1,184 research outputs found

    Anti-arrhythmic effects of hypercalcemia in hyperkalemic, Langendorff-perfused mouse hearts

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    Isolated heart models for studying cardiac electrophysiology: a historical perspective and recent advances

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    Experimental models used in cardiovascular research range from cellular to whole heart preparations. Isolated whole hearts show higher levels of structural and functional integration than lower level models such as tissues or cellular fragments. Cardiovascular diseases are multi-factorial problems that are dependent on highly organized structures rather than on molecular or cellular components alone. This article first provides a general introduction on the animal models of cardiovascular diseases. It is followed by a detailed overview and a historical perspective of the different isolated heart systems with a particular focus on the Langendorff perfusion method for the study of cardiac arrhythmias. The choice of species, perfusion method, and perfusate composition are discussed in further detail with particular considerations of the theoretical and practical aspects of experimental settings

    Isolated heart models for studying cardiac electrophysiology: a historical perspective and recent advances

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    Experimental models used in cardiovascular research range from cellular to whole heart preparations. Isolated whole hearts show higher levels of structural and functional integration than lower level models such as tissues or cellular fragments. Cardiovascular diseases are multi-factorial problems that are dependent on highly organized structures rather than on molecular or cellular components alone. This article first provides a general introduction on the animal models of cardiovascular diseases. It is followed by a detailed overview and a historical perspective of the different isolated heart systems with a particular focus on the Langendorff perfusion method for the study of cardiac arrhythmias. The choice of species, perfusion method, and perfusate composition are discussed in further detail with particular considerations of the theoretical and practical aspects of experimental settings.published_or_final_versio

    Lack of Cardiac Nerve Sprouting after Intramyocardial Transplantation of Bone Marrow-Derived Stem Cells in a Swine Model of Chronic Ischemic Myocardium

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    Previous experimental studies suggested that mesenchymal stem cell transplantation causes cardiac nerve sprouting; however, whether bone marrow (BM)-derived mononuclear cells (MNC) and endothelial progenitor cells (EPC) can also lead to cardiac nerve sprouting and alter gap junction expression remains unclear. We investigated the effect of electroanatomical mapping-guided direct intramyocardial transplantation of BM-MNC (n = 8) and CD31+EPC (n = 8) compared with saline control (n = 8) on cardiac nerve sprouting and gap junction expression in a swine model of chronic ischemic myocardium. At 12 weeks after transplantation, the distribution and density of cardiac nerve sprouting were determined by staining of tyrosine hydroxylase (TH) and growth associated protein 43(GAP-43) and expression of connexin 43 in the targeted ischemic and remote normal myocardium. After 12 weeks, no animal developed sudden death after the transplantation. There were no significant differences in the number of cells with positive staining of TH and GAP-43 in the ischemic and normal myocardium between three groups. Furthermore, expression of connexin 43 was also similar in the ischemic and normal myocardia in each group of animals (P > 0.05). The results of this study demonstrated that intramyocardial BM-derived MNC or EPC transplantation in a large animal model of chronic myocardial ischemia was not associated with increased cardiac nerve sprouting over the ischemic myocardium

    Tpeak-Tend, Tpeak-Tend/QT ratio and Tpeak-Tend dispersion for risk stratification in Brugada Syndrome:A systematic review and meta-analysis

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    Background: Brugada syndrome is an ion channelopathy that predisposes affected subjects to ventricular tachycardia/fibrillation (VT/VF), potentially leading to sudden cardiac death (SCD). Tpeak-Tend intervals, (Tpeak-Tend)/QT ratio and Tpeak-Tend dispersion have been proposed for risk stratification, but their predictive values in Brugada syndrome have been challenged recently. Methods: A systematic review and meta-analysis was conducted to examine their values in predicting arrhythmic and mortality outcomes in Brugada Syndrome. PubMed and Embase databases were searched until 1 May 2018, identifying 29 and 57 studies. Results: Nine studies involving 1740 subjects (mean age 45 years old, 80% male, mean follow-up duration was 68 ± 27 months) were included. The mean Tpeak-Tend interval was 98.9 ms (95% CI: 90.5-107.2 ms) for patients with adverse events (ventricular arrhythmias or SCD) compared to 87.7 ms (95% CI: 80.5-94.9 ms) for those without such events, with a mean difference of 11.9 ms (95% CI: 3.6-20.2 ms, P = 0.005; I2 = 86%). Higher (Tpeak-Tend)/QT ratios (mean difference = 0.019, 95% CI: 0.003-0.036, P = 0.024; I2 = 74%) and Tpeak-Tend dispersion (mean difference = 7.8 ms, 95% CI: 2.1-13.4 ms, P = 0.007; I2 = 80%) were observed for the event-positive group. Conclusion: Tpeak-Tend interval, (Tpeak-Tend)/QT ratio and Tpeak-Tend dispersion were higher in high-risk than low-risk Brugada subjects, and thus offer incremental value for risk stratification

    What Is the Arrhythmic Substrate in Viral Myocarditis? Insights from Clinical and Animal Studies

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    Sudden cardiac death (SCD) remains an unsolved problem in the twenty-first century. It is often due to rapid onset, ventricular arrhythmias caused by a number of different clinical conditions. A proportion of SCD patients have identifiable diseases such as cardiomyopathies, but for others, the causes are unknown. Viral myocarditis is becoming increasingly recognized as a contributor to unexplained mortality, and is thought to be a major cause of SCD in the first two decades of life. Myocardial inflammation, ion channel dysfunction, electrophysiological, and structural remodeling may play important roles in generating life-threatening arrhythmias. The aim of this review article is to examine the electrophysiology of action potential conduction and repolarization and the mechanisms by which their derangements lead to triggered and reentrant arrhythmogenesis. By synthesizing experimental evidence from pre-clinical and clinical studies, a framework of how host (inflammation), and viral (altered cellular signaling) factors can induce ion electrophysiological and structural remodeling is illustrated. Current pharmacological options are mainly supportive, which may be accompanied by mechanical circulatory support. Heart transplantation is the only curative option in the worst case scenario. Future strategies for the management of viral myocarditis are discussed.GT was awarded a BBSRC Doctoral Training Award and thanks for the Croucher Foundation for its generous support

    Hypoxia causes transgenerational impairments in reproduction of fish

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    Channel Capacities for Different Antenna Arrays with Various Transmitting Angles in Tunnels

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    [[abstract]]This paper focuses on the research of channel capacity of multiple-input multipleoutput (MIMO) system with different transmitting angles in straight and curvy tunnels.Araytracing technique is developed to calculate channel frequency responses for tunnels, and the channel frequency response is further used to calculate corresponding channel capacity. The channel capacities are calculated based on the realistic environment. The channel capacities of MIMO long term evolution system using spatial and polar antenna arrays by different transmitting angles are computed. Numerical results show that, The channel capacity for transmitting angle at 15◦ is largest compared to the other angles in the tunnels. Moreover, the channel capacity of polar array is better than that of spatial array both in the straight and curvy tunnels. Besides, the channel capacity for the tunnels with traffic is larger than that without traffic. Finally, it isworth noting that in these cases the presentwork provides not only comparative information but also quantitative information on the performance reduction.[[notice]]補正完畢[[incitationindex]]SC
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