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Puneet Kaur Randhawa, Amteshwar Singh Jaggi
Remote ischemic preconditioning (RIPC) treatment strategy is a breakthrough in the field of cardiovascular pharmacology as it has the potential to attenuate myocardial ischemia-reperfusion injury. However, the underlying intracellular pathways have not been widely explored. The present study intends to explore the possible role of TRPV1 channels in mediating remote hind limb preconditioning-induced cardioprotection. Remote hind limb preconditioning stimulus (4 cycles in succession) was delivered by tying the blood pressure cuff at the inguinal level of the rat...
October 17, 2016: Naunyn-Schmiedeberg's Archives of Pharmacology
Nicole Kurhanewicz, Rachel McIntosh-Kastrinsky, Haiyan Tong, Allen Ledbetter, Leon Walsh, Aimen Farraj, Mehdi Hazari
Short-term exposure to ambient air pollution is linked with adverse cardiovascular effects. While previous research focused primarily on particulate matter-induced responses, gaseous air pollutants also contribute to cause short-term cardiovascular effects. Mechanisms underlying such effects have not been adequately described, however the immediate nature of the response suggests involvement of irritant neural activation and downstream autonomic dysfunction. Thus, this study examines the role of TRPA1, an irritant sensory receptor found in the airways, in the cardiac response of mice to acrolein and ozone...
October 13, 2016: Toxicology and Applied Pharmacology
Kyung Hye Lee, Sang Jin Ha, Jong-Shin Woo, Gi-Ja Lee, So-Ra Lee, Jung Wook Kim, Hun Kuk Park, Weon Kim
BACKGROUND: Exenatide exerts cardioprotective effects by attenuating ischaemic reperfusion injury, possibly through activating the opening of mitochondrial ATP-sensitive potassium channels. We used atomic force microscopy (AFM) to investigate changes in mitochondrial morphology and properties in order to assess exenatide-mediated cardioprotection in IR injury. METHODS: We used an in vivo Sprague-Dawley rat IR model and ex vivo Langendorff injury model. In the left anterior descending artery (LAD) occlusion model, animals were randomly divided into three groups: sham-operated rats (Sham, n=5), IR-injured rats treated with placebo (IR, n=6), and IR-injured treated with exenatide (IR + EXE, n=6)...
September 23, 2016: Heart, Lung & Circulation
Tobias Opthof, Carol Ann Remme, Esther Jorge, Francisco Noriega, Rob F Wiegerinck, Arlin Tasiam, Leander Beekman, Jesus Alvarez-Garcia, Cristian Munoz-Guijosa, Ruben Coronel, Juan Cinca
BACKGROUND: The repolarization pattern of the human heart is unknown. OBJECTIVE: We performed a multisite analysis of the activation-repolarization patterns and mRNA expression patterns of ion channel subunits in isolated human hearts. METHODS: Hearts from three donors without reported cardiac disease were Langendorff perfused with the patient's own blood. A standard ECG was obtained prior to explantation. Up to 92 unipolar electrograms from 24 transmural needles were obtained during right atrial pacing...
October 10, 2016: Heart Rhythm: the Official Journal of the Heart Rhythm Society
Jeppe Egedal Kirchhoff, Jonas Goldin Diness, Lea Abildgaard, Majid Sheykhzade, Morten Grunnet, Thomas Jespersen
Dose is an important parameter in terms of both efficacy and adverse effects in pharmacological treatment of atrial fibrillation (AF). Both of the class III antiarrhythmics dofetilide and amiodarone have documented anti-AF effects. While dofetilide has dose-related ventricular side effects, amiodarone primarily has adverse non-cardiac effects. Pharmacological inhibition of small conductance Ca(2+)-activated K(+) (SK) channels has recently been reported to be antiarrhythmic in a number of animal AF models. In a Langendorff model of acutely induced AF on guinea pig hearts, it was investigated whether a combination of the SK channel blocker N-(pyridin-2-yl)-4-(pyridin-2-yl)thiazol-2-amine (ICA) together with either dofetilide or amiodarone provided a synergistic effect...
October 8, 2016: Pflügers Archiv: European Journal of Physiology
Aude Belliard, Gaurav K Gulati, Qiming Duan, Rosana Alves, Shannon Brewer, Namrata Madan, Yoann Sottejeau, Xiaoliang Wang, Jennifer Kalisz, Sandrine V Pierre
Cardiac glycosides (CG) are traditionally known as positive cardiac inotropes that inhibit Na(+)/K(+)-ATPase-dependent ion transport. CG also trigger-specific signaling pathways through the cardiac Na(+)/K(+)-ATPase, with beneficial effects in ischemia/reperfusion (I/R) injury (e.g., ouabain preconditioning, known as OPC) and hypertrophy. Our current understanding of hypersensitivity to CG and subsequent toxicity in the ischemic heart is mostly based on specific I/R-induced alterations of the Na(+)/K(+)-ATPase enzymatic function and has remained incomplete...
October 2016: Physiological Reports
Xiongwen Chen, Timothy D O'Connell, Yang K Xiang
No abstract text is available yet for this article.
September 30, 2016: Circulation Research
Justin Judd, Jonathan Lovas, Guo N Huang
Cultured cardiomyocytes can be used to study cardiomyocyte biology using techniques that are complementary to in vivo systems. For example, the purity and accessibility of in vitro culture enables fine control over biochemical analyses, live imaging, and electrophysiology. Long-term culture of cardiomyocytes offers access to additional experimental approaches that cannot be completed in short term cultures. For example, the in vitro investigation of dedifferentiation, cell cycle re-entry, and cell division has thus far largely been restricted to rat cardiomyocytes, which appear to be more robust in long-term culture...
2016: Journal of Visualized Experiments: JoVE
Virginia Perez, Verónica D Annunzio, Tamara Mazo, Timoteo Marchini, Lourdes Caceres, Pablo Evelson, Ricardo J Gelpi
Thioredoxin-1 maintains the cellular redox status and decreases the infarct size in ischemia/reperfusion injury. However, whether the increase of thioredoxin-1 expression or its lack of activity modifies the protection conferred by ischemic postconditioning has not been yet elucidated. The aim was to evaluate if the thioredoxin-1 overexpression enhances the posctconditioning protective effect, and whether the lack of the activity abolishes the reduction of the infarct size. Wild type mice hearts, transgenic mice hearts overexpressing thioredoxin-1, and a dominant negative mutant (C32S/C35S) of thioredoxin-1 were used...
September 25, 2016: International Journal of Biochemistry & Cell Biology
Ngonidzashe B Madungwe, Netanel F Zilberstein, Yansheng Feng, Jean C Bopassa
Reactive oxygen species (ROS) generation has been implicated in many pathologies including ischemia/reperfusion (I/R) injury. This led to multiple studies on antioxidant therapies to treat cardiovascular diseases but paradoxically, results have so far been mixed as ROS production can be beneficial as a signaling mechanism and in cardiac protection via preconditioning interventions. We investigated whether the differential impact of increased ROS in injury as well as in protection could be explained by their site of production on the mitochondrial electron transport chain...
2016: American Journal of Cardiovascular Disease
Lei Yang, Yan Zhang, Mengmeng Zhu, Qiong Zhang, Xiaoling Wang, Yanjiao Wang, Jincai Zhang, Jing Li, Liang Yang, Jie Liu, Fei Liu, Yinan Yang, Licheng Kang, Yanna Shen, Zhi Qi
The objective was to examine the protective effect of resveratrol (RSV) on myocardial ischemia/reperfusion (IR) injury and whether the mechanism was related to vascular endothelial growth factor B (VEGF-B) signaling pathway. Rat hearts were isolated for Langendorff perfusion test and H9c2 cells were used for in vitro assessments. RSV treatment significantly improved left ventricular function, inhibited CK-MB release, and reduced infarct size in comparison with IR group ex vivo. RSV treatment markedly decreased cell death and apoptosis of H9c2 cells during IR...
September 22, 2016: Free Radical Biology & Medicine
Farzaneh Faraji Shahrivar, Mohammad Badavi, Mahin Dianat, Ali Mard, Akram Ahangarpour, Alireza Samarbaf-Zadeh
The most important conditions associated with hypothyroidism is the cardiac dysfunction. Apelin is an endogenous ligand, involved in energy storage and metabolism which improves cardiac contractility. This study was done to evaluate the effects of apelin, l-Thyroxin (T4) or a combination of both, on cardiac function and mRNA expression of two contractile proteins, α and β myosin heavy chain (α-MHC and β-MHC), in 6-propyl-2-thiouracil (PTU)-induced hypothyroid rats. Forty male Wistar rats were randomly assigned into five groups: Ctrl (Control), and 4 hypothyroid groups (H, HA, HT, and HAT)...
September 20, 2016: Gene
Sebastian Kötter, Malgorzata Kazmierowska, Christian Andresen, Katharina Bottermann, Maria Grandoch, Simone Gorressen, Andre Heinen, Jens M Moll, Jürgen Scheller, Axel Gödecke, Jens W Fischer, Joachim P Schmitt, Martina Krüger
RATIONALE: Myocardial infarction (MI) increases the wall stress in the viable myocardium and initiates early adaptive remodeling in the left ventricle to maintain cardiac output. Later remodeling processes include fibrotic reorganization that eventually leads to cardiac failure. Understanding the mechanisms that support cardiac function in the early phase post MI and identifying the processes that initiate transition to maladaptive remodeling are of major clinical interest. OBJECTIVE: To characterize MI-induced changes in titin-based cardiac myocyte stiffness and to elucidate the role of titin in ventricular remodeling of remote myocardium in the early phase after MI...
October 14, 2016: Circulation Research
Kiyoshi Takasuna, Keiichi Asakura, Seiichi Araki, Hiroyuki Ando, Katsuyuki Kazusa, Takashi Kitaguchi, Takeshi Kunimatsu, Shinobu Suzuki, Norimasa Miyamoto
Recent increasing evidence suggests that the currently-used platforms in vitro IKr and APD, and/or in vivo QT assays are not fully predictive for TdP, and do not address potential arrhythmia (VT and/or VF) induced by diverse mechanisms of action. In addition, other cardiac safety liabilities such as functional dysfunction of excitation-contraction coupling (contractility) and structural damage (morphological damage to cardiomyocytes) are also major causes of drug attrition, but current in vitro assays do not cover all these liabilities...
September 17, 2016: Journal of Pharmacological and Toxicological Methods
Heike A Hildebrandt, Vincent Kreienkamp, Sabine Gent, Philipp Kahlert, Gerd Heusch, Petra Kleinbongard
Although remote ischemic pre-conditioning (RIPC) reduced infarct size in animal experiments and proof-of-concept clinical trials, recent phase III trials failed to confirm cardioprotection during cardiac surgery. Here, we characterized the kinetic properties of humoral factors that are released after RIPC, as well as the signal transduction pathways that were responsible for cardioprotection in an ex vivo model of global ischemia reperfusion injury. Venous blood from 20 healthy volunteers was collected at baseline and 5 min, 30 min, 1 h, 6 h, and daily from 1 to 7 days after RIPC (3 × 5/5 min upper-limb ischemia/reperfusion)...
January 2016: JACC. Basic to Translational Science
Gary Tse, Jie Ming Yeo, Vivian Tse, Joseph Kwan, Bing Sun
In the current study, arrhythmogenic effects of the gap junction inhibitor heptanol (0.05 mM) were examined in Langendorff-perfused mouse hearts. Monophasic action potential recordings were obtained from the left ventricular epicardium during right ventricular pacing. Regular activity was observed both prior and subsequent to application of heptanol in all of the 12 hearts studied during 8 Hz pacing. By contrast, induced ventricular tachycardia (VT) was observed after heptanol treatment in 6/12 hearts using a S1S2 protocol (Fisher's exact test; P<0...
September 13, 2016: Molecular Medicine Reports
Bochra Tourki, Philippe Matéo, Jessica Morand, Mohamed Elayeb, Diane Godin-Ribuot, Naziha Marrakchi, Elise Belaidi, Erij Messadi
Cardiac ischemia is one of the leading causes of death worldwide. It is now well established that natriuretic peptides can attenuate the development of irreversible ischemic injury during myocardial infarction. Lebetin 2 (L2) is a new discovered peptide isolated from Macrovipera lebetina venom with structural similarity to B-type natriuretic peptide (BNP). Our objectives were to define the acute cardioprotective actions of L2 in isolated Langendorff-perfused rat hearts after regional or global ischemia-reperfusion (IR)...
2016: PloS One
Veronique M F Meijborg, Mark Potse, Chantal E Conrath, Charly N W Belterman, Jacques M T De Bakker, Ruben Coronel
BACKGROUND: J-waves in inferolateral leads are associated with a higher risk for idiopathic ventricular fibrillation. We aimed to test potential mechanisms (depolarization or repolarization dependent) responsible for inferolateral J-waves. We hypothesized that inferolateral J-waves can be caused by regional delayed activation of myocardium that is activated late during normal conditions. METHODS: Computer simulations were performed to evaluate how J-point elevation is influenced by reducing sodium current conductivity (GNa), increasing transient outward current conductivity (Gto), or cellular uncoupling in three predefined ventricular regions (lateral, anterior, or septal)...
2016: Frontiers in Physiology
Lara Testai, Alice Marino, Ilaria Piano, Vincenzo Brancaleone, Kengo Tomita, Lorenzo Di Cesare Mannelli, Alma Martelli, Valentina Citi, Maria C Breschi, Roberto Levi, Claudia Gargini, Mariarosaria Bucci, Giuseppe Cirino, Carla Ghelardini, Vincenzo Calderone
The endogenous gasotransmitter hydrogen sulphide (H2S) is an important regulator of the cardiovascular system, particularly of myocardial function. Moreover, H2S exhibits cardioprotective activity against ischemia/reperfusion (I/R) or hypoxic injury, and is considered an important mediator of "ischemic preconditioning", through activation of mitochondrial potassium channels, reduction of oxidative stress, activation of the endogenous "anti-oxidant machinery" and limitation of inflammatory responses. Accordingly, H2S-donors, i...
September 9, 2016: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
Ernestina M De Francesco, Carmine Rocca, Francesco Scavello, Daniela Amelio, Teresa Pasqua, Damiano C Rigiracciolo, Andrea Scarpelli, Silvia Avino, Francesca Cirillo, Nicola Amodio, Maria C Cerra, Marcello Maggiolini, Tommaso Angelone
The use of Doxorubicin (Dox), a frontline drug for many cancers, is often complicated by dose-limiting cardiotoxicity in approximately 20% of patients. The G-protein estrogen receptor GPER/GPR30 mediates estrogen action as the cardioprotection under certain stressful conditions. For instance, GPER activation by the selective agonist G-1 reduced myocardial inflammation, improved immunosuppression, triggered pro-survival signaling cascades, improved myocardial mechanical performance and reduced infarct size after ischemia/reperfusion (I/R) injury...
September 8, 2016: Journal of Cellular Physiology
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