MC, 3Neonatology, Erasmus MC Here we present a protocol to assess cardiopulmonary function in awake swine, at rest and during graded treadmill exercise. Chronic instrumentation allows for repeated hemodynamic measurements uninfluenced by cardiodepressive anesthetic agents.
Other articles by Dirk J Duncker on PubMed
Limitation of Infarct Size and No-Reflow By Intracoronary Adenosine Depends Critically on Dose and Duration JACC. Cardiovascular Interventions. Dec, 2015 | Pubmed ID: 26738671 In the absence of effective clinical pharmacotherapy for prevention of reperfusion-mediated injury, this study re-evaluated the effects of intracoronary adenosine on infarct size and no-reflow in a porcine model of acute myocardial infarction using clinical bolus and experimental high-dose infusion regimens.
UM206, a Selective Frizzled Antagonist, Attenuates Adverse Remodeling After Myocardial Infarction in Swine Laboratory Investigation; a Journal of Technical Methods and Pathology. Feb, 2016 | Pubmed ID: 26658451 Modulation of Wnt/Frizzled signaling with UM206 reduced infarct expansion and prevented heart failure development in mice, an effect that was accompanied by increased myofibroblast presence in the infarct, suggesting that Wnt/Frizzled signaling has a key role in cardiac remodeling following myocardial infarction (MI). This study investigated the effects of modulation of Wnt/Frizzled signaling with UM206 in a swine model of reperfused MI. For this purpose, seven swine with MI were treated with continuous infusion of UM206 for 5 weeks. Six control swine were treated with vehicle. Another eight swine were sham-operated. Cardiac function was determined by echo in awake swine. Infarct mass was estimated at baseline by heart-specific fatty acid-binding protein ELISA and at follow-up using planimetry. Components of Wnt/Frizzled signaling, myofibroblast presence, and extracellular matrix were measured at follow-up with qPCR and/or histology. Results show that UM206 treatment resulted in a significant decrease in infarct mass compared with baseline (-41±10%), whereas infarct mass remained stable in the Control-MI group (+3±17%). Progressive dilation of the left ventricle occurred in the Control-MI group between 3 and 5 weeks after MI, while adverse remodeling was halted in the UM206-treated group. mRNA expression for Frizzled-4 and the Frizzled co-receptor LRP5 was increased in UM206-treated swine as compared with Control-MI swine. Myofibroblast presence was significantly lower in infarcted tissue of the UM206-treated animals (1.53±0.43% vs 3.38±0.61%) at 5 weeks follow-up. This study demonstrates that UM206 treatment attenuates adverse remodeling in a swine model of reperfused MI, indicating that Wnt/Frizzled signaling is a promising target to improve infarct healing and limit post-MI remodeling.