TY - JOUR. T1 - Optimal conditions for palmitate oxidation by rat heart homogenates. AU - Passeron, Susana. AU - Savageau, Michael A.. AU - Harary, Isaac. PY - 1968/10. Y1 - 1968/10. N2 - A study of the oxidation of palmitate-1-C14 to C14O2 by heart homogenates was undertaken and the optimal conditions were determined. The system has an absolute requirement for carnitine, CoA, ATP, and Mg2+. The levels of ATP and Mg2+ for the optimal rate of palmitate oxidation are interdependent. Excess of ATP or Mg2+ inhibits the production of CO2. The amount of fatty acid oxidized is dependent on the molar ratio of fatty acid to albumin in the incubation medium: an optimal ratio of approximately 5 was found for all the concentrations of fatty acid and albumin tested. A tentative mechanism for the albumin effect is presented.. AB - A study of the oxidation of palmitate-1-C14 to C14O2 by heart homogenates was undertaken and the optimal conditions were determined. The system has an absolute requirement for ...
294596050 - EP 1064356 A2 2001-01-03 - CARDIAC-DERIVED STEM CELLS - [origin: WO9949015A2] The invention provides cardiac-derived pluripotent stem cells, which on proliferation and differentiation can produce a variety of cell types including cardiocytes, fibroblasts, smooth muscle cells, skeletal muscle cells, keratinocytes, osteoblasts and chondrocytes. The cells can be used in methods of treating patients suffering from necrotic heart tissue. The stem cells proliferate and differentiate to produce cardiocytes replacing the necrotic tissue. The cells can also be used to screen compounds for activity in promoting proliferation and/or differentiation of cardiac-derived stem cells.[origin: WO9949015A2] The invention provides cardiac-derived pluripotent stem cells, which on proliferation and differentiation can produce a variety of cell types including cardiocytes, fibroblasts, smooth muscle cells, skeletal muscle cells, keratinocytes, osteoblasts and chondrocytes. The cells can be used in methods of
Fiction is the lie through which we tell the truth". One of the fundamental principles behind urgent revascularization of the culprit coronary vessel in patients with acute myocardial infarction (AMI) is to salvage ischemic but still viable myocardium and thereby reduce final infarct size and improve survival.1 Cardiovascular magnetic resonance (CMR) imaging can quantify salvaged myocardium by comparing edema extent in T2-weighted sequences (myocardium at risk [MAR]) with infarcted myocardium in T1-weighted late gadolinium enhancement images.2 Accordingly, CMR parameters of myocardial injury are widely used as measures of reperfusion efficacy and prognostic markers after AMI in both routine clinical practice and as a surrogate endpoint in clinical trials.3, 4 However, the accurate delineation of MAR is crucial to correctly estimate myocardial salvage. Whether or not the regions with high T2 signal intensity in CMR imaging correspond to the true MAR is hotly debated within the CMR community.5, 6 ...
We have examined the expression of 13 proto-oncogenes in proliferating and terminally differentiated cardiac and skeletal muscle. Total RNA was prepared from intact ventricular cardiac-muscle tissue and from purified ventricular cardiac-muscle cells of neonatal and adult rats and from cultured proliferating and terminally differentiated L6A1 rat skeletal-muscle cells. cDNA probes for histone H4, thymidine kinase, myosin heavy chain and M-creatine kinase were used to assess cellular proliferation and differentiation. Oncogenes c-myc, c-raf, c-erb-A, c-ras-H, c-ski, and c-sis were expressed in both proliferating and differentiated cardiac muscle tissue and cells, whereas c-myb expression was not observed in either. c-src was expressed only in neonatal cardiac muscle tissue and cells. c-fms, c-abl, and c-ras-K were expressed in tissue from both neonatal and adult animals but only in purified cells from neonatal animals. c-fes/fps was expressed only in neonatal cardiac muscles cells. c-fos ...
Dutch researchers have made a breakthrough in stem cell research by successfully growing stem cells from adult human heart into new heart muscle cells.
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Recently published studies suggest that the procoagulant receptor protein tissue factor (TF) is involved in vitro in cell adhesion and migration, via an interaction of its cytoplasmic domain with cytoskeletal proteins. Interestingly, TF is abundantly expressed in myocardium, but not in skeletal muscle. To elucidate the possible roles of TF in the myocardium, this study examined the cellular distribution of TF in relation to cytoskeletal proteins, as well as its relative amounts in different segments of premature, mature, and pathologically altered cardiac muscle. In juvenile and adult hearts, TF was predominantly detectable in the transverse part of the intercalated discs, where it co-localized with cytoskeletal proteins such as desmin and vinculin. The lowest amount of TF was observed in right atrial and the highest in left ventricular myocardium, which correlated with the number of contact sites of cardiomyocytes in these segments of the cardiac muscle. Lower levels of TF were present in structurally
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Cardiac Pathophysiology * Treatment: relieve symptoms of heart failure, decrease workload, and anticoagulants; transplants Chest pain Dizziness Fainting, especially ... – A free PowerPoint PPT presentation (displayed as a Flash slide show) on PowerShow.com - id: 48655e-OWMyZ
The current study reveals several key findings with regard to endogenous cardiac TAG metabolism under both baseline (i.e., normoxia) and I-R conditions. First, increased TAG content and turnover as a result of DGAT1 overexpression do not adversely affect cardiac function, energetics, or the oxidation of exogenous substrates. Second, DGAT1 overexpression significantly increased the incorporation rates of various LCFAs into the TAG pool. Third, our data show that maintaining elevated TAG turnover rates during reperfusion after acute ischemia is cardioprotective, in part, by sequestering fatty acids into the TAG pool and reducing the accumulation of ceramides. Last, we show that when palmitate is the sole source of exogenous fatty acids during the reperfusion period, there are deleterious effects on recovery from ischemia in DGAT1 transgenic hearts. All told, our findings demonstrate an important role of endogenous cardiac TAG metabolism in determining outcomes of cardiac stress. Moreover, they ...
PURPOSE: A quantitative 31P-MR-spectroscopic technique was used to assess the energy metabolism in healthy and diseased myocardium. METHODS: 31P spectra were acquired on a 1.5 T scanner using a 3D-chemical shift imaging technique. Based on the anatomical information provided by 1H images, SLOOP (Spatial Localization with Optimal Pointspread Function) allows to obtain spectra from defined compartments. With SLOOP a free voxel shape with adaption to anatomic structures, e.g. the myocardium, is possible. Absolute values for phosphocreatine (PCr) and adenosine triphosphate (ATP) were determined using an external standard. RESULTS: 31P-spectra showed only minimal contamination by surrounding tissue. The standard deviation for the determined values of healthy volunteers was low. Compared to healthy volunteers, reduced PCr and ATP concentrations were seen for dilative cardiomyopathies and coronary artery disease and unchanged concentrations were observed for hypertensive heart disease. CONCLUSION: 31P-MR
In the present study, we have quantified levels of myotrophin concentration in the hearts of SHR and normal rats of different age groups. Myotrophin was quantified in normal and hypertrophied rat hearts for various age groups by using the specific antibody raised against MAP. The antibody was characterized by solid-phase radioimmunoassays and Western blot analysis. To define the specificity of the polyclonal antibody raised against myotrophin, the affinity constant was calculated from the Scatchard plot. The accuracy of the quantification depends on the specificity of the antibody raised against MAP and its affinity toward the antigen (myotrophin). The specificity of the antibody has been established by three methods. First, we determined the affinity constant of the myotrophin antibody from the Scatchard plot as described in "Materials and Methods." The Scatchard plot was constructed by plotting the ratio of bound to free myotrophin against the concentration of bound myotrophin. The ...
Hello, are you looking for article NursingCrib.com Nursing Care Plan Myocardia Infarction by ? If it is true we are very fortunate in being able to provide information NursingCrib.com Nursing Care Plan Myocardia Infarction by And good article NursingCrib.com Nursing Care Plan Myocardia Infarction by This could benefit/solution for you. ...
Despite normal blood pressures, overweight teenage boys might be at an increased risk of suffering from heart damage, according to a new study led by Indian-origin researcher.
G protein-coupled receptor (GPCR) kinases (GRKs) are critical regulators of cellular signaling and function. In cardiomyocytes, GRK2 and GRK5 are two GRKs important for myocardial regulation, and both have been shown to be up-regulated in the dysfunctional heart. We report that increased levels and activity of GRK5 in failing myocardium may have unique significance due to its nuclear localization, a property not shared by GRK2. We find that transgenic mice with elevated cardiac GRK5 levels have exaggerated hypertrophy and early heart failure compared with control mice after pressure overload. This pathology is not present in cardiac GRK2-overexpressing mice or in mice with overexpression of a mutant GRK5 that is excluded from the nucleus. Nuclear accumulation of GRK5 is enhanced in myocytes after aortic banding in vivo and in vitro in myocytes after increased Gαq activity, the trigger for pressure-overload hypertrophy. GRK5 enhances activation of MEF2 in concert with Gq signals, demonstrating ...
MP Biomedicals has a wide range of Rapid test & Immuno assay test Kits to diagnose different Cardiac markers like, serum accute phase proteins (CRP proteins) and other Cardiac proteins. These diferent cardiac markers cover some enzymes to screen myocardial infraction.It also consists of some proteins, motor proteins helps to make cardiac muscle contraction and relaxation. Learn More ...
Here we describe a novel method to reproducibly fabricate cardiac network patches with pores of controlled size and elongation in order to improve oxygen diffusion and locally control 3D cell alignment inside the patch. Specifically, PDMS molds were cast against a microfabricated master made of UV-curable resin and injected with a mixture of neonatal rat cardiac cells, fibrin gel, and matrigel (Fig. A1- 4⇓). After a week of culture, initial cell density was increased an order of magnitude by gel compaction. After 4 weeks, differentiated cardiomyocytes were densely packed, highly aligned and interconnected throughout the patch (Fig. B⇓). The majority of non-cardiomyocytes were localized at the outer surface of the networks. Transmembrane voltage was optically mapped using a voltage sensitive dye (di-4-ANEPPS) and a 504 channel photodiode array. Tissue networks vigorously and synchronously contracted at rates that decreased over time in culture from 4~5Hz to~1Hz. At week 4, electrical ...
By manipulating stem cells, scientists have found they can grow beating cardiac tissue in a petri dish. The cells self-organized to form microchamber ...
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Whole hearts and cardiac muscle sections. Hearts from 10 week old Destm1Cap/Destm1Cap (-/-, A) and wild type (WT, E) mice demonstrate extensive areas of degeneration and calcification throughout the myocardium of mutant mice. Sections from mutant mice (B and C) and corresponding areas in wild type (F and G) were stained with Massons trichrome to reveal areas of interstitial fibrosis and degeneration. High magnification of cardiac myofibers taken from nonfibrotic regions of mutant myocardium (D) and wild type (H) myocardium stained with hematoxylin and eosin. Several of the fibers from the mutant myocardium appear to be disrupted and disintegrating. Bars: D and H, 5um; C and G, 10um ...
Read and get a deeper understanding with our free articles on the topic: The cardiac muscle tissue is found in the myocardium and is responsible for the contraction of the heart.
Several investigators have used stereological methods to estimate the volume fraction of the heart occupied by its major constituent cell types.1-4,11 In rat or human heart sections imaged by light microscopy, the volume fraction occupied by cardiomyocytes, ECs, and interstitial cells was 70% to 80%, 3.2% to 5.3%, and 1.4% to 1.9%, respectively.1-3,11 Because the mean volume of cardiomyocytes is 20× to 25× that of ECs or fibroblasts,1,2 this leads to an estimated proportion of ECs to cardiomyocytes of 0.8 to 1.9 and fibroblasts to cardiomyocytes of 0.4 to 0.7, that is, based on these studies, ECs are among the most abundant cell types in the heart, whereas fibroblasts are 2- to 3-fold less abundant (Figure).. Heart dissociation followed by immunostaining and flow cytometric analysis has also been used to measure the cellular composition of the heart. Using this strategy, Banerjee et al6 evaluated the composition of the mouse and the rat hearts, marking cardiomyocytes, ECs, and fibroblasts with ...
Pouleur, H. ; Rousseau, MF. ; van Eyll, Christian. Evidence for a Selective Improvement of the Chronically Ischemic Myocardium After Calcium-antagonist Administration.In: Circulation (Baltimore), Vol. 68, no. 4, p. 402-402 (1983 ...
Histoenzymological techniques were used to examine ATPase activity in rat heart muscle fibres after experimental infarction. 25 hours after coronary ligation, ATPase activity in all ventricular section fibres was high, homogeneous at pH 9.4, sections
Cardiac enzymes are sometimes called heart damage markers because they are released into the bloodstream when heart muscle cells are damaged. ...
Cardiac enzymes are sometimes called heart damage markers because they are released into the bloodstream when heart muscle cells are damaged. ...
Expression levels of miRs specifically up-regulated in CMC (A) or in both cultured cardiac interstitial cells and NIH3T3 fibroblasts (B). The relative expressio
Absence of PTPσ restores innervation to the infarcted myocardium and prevents arrhythmias.Heart sections from HET (a) and KO (b) mice were stained for TH (gree
In this guide we explain how alcohol is capable of damaging your heart. We also explain a number of steps you may take to reduce these risks.
infection is the thing to stop, trying to make well a person already infected is a medical emergency.. Covid is a series of infectious viruses.. S protein on virus surface has two parts: The S1 interacts with the ACE-2 Receptor on the human cell to decoy and S2 from clamping to the surface of the exposed target cell membrane, an thereafter disrupting the membrane between virus and the cell cytosole, that disruption causes the cell to open a pore tunnel thru both layers of membrane which enables the virus to crawl into into the cytosol of the live living human cell (this stage, the first, is called infection). Everything after that is up to immune system to overcome until after the 10 th day or so, then the damage the Immune system caused becomes a factor in whether or not the patient recovers or dies. The focus should be on preventing infection. But no body wants to hear that.. Wear a mask and gloves. Infected patients are at the mercy of their own immune system to win the battle with the virus, ...
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Washington, May 12 - In a first, scientists have merged stem cell and organ-on-a-chip technologies to grow functioning human heart tissue carrying an inherited cardiovascular disease.The research is a big step forward for personalised medicine as now, a
Researchers at the UC College of Medicine have shown that a new targeted treatment could benefit patients with certain pancreatic tumors.
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01:06, 16 April 2011 (diff , hist) . . (+4,557)‎ . . N LavaMD ‎ (Created page with Myocyte application models cardiac myocyte (heart muscle cell) and simulates its behavior according to the work by Saucerman and Bers [8]. The model integrates cardiac myocyte el...) ...
Lack of understanding of basic stem cell mechanisms limits current therapeutic approaches. In this renewal application, we will focus on the use of c-kit* cardi...
A resting radionuclide scan that can identify metabolically impaired myocardium may be able to stratify patients with end-stage renal disease (ESRD) but no apparent heart disease, according to risk of death from cardiac causes, suggests a study in the Jan.15 issue Journal of the American College of Cardiology.
We`re excited to receive this funding, which represents our first major grant to explore the potential of stem cells to repair heart damage,says Darwin Prockop, the center`s director. This is a medical problem of tremendous importance, because heart disease is the leading cause of death of American adults ...
The increased activity of pyruvate dehydrogenase (PDH) kinase induced in hearts of rats by starvation for 48 h was maintained following preparation of cardiac myocytes, and it was also maintained, though at a decreased level, after 25 h of culture in medium 199. This loss of PDH kinase activity was not prevented by n-octanoate, dibutyryl cyclic AMP or glucagon. The PDH kinase activity of myocytes from fed rats was increased to that of starved rats after 25 h of culture with n-octanoate, dibutyryl cyclic AMP or both agents together. ...
In our laboratory, recent single cell electrophysiologic studies have demonstrated the absence of voltage-gated Ca2+ channels in human cardiac fibroblasts. The more positive membrane potential found in these cells suggests that Ca2+ entry occurs through a different mechanism. We hypothesized that non-voltage-gated Ca2+-permeable TRP channels are responsible for Ca2+ entry in human cardiac fibroblasts. With informed consent, right atrial biopsies were obtained from patients undergoing cardiac surgery (n=4:.3M, 1F; mean age 65±8 yrs, EF 63±5%, LVEDP 24±4 mm Hg). Fibroblasts were dissociated and cultured for 7 to 10 days. We found that TRPC1, TRPC4, TRPC6, TRPV4, TRPV5, TRPV6, TRPM4 and TRPM7 were detectable at message levels by RT-PCR. Functional expression of these channels was evaluated by patch-clamp technique. An outward rectifying current with typical I-V relation of TRPM7 was readily recorded in the fibroblasts. The averaged current density was 14.5±0.8 pA/pF (mean±SEM, n=60 from four ...
The Neonatal Cardiac Fibroblast Isolation Kit, rat has been designed for the enrichment of cardiac fibroblasts from dissociated neonatal rat hearts. The isolation of cardiac fibroblasts has been successfully tested using neonatal rat hearts from postnatal day 0 to day 3 (P0- P3). - Österreich
The second messenger cyclic adenosine monophosphate (cAMP) is the most important modulator of sympathetic control over cardiac contractility. In cardiac myocytes and many other cell types, however, cAMP transduces the signal generated upon stimulation of various receptors and activates different cellular functions, raising the issue of how specificity can be achieved. In the general field of signal transduction, the view is emerging that specificity is guaranteed by tight localization of signaling events. Here, we show that in neonatal rat cardiac myocytes, beta-adrenergic stimulation generates multiple microdomains with increased concentration of cAMP in correspondence with the region of the transverse tubule/junctional sarcoplasmic reticulum membrane. The restricted pools of cAMP show a range of action as small as approximately 1 micrometer, and free diffusion of the second messenger is limited by the activity of phosphodiesterases. Furthermore, we demonstrate that such gradients of cAMP specifically
BioAssay record AID 705505 submitted by ChEMBL: Binding affinity to PX domain-containing protein kinase-like protein in Sprague-Dawley rat heart homogenate after 15 mins by chromatographic analysis relative to pioglitazone.
TY - JOUR. T1 - Increased Ca2+-sensitivity of the contractile apparatus in end-stage human heart failure results from altered phosphorylation of contractile proteins. AU - Van der Velden, J.. AU - Papp, Z.. AU - Zaremba, R.. AU - Boontje, N. M.. AU - De Jong, J. W.. AU - Owen, V. J.. AU - Burton, P. B.J.. AU - Goldmann, P.. AU - Jaquet, K.. AU - Stienen, G. J.M.. PY - 2003/1/1. Y1 - 2003/1/1. N2 - Objective: The alterations in contractile proteins underlying enhanced Ca2+-sensitivity of the contractile apparatus in end-stage failing human myocardium are still not resolved. In the present study an attempt was made to reveal to what extent protein alterations contribute to the increased Ca2+-responsiveness in human heart failure. Methods: Isometric force and its Ca2+-sensitivity were studied in single left ventricular myocytes from non-failing donor (n=6) and end-stage failing (n=10) hearts. To elucidate which protein alterations contribute to the increased Ca2+-responsiveness isoform composition ...
Background: There is an ongoing debate about the significance of cardiac troponin T (cTnT) elevation after strenuous exercise: heart muscle cell death versus physiologic mechanism of release through an intact cell membrane. While cTnT is a small molecule (37 kDa), cardiac specific myosin heavy chain-alpha (MHC-α) is much larger (224 kDa) and an increase after exercise could hardly be explained by passage through an intact cardiac cell membrane. PURPOSE: To measure MHC-α, and other biomarkers (C-reactive protein (CRP); cTnT, creatine kinase (CK), myoglobin (MG), creatinine (C), and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) before and after a full distance Ironman in order to answer the question of heart muscle cell death versus physiologic changes. Methods: In 52 non-elite athletes (14 female, 38 male; age 41.1 ± 9.7, range 24-70 years; all completed the race) biomarkers were measured by standard laboratory methods 7 days before, directly after, and day 1, 4 and 6 after ...
The authors investigated the regulatory effects of sulfur dioxide (SO2) on myocardial injury induced by isopropylarterenol (ISO) hydrochloride and its mechanisms. Wistar rats were divided into four groups: control group, ISO group, ISO plus SO2 group, and SO2 only group. Cardiac function was measured and cardiomyocyte apoptosis was detected. Bcl-2, bax and cytochrome c (cytc) expressions, and caspase-9 and caspase-3 activities in the left ventricular tissues were examined in the rats. The opening status of myocardial mitochondrial permeability transition pore (MPTP) and membrane potential were analyzed. The results showed that ISO-treated rats developed heart dysfunction and cardiac injury. Furthermore, cardiomyocyte apoptosis in the left ventricular tissues was augmented, left ventricular tissue bcl-2 expression was down-regulated, bax expression was up-regulated, mitochondrial membrane potential was significantly reduced, MPTP opened, cytc release from mitochondrion into cytoplasm was ...
Embryonic Heart Exhibits Impressive Regenerative Capacity Monday, 13 October 2008 A new study demonstrates that the embryonic mouse heart has an astounding capacity to regenerate, a phenomenon previously observed only in non-mammalian species. The research, published by Cell Press in the October 14th issue of the journal Developmental Cell, describes the previously unrecognized potential of the embryonic heart to replace diseased tissue through compensatory proliferation of healthy cells. Disorders of the mitochondria, a cell structure required for energy production, are one of the leading causes of fatal early onset cardiomyopathies. To investigate how mutations that interfere with mitochondrial function impact the heart during development, Professor Timothy C. Cox from the University of Washington in Seattle and colleagues from Australia, used a heart-specific knockout approach in mice to inactivate a gene crucial for normal mitochondrial function. Their experimental methods established ...
Accumulating evidence supports the notion that the renin-angiotensin system exists not only in the blood circulation but also in cardiac tissues.34 35 Recently, it has been reported that Ang II induces hypertrophy of cultured cardiac myocytes from neonatal rats9 and embryonic chick8 and also causes the proliferation of cultured neonatal rat cardiac fibroblasts.9 Furthermore, very recently, using an in vitro model of load (stretch)-induced cardiac hypertrophy, Sadoshima et al10 have obtained evidence showing that mechanical stretch leads to release of Ang II from neonatal rat ventricular myocytes and the released Ang II acts as an initial mediator of the stretch-induced hypertrophic response. All these findings, obtained by in vitro studies,8 9 10 support the notion that autocrine release of Ang II from cardiac myocytes is involved in load (stretch)-induced growth of ventricular myocytes, thereby suggesting the central role of Ang II in cardiac hypertrophy and remodeling. However, it remains to ...
This study describes the use of a microperfusion system to create rapid, large regional changes in intracellular pH (pH(i)) within single ventricular myocytes. The spatial distribution of pH(i) in single myocytes was measured with seminaphthorhodafluor-1 fluorescence using confocal imaging. Changes in pH(i) were induced by local external application of NH(4)Cl, CO(2), or sodium propionate. Local application was achieved by simultaneously directing two parallel square microstreams, each 275 microm wide, over a single myocyte oriented perpendicular to the direction of flow. One stream contained the control solution, and the other contained a weak acid or base. End-to-end, stable pH(i) gradients as large as 1 pH unit were readily created with this technique. This result indicates that pH within a single cardiac cell may not always be spatially uniform, particularly when weak acid or base gradients are present, which can occur, for example, in regional myocardial ischemia. The microperfusion method should
Most heart muscle cells formed during childhood New human heart muscle cells can be formed, but this mainly happens during the first 10 years of life. Other cell types, however, are replaced more quickly. The study demonstrates that the heart muscle is regenerated throughout a persons life, supporting the idea that it is possible to stimulate the rebuilding of lost heart tissue. ...
TY - JOUR. T1 - Calcium sensitivity of force in human ventricular cardiomyocytes from donor and failing hearts. AU - Van Der Velden, J.. AU - Boontje, N. M.. AU - Papp, Z.. AU - Klein, L. J.. AU - Visser, F. C.. AU - De Jong, J. W.. AU - Owen, V. J.. AU - Burton, P. B J. AU - Stienen, G. J M. PY - 2002. Y1 - 2002. N2 - In failing human myocardium changes occur, in particular, in isoform composition and phosphorylation level of the troponin T (TnT) and troponin I (TnI) subunits of the actin filament and the myosin light chains (MLC-1 and -2), but it is unclear to what extent they influence cardiac performance. This overview concentrates on the relation between contractile function, contractile protein composition and phosphorylation levels in small biopsies from control (donor) hearts, from biopsies obtained during open heart surgery (NYHA Class I - IV) and from end-stage failing (explanted, NYHA class IV) hearts. Furthermore, attention is paid to the effect of the catalytic subunit of protein ...
TY - JOUR. T1 - Hibernating myocardium in patients with coronary artery disease. T2 - Identification and clinical importance. AU - Ferrari, R.. AU - La Canna, G.. AU - Giubbini, R.. AU - Alfieri, O.. AU - Visioli, O.. PY - 1992/6. Y1 - 1992/6. N2 - The term hibernating myocardium describes a particular outcome of myocardial ischemia in which myocytes show a chronically depressed contractile ability but remain viable. Revascularization of hibernating tissue causes a recovery of mechanical function that correlates with long-term survival. Therefore it is important clinically to distinguish hibernating from infarcted myocardium, since asynergies due to hibernation will improve on reperfusion, whilst those due to infarct will not. One suggested technique to identify hibernating myocardium is to stimulate the myocytes acutely, but briefly, by administration of inotropic agents while monitoring contractile function by echocardiography. We report our experience on the use of low dosages of dobutamine. ...
Human Cardiac Fibroblast cDNA https://www.sciencepro.com.br/produtos/sc-6304 https://www.sciencepro.com.br/@@site-logo/logo-novo.png ...
Physiological cardiac growth occurs during postnatal development, and in response to long-term exercise training (15). This form of hypertrophy is associated with normal or enhanced cardiac function and normal cardiac structure. In contrast, pathological cardiac hypertrophy may arise as a compensatory mechanism against increased myocyte stress in many disease states. Any initial benefit is however overridden by eventual derangement of myocardial architecture and deterioration of function (15). Diabetic cardiomyopathy is characterized by adverse structural changes to the heart, including increased cardiac fibrosis (pathological in nature) and cardiomyocyte hypertrophy. Our results show that diabetes increased several markers of cardiomyocyte hypertrophy, including cardiomyocyte width as well as gene expression of β-myosin heavy chain, ANP, and BNP as previously described (13). No changes in heart weight-to-body weight or heart weight-to-tibia length ratios were observed in Ntg diabetic mice, ...
The surgical repair of congenital heart defects (CHDs) often requires a bloodless/motionless field achieved by arresting the neonatal...
Surgery for problems unrelated towards the heart can harm heart cells - and it may be deadly for many patients, new research finds.. Research printed Monday within the American Heart Associations journal Circulation discovered that heart cell damage occurring during or following a non-heart-related operation was connected by having an elevated chance of dying among patients who have been 65 or older or whod a pre-existing heart problem.. Heart damage that develops during or after surgical treatment is known as perioperative myocardial injuries, or PMI.. "Patients with PMI are often missed simply because they show no signs and symptoms of cardiovascular disease in nearly all cases and just hardly ever experience chest discomfort, the typical characteristic of cardiac arrest,Inches stated the studys lead author Christian Puelacher, M.D., Ph.D., a clinical investigator at Cardiovascular Research Institute Basel in Europe, in an announcement.. The research incorporated greater than 2,000 men and ...
Surgery for problems unrelated towards the heart can harm heart cells - and it may be deadly for many patients, new research finds.. Research printed Monday within the American Heart Associations journal Circulation discovered that heart cell damage occurring during or following a non-heart-related operation was connected by having an elevated chance of dying among patients who have been 65 or older or whod a pre-existing heart problem.. Heart damage that develops during or after surgical treatment is known as perioperative myocardial injuries, or PMI.. "Patients with PMI are often missed simply because they show no signs and symptoms of cardiovascular disease in nearly all cases and just hardly ever experience chest discomfort, the typical characteristic of cardiac arrest,Inches stated the studys lead author Christian Puelacher, M.D., Ph.D., a clinical investigator at Cardiovascular Research Institute Basel in Europe, in an announcement.. The research incorporated greater than 2,000 men and ...
Yet not much is known about patients with PA, VSD at a cellular level, so any available new data for this group is taken along in the understanding of this disease. As mentioned earlier, we studied limited numbers of patients and controls. Therefore the conclusions can only be drawn with caution. It may be added here that the limited clinical data on normal myocardium in young healthy children is a limitation of our study as well. We are currently accumulating appropriate tissue biopsies to increase the number of contro ls. Two of these mutations are found within a troponin T binding site, located at amino acids 175 and 180. In this study, we analyze a transgenic mouse model for one of the mutations that occur at codon 180: a substitution of a glutami c acid for a glycine. These mice develop severe cardiac hypertrophy, substantial interstitial fibrosis, and have an increased heart weight! body weight ratio . Results show that calcium-handling proteins associated with the sarcoplasmic reticulum ...
After coronary occlusion, myocardium originally supplied by the occluded vessel ultimately separates into infarct and surviving muscle. To clarify this process, evolution of collateral blood flow to infarct and to surviving myocardium was retrospectively analyzed after permanent left anterior descending occlusion in 24 closed chest dogs. Microspheres were injected before occlusion and 5 and 20 minutes and 4 hours after occlusion. Ten minutes after occlusion, dogs received either verapamil, 0.4 mg/kg, followed by 0.6 mg/kg per hour for 6 hours (n = 10) or equivalent saline solution (n = 14). These dogs were sacrificed 3 days later, the distribution of the occluded artery was defined by dye perfusion and infarcted myocardium was determined by triphenyltetrazolium staining of heart slices. Surviving muscle within the distribution of the occluded artery was divided into medial regions adjacent to the infarct (medial adjacent) and remote from the infarct (medial remote) and lateral regions adjacent ...
Looking for myocardium? Find out information about myocardium. the muscular tissue of the heart the muscular layer that constitutes most of the heart. It consists of striated muscle tissue made up of a dense aggregation... Explanation of myocardium
TY - JOUR. T1 - Intermittent hypoxic training protects canine myocardium from infarction. AU - Zong, Pu. AU - Setty, Srinath. AU - Sun, Wei. AU - Martinez, Rodolfo. AU - Tune, Johnathan D.. AU - Ehrenburg, Igor V.. AU - Tkatchouk, Elena N.. AU - Mallet, Robert T.. AU - Downey, H. Fred. PY - 2004/9. Y1 - 2004/9. N2 - This investigation examined cardiac protective effects of normobaric intermittent hypoxia training. Six dogs underwent intermittent hypoxic training for 20 consecutive days in a normobaric chamber ventilated intermittently with N2 to reduce fraction of inspired oxygen (FIO2) to 9.5%-10%. Hypoxic periods, initially 5 mins and increasing to 10 mins, were followed by 4-min normoxic periods. This hypoxia-normoxia protocol was repeated, initially 5 times and increasing to 8 times. The dogs showed no discomfort during intermittent hypoxic training. After 20 days of hypoxic training, the resistance of ventricular myocardium to infarction was assessed in an acute experiment. The left ...
, Human Heart Ventricle, right (Arrhythmia, infarct) tissue lysate, GTX25574, Applications: ELISA, IP, WB; ELISA, Immunoprecipitation, Western Blot (WB); CrossReactivity:
Cardiomyocyte apoptosis has been demonstrated to occur months after acute MI, both in humans [113, 120, 136-138] and experimental animals [139-141]. Apoptotic rate was higher in the periinfarct region especially if persistent or recurrent ischemia was present, and lower in the remote myocardium, but still higher than in the control hearts. A gradual decrease of apoptotic rate over time has been reported, with end-stage ischemic heart failure having only a modest, but significant increase vs controls [120].. Ongoing apoptosis in the border zone and remote myocardium results in a reduction in cardiomyocyte number and might be therefore an important pathogenetic mechanism of ventricular remodeling after MI. Ventricular remodeling is characterized by progressive chamber dilatation, wall thinning, and systolic/diastolic dysfunction [142] beginning days after MI and persisting for weeks and months after the initial insult both at the site of MI and in the healthy myocardium [120, 143-146].. Apoptosis ...
This in utero echocardiographic study showed morphological cardiac changes in Akt1−/− fetuses resulting in abnormal mitral flow patterns and diastolic as well as systolic cardiac dysfunction. Ex vivo 3D μCT analysis revealed a reduced left ventricular volume, a dilated morphology with thinner fetal myocardium. Ex vivo histology confirmed altered cardiac morphology, and illustrated a reduced number of coronary blood vessels and myocardial capillaries in Akt1−/− fetuses. In neonatal Akt1−/− mice in vivo cardiac MRI and histology confirmed altered cardiac function and structure. Impaired myocardial angiogenesis with concomitant aberrant fibrinogenesis proceeded after birth in neonatal Akt1−/− mice displaying reduced survival.. In this study we used multiple imaging modalities leading to unique and powerful datasets to generate simultaneous high‐resolution anatomical and functional information. Multiparameter in utero echocardiographic analyses could associate a functional ...
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The purpose of this study is to investigate the safety of intracoronary cardiac stem cells (CSCs) therapy in humans. Currently, there is no effective intervention to regenerate (regrow) dead heart muscle after a heart attack.. The central hypothesis is that CSCs infused into nonviable myocardial segments will regenerate infarcted myocardium by differentiating into cardiomyocytes and other cell types. According to our hypothesis, CSC infusion regenerates myocardium with consequent improvement in contractile function of the heart and general clinical status. ...
Family 2 (Figure 1). This was a 15-year-old boy who was experiencing low-grade fever, present in individuals in his school class. Genetic analysis revealed 4 missense variants. The variant DSP_p.E290K, rs397816974, not identified in global databases, was predicted in silico as deleterious. The variant PKP2_p.Q62K, rs199601548, present in very low frequency, was classified as of unknown significance. Other 2 genetic variants were predicted in silico as benign (JPH2_p.A181T) and deleterious (TTN_p.S30475G). His sisters CMR (III.2) showed wide fibrotic areas in the left ventricular myocardium. She carried DSP (p.E290K) and TTN (p.S30475G). The mothers CMR (II.2) showed fibrotic interstitial areas in the left ventricle. She carried DSP (p.E290K) and JPH2 (p.A181T). His father (II.1) had normal CMR and carried PKP2 (p.Q62K) and TTN (p.S30475G). Thus, the only segregating pathogenic variant was DSP (p.E290K). The grandfather (I.1) died suddenly at a young age without autopsy.. Family 3 (Figure 1). ...
An injector for delivering an injectate into the myocardium of the heart may be implemented as a catheter or a handheld unit. The injector includes a body, a stabilizer secured to a distal end of the body, and a needle that may be controllably advanced from the distal end of the body. The stabilizer stabilizes the distal end of the body relative to the myocardium while the heart beats. An enlarged region disposed along the needle prevents the needle from being advanced into the myocardium beyond a desired penetration depth. To make an injection, the physician brings the distal end of the body in proximity to the myocardium, actuates the stabilizer to stabilize the distal end relative to the myocardium, and advances the needle into the myocardium. Advancement of the needle is impeded by the enlarged region, thereby placing the needle tip at the desired penetration depth for the injection.
Methods 42 SD rat models of DCM, established by combination of insulin resistance by a high-fat diet with intraperitoneal injection of high dose streptozotocin (50 mg/kg), were evaluated in the damage of the myocardium by ECG at the twelveth week after modelling, and the serum are analysed for blood glucose (GLU), cholesterol and triglyceride (TG); the content of the left cardiac ventricle myocardial collagen was quantified by Masson staining test; the level of myocardial cell apoptosis was tested with Tunel apoptosis kit; the damage extent of the myocardial subcellular structure was observed by electron microscopy; the expression levels of cardiac TSP-1, TGF-β1 and TRB-3 proteins were detected by immunohistochemistry, the changes of the expression levels of the cardiac TSP-1, A-TGFβ1 and L-TGF-β1 protein were detected by Western blotting; and the changes of the mRNA expression levels of TSP-1 and TRB-3 were detected by real-time quantitative PCR.. ...
In the present study, vehicle-treated MI rats had depressed cardiac function that was characterized by reduced cardiac index and stroke volume index and increased systemic vascular resistance, indicating that heart failure developed in this animal model. Intravenous infusion of HGF, for 6 days beginning the day after ischemia/reperfusion, resulted in a significant improvement in cardiac performance, measured 8 weeks post-MI. Compared with rats with vehicle-treated MI, animals receiving HGF had significantly higher cardiac index and stroke volume index and reduced systemic vascular resistance. These three parameters were improved to near normal levels. To our knowledge, this is the first demonstration that HGF improves cardiac function in conscious animals with heart failure induced by MI.. The premise for this work was based on the observations that myocardial HGF and c-Met were induced for several days after MI (Ono et al., 1997;Ueda et al., 2001) and that the peak levels occurred well past the ...
Learn more about Drugs That May Lead to Heart Damage at Reston Hospital Center If you are taking medication for a condition, or using illegal drugs ...
In our rat model for ICM, pharmacological inhibition of CatA activity did not significantly improve LV global systolic function at rest; however, it did prevent wall thinning and preserve more viable myocardium in the LV infarct area and the LV noninfarcted remote myocardium without reducing LV fibrosis. In each of these parameters, SAR was more efficacious than ramipril.. We showed that this antiremodeling effect occurred not only in the ventricular infarct area and noninfarcted remote myocardium but also in the atrium. Inhibition of CatA activity hampered LA fibrosis formation and reduced gene expression of fibrillary collagen types I and III, which are known to be dysregulated in cardiac disease (14,30,31). In the heart, the predominant fibrillary collagens are the rigid type I (80%) and the elastic type III (11%), providing structure and elasticity to the ECM (14,31). The extent of this remodeling process is controlled by the balance between ECM synthesis and degradation, which is tightly ...
Background -Here, we generated human cardiac muscle patches (hCMPs) of clinically relevant dimensions (4 cm × 2 cm × 1.25 mm) by suspending cardiomyocytes, smooth-muscle cells, and endothelial cells that had been differentiated from human induced-pluripotent stem cells (hiPSCs) in a fibrin scaffold and then culturing the construct on a dynamic (rocking) platform. Methods -In vitro assessments of hCMPs suggest maturation in response to dynamic culture stimulation. In vivo assessments were conducted in a porcine model of myocardial infarction (MI). Animal groups included: MI hearts treated with two hCMPs (MI+hCMP, N=13), treated with two cell-free open fibrin patches (MI+OP, n=14), or with neither experimental patches (MI, n=15); a fourth group of animals underwent sham surgery (SHAM, n=8). Cardiac function and infarct size were evaluated by magnetic resonance imaging, arrhythmia incidence by implanted loop recorders, and the engraftment rate by calculation of quantitative PCR measurements of ...
Experiments with selective agonists and antagonists of purinoceptors allowed us to evaluate the subtype of P2X receptors. We showed that the myocardium of 14-100-day-old rats contains functionally active P2X1 receptors. These receptors are involved in the realization of the positive inotropic effect of the atria and ventricles. Selective P2X1 receptor agonist β,γ-methylene-ATP induced a dose-dependent increase in the strength of atrial and ventricular contractions. P2X1 receptor antagonist TNP-ATP abolished the effect of the agonist in rats of all age groups.
Fibroblasts, including Cardiac Fibroblasts, & other primary cells at Cell Applications, your worldwide provider of human & animal cells, antibodies, & cell culture & molecular biology tools.
A large number of cardiomyocytes and coronary vessels were created in a rather short period of time from the delivery, engraftment, and differentiation of cardiac progenitor cells from the recipient. A proportion of newly formed cardiomyocytes acquired adult characteristics and was integrated structurally and functionally within the transplant. Similarly, the regenerated arteries, arterioles, and capillaries were operative and contributed to the oxygenation of the chimeric myocardium. Attenuation in the extent of acute damage by repopulating cardiomyocytes and vessels decreased significantly the magnitude of myocardial scarring preserving partly the integrity of the donor heart.. ...
Smith SJ, Towers N, Saldanha JW, Shang CA, Mahmood SR, Taylor WR, Mohun TJ. The cardiac-restricted protein ADP-ribosylhydrolase-like 1 is essential for heart ch
TY - JOUR. T1 - Targeted Sprouty1 overexpression in cardiac myocytes does not alter myocardial remodeling or function. AU - Charles, Nathan J.. AU - Huebert, Robert C.. AU - Lee, Sangjin. AU - Adhikari, Neeta. AU - Polster, Sean. AU - Rider, James E.. AU - Braunlin, Elizabeth. AU - Mariash, Ami. AU - Robledo, Maggie. AU - Schuweiler, David. AU - Hall, Jennifer L.. PY - 2010/9/1. Y1 - 2010/9/1. N2 - The mitogen activated protein kinase (MAPK) signaling pathway regulates multiple events leading to heart failure including ventricular remodeling, contractility, hypertrophy, apoptosis, and fibrosis. The regulation of conserved intrinsic inhibitors of this pathway is poorly understood. We recently identified an up-regulation of Sprouty1 (Spry1) in a targeted approach for novel inhibitors of the MAPK signaling pathway in failing human hearts following reverse remodeling. The goal of this study was to test the hypothesis that up-regulated expression of Spry1 in cardiac myocytes would be sufficient to ...
Lauren Blacks research interests lie in understanding the biophysical signaling mechanisms responsible for the development of healthy and diseased myocardium inclusive of mechanical stress/strain, electrical stimulation, and cell-cell/ cell-matrix interactions. The ultimate goal of his research is to design and develop new methods for repairing diseased or damaged myocardium.. ...
The current studies provide evidence that TrpC4α, but not the closely related TrpC4β, is involved in pathways downstream of PLCβ1b and contributes to cellular hypertrophic responses. PLCβ1b is an immediate effector of signaling responses downstream of Gq-coupled receptors and is required for Gq-initiated cardiomyocyte hypertrophy (Filtz et al., 2009). PLCβ1b expression and activity are elevated in diseased myocardium from humans, rats, mice, and sheep, and, furthermore, activity increases with disease progression (Woodcock et al., 2009). Thus, PLCβ1b and its downstream effectors, including TrpC4α, may contribute to disease. TrpC4α differs from the other splice variant, TrpC4β, only in the inclusion of an 84-amino-acid sequence located close to, but not at, the extreme C-terminal end of the protein (Fig. 2A). Despite the apparently small sequence difference between the two splice variants, we found that TrpC4α, but not TrpC4β, associated with both PLCβ1b and Shank3 (Fig. 2) and ...
Cardiac arrhythmias are one of the most frequent causes of death worldwide. A popular biological model used to study arrhythmogenesis is the cultured cardiac cell monolayer, which provides a good trade-off between physiological relevance and experimental access. Excitation wave patterns are imaged using high-bandwidth detectors, producing large data sets that are typically analyzed manually. To make such analysis less time consuming and less subjective, we have designed and implemented a toolkit for segmentation and tracking of cardiac waves in optical mapping recordings. The toolkit is optimized for high-resolution detectors to accommodate the growing availability of inexpensive high-resolution detectors for life science imaging applications (e.g., scientific CMOS cameras). The software extracts key features of propagating waves, such as wavefront speed and entropy. The methods have been validated using synthetic data, and real-world examples are provided, showing a difference in conduction velocity
Participants (par.) who met eligibility criteria and completed a 30 day Screening were then randomized to a 13-week Treatment Period, followed by a Follow-up visit 28 days post-treatment. The duration of the study was approximately 20 weeks from Screening to Follow-up. A total of 100 par. were planned, and 82 par. were randomized ...
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The dynamics of morphologic and biochemical lesions of the myocardial fiber during the first ten days after an experimental myocardial infarction showed an unequal evolution of the lesional picture in the ischaemic area, the intervention of lysosomal
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My laboratory is interested in bi-directional crosstalk between vascular endothelium and cardiomyocytes that regulates cardiac size and function. As an alternative to myocyte-driven hypertrophy in response to hemodynamic stress we recently reported a cross-talk loop induction of myocardial hypertrophy by expanding vascular endothelium in the absence of traditional hypertrophy stimuli. This reveals a new and unexplored role played by the endothelium in regulation of adult organ growth and size that would be of great interest in formulating new therapeutic angiogenic approaches to the treatment of heart disease.. Our hypothesis is that an increase in vascular endothelium in the adult heart results in increased nitric oxide (NO) production that in turn drives the growth of cardiomyocytes by sustained ubiquitination of the negative regulator of G protein signaling subtype 4 (RGS4) and derepression of the hypertrophic program via heterotrimeric G protein signaling. To investigate this crosstalk we ...
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Heart tissue. Fluorescence deconvolution micrograph of a section through heart tissue. The heart largely consists of fibres (green) of cardiac muscle (the myocardium) that contract to pump blood around the heart. It also includes blood vessels that supply oxygen to the heart muscle. One such blood vessel is shown here in cross-section, with the blood vessel wall surrounding the lumen (black). Cellular proteins are highlighted with fluorescent markers: g-actin (red), f-actin (green) and smooth muscle actin (blue). - Stock Image C010/5810
Hello, I'm rather new to ImageJ and the different tools and plug-ins out there. I have stained rat myocardium with antibodies against CD31, aSMA, and von Willibrand Factor to stain arteries and capillaries. Images are …
As more data comes in from China and Italy, as well as Washington state and New York, more cardiac experts are coming to believe the COVID-19 virus can infect the heart muscle.
Heart tissue. Fluorescence deconvolution micrograph of a section through heart tissue. The heart largely consists of fibres (green) of cardiac muscle (the myocardium) that contract to pump blood around the heart. This tissue sample includes intercalated discs (orange) and muscle striations. Cellular proteins are highlighted with fluorescent markers: g-actin (red), f-actin (green) and cell nuclei (blue). - Stock Image C010/5815
A mutation of a massive heart protein that keeps the heart beating has been discovered to be the cause of sudden deaths in heart patients.
A cardiac electro-stimulatory device and method for operating same in which stimulation pulses are distributed among a plurality of electrodes fixed at different sites of the myocardium in order to reduce myocardial hypertrophy brought about by repeated pacing at a single site and/or increase myocardial contractility. In order to spatially and temporally distribute the stimulation, the pulses are delivered through a switchable pulse output configuration during a single cardiac cycle, with each configuration comprising one or more electrodes fixed to different sites in the myocardium.
Cardiac injury occurs when there is disruption of normal cardiac myocyte membrane integrity. This results in the loss into the extracellular space (including blood) of intracellular constituents, including detectable levels of a variety of biological
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A központi idegrendszer és a myocardium szabályozásában szerepet játszó adenozin-receptorok és PET izotóppal jelölt ligandjaik kötődés kinetikájának vizsgálata PET technikával
Cardiovascular diseases are a leading cause of death, in part due to limitations of existing models of the myocardium. Myocardium consists of aligned, contractile cardiac myocytes interspersed with fibroblasts that synthesize extracellular matrix (ECM). The cellular demographics and biochemical and mechanica
Enhanced sympathetic activity at the ventricular myocardium can destabilize repolarization, increasing the risk of death. Sympathetic activity is known to cluster in low-frequency bursts; therefore, we hypothesized that sympathetic activity induces periodic low-frequency changes of repolarization. We developed a technique to assess the sympathetic effect on repolarization and identified periodic components in the low-frequency spectral range (≤0.1 Hz), which we termed periodic repolarization dynamics (PRD). ...
... At rest, the ventricular myocyte membrane potential is about -90 mV, which is close to the potassium reversal potential. When an
The heart requires highly efficient metabolism to maintain the levels of ATP needed for contractility and pump function. Aberrant cardiac metabolism is associat...