July 25, 2016
How well do we understand the post-translational molecular mechanisms regulating changes in metabolism in the newborn heart? This podcast seeks the answer, as Associate Editor Ajay Shah (King’s College London, British Heart Foundation Centre of Excellence) interviews lead author Gary Lopaschuk (University of Alberta) and content expert Luc Bertrand (Université catholique de Louvain) about the work by Fukushima et al, which found rapid acetylation of a number of fatty acid oxidative enzymes, and increased fatty acid oxidation activity, in the newborn rabbit heart. Why is increased expression of mitochondrial acetyltransferase GCN5L1 important in the changes observed by Lopaschuk and colleagues? Could this be a “master regulator” of protein acetylation? Listen and find out.
Arata Fukushima, Osama Abo Alrob, Liyan Zhang, Cory S Wagg, Tariq Altamimi, Sonia Rawat, Ivan M. Rebeyka, Paul F. Kantor, Gary D. Lopaschuk Acetylation and Succinylation Contribute to Maturational Alterations in Energy Metabolism in the Newborn Heart Am J Physiol Heart Circ Physiol, published June 3, 2016. DOI: 10.1152/ajpheart.00900.2015
July 21, 2016
Can restoring parasympathetic nerve activity in patients with primary hypertension prevent cardiovascular end organ damage? In this podcast Associate Editor Debra Diz (Wake Forest University School of Medicine) interviews lead author Harald Stauss (University of Iowa) and content expert Douglas Martin (University of South Dakota) about the study by Chapleau et al. Referred to as a “a technological tour de force” that combined chronic vagal nerve stimulation, chronic telemetric blood pressure measurements, and in vivo imaging of the long posterior ciliary artery (LPCA) using the slit lamp approach to assess endothelial function, the authors found that endothelial function improved, without changes in blood pressure. Does this approach have the potential to interrupt the pathway between blood pressure and end organ damage, when lowering blood pressure could lead to adverse clinical ramifications in elderly fall risk patients, for example? Listen and learn.
Mark W. Chapleau, Diane L Rotella, John J Reho, Kamal Rahmouni, Harald M. Stauss Chronic Vagal Nerve Stimulation Prevents High-Salt Diet-Induced Endothelial Dysfunction and Aortic Stiffening in Stroke-Prone Spontaneously Hypertensive Rats Am J Physiol Heart Circ Physiol, published May 20, 2016. DOI: 10.1152/ajpheart.00043.2016
July 20, 2016
What is the connection between Tromso, Norway, hypothermia, rewarming, heart failure…and AJP-Heart and Circ? Listen to this fascinating new podcast as Associate Editor Leon De Windt (Cardiovascular Research Institute Maastricht) interviews lead author Gary Sieck (Mayo Clinic) and content expert Jolanda van der Velden (VU University Medical Center Amsterdam) about the intriguing and entirely unique work by Schaible at al, which explores how to protect the heart during rewarming after hypothermia. Whatever the cause of hypothermia—falling into a fjord, skiing accident—inadequate rewarming at a trauma center and/or restarting the heart in the field by first responders can both lead to heart failure. Listen as we discuss how hypothermia can inhibit the SERCA pump, as well as affect the sodium-calcium exchanger, slowing the clearance of calcium. Is it possible for a hypothermic person in asystole, if CPR is administered to restore circulation, to later be rewarmed and survive without any deficits or long-term side effects? Listen and find out.
Niccole Schaible, Young Soo Han, Thuy Hoang, Grace Arteaga, Torkjel Tveita, Gary Sieck Hypothermia/rewarming disrupts excitation-contraction coupling in cardiomyocytes Am J Physiol Heart Circ Physiol, published June 1, 2016. DOI: 10.1152/ajpheart.00840.2015
July 11, 2016
What role do circulating nucleotides play in the pathobiology of pulmonary arterial hypertension (PAH)? In this new podcast Associate Editor Robert Hester (University of Mississippi Medical Center) interviews lead author Scott Visovatti (University of Michigan) and content expert Nikki Jernigan (University of New Mexico Health Sciences Center) about the clinically important work by Visovatti and colleagues investigating whether CD39—an extracellular nucleotidase responsible for the dephosphorylation of ATP—could be a key trigger for idiopathic PAH. By first investigating human blood and tissue samples of pulmonary arterial hypertension patients, followed by data from a unique CD39 knockout hypoxic mouse model, Visovatti and co-authors gained valuable insight into the PAH phenotype. What two “rescue approaches” did the authors use to lower right ventricular and pulmonary pressures in the CD39 mouse model? Listen and find out.
Scott H Visovatti, Matthew C Hyman, Sascha N Goonewardena, Anuli C. Anyanwu, Yogendra Kanthi, Patrick Robichaud, Jintao Wang, Danica Petrovic-Djergovic, Rahul Rattan, Charles F. Burant, David J Pinsky Purinergic dysregulation in pulmonary hypertension Am J Physiol Heart Circ Physiol, published May 20, 2016. DOI: 10.1152/ajpheart.00572.2015