Myocardium cells

Muscle-specific actin HHF-35 42-kD protein in preparations of purified skeletal muscle actin and extracts of aorta, uterus, diaphragm, and heart SDS extracted protein fraction of human myocardium Cell Marque NA HIER... 

One of the disadvantages of cell injection is that great precision is required for the effective administration of the cells. Furthermore, very low retention rates are generally observed using these techniques. While the reason for this is not completely understood, it is likely that inflammation, nutrient limitations, and damage due to the injection procedure could be responsible. Scaffold-based cell therapy approaches for the treatment of the myocardium could present a possible solution to this problem. A number of recent studies have described using cell-seeded scaffolds instead of cell injections for cell-based therapy of the myocardium cells. Delivery of cardiomyocytes (Zimmermann et al., 2004), mesenchymal stem... 

Inhibition of the Na+/K+-ATPase leads to a loss of potassium and an increase of sodium within the cell. Secondary intracellular calcium is increased via the Na VCa -exchanger. This results in a positive inotropic effect in the myocardium, with an increase of peak force and a decrease in time to peak tension. Besides this, cardiac glycosides increase vagal activity by effects on the central vagal nuclei, the nodose ganglion and increase in sensitivity of the sinus node to acetylcholine. 

Endothelial cells are the major source of ET-1-synthesis. ET-1 is also produced by astrocytes, neurons, hepatocytes, bronchial epithelial cells, renal epithelial and mesangial cells. Physiological stimuli of ET-1-synthesis in endothelial cells are angiotensin II, catecholamines, thrombin, growth factors, insulin, hypoxia and shear stress. Inhibitors of ET-1 synthesis are atrial natriuretic peptide, prostaglandin E2 and prostacyclin. ET-2 is mainly synthesized in kidney, intestine, myocardium and placenta and ET-3 is predominantely produced by neurons, astrocytes and renal epithelial cells. 

CR is distributed in various organs with highest concentrations in skeletal muscle, myocardium, and brain and lesser amounts in the gastrointestinal tract, uterus, urinary bladder, and kidney ( ). The CR content of liver and red blood cells is negligible so that diseases of these tissues are unlikely to increase the serum CR activity. The serum CR level begins to increase in 2-4 hours after myocardial infarction and reaches a peak in 24-36 hours and returns to normal in about 3 days. 

Hearse, D.J., Humphrey, S.M., Nayler, W.G., Slade, A. and Border, D. (1975). Ultrastructural damage associated with reoxygenation of the anoxic myocardium. J. Mol. Cell. Cardiol. 7, 315-324. 

Potassium is the second most abundant cation in the body and is found primarily in the intracellular fluid. Potassium has many important physiologic functions, including regulation of cell membrane electrical action potential (especially in the myocardium), muscular function, cellular metabolism, and glycogen and protein synthesis. Potassium in PN can be provided as chloride, acetate, and phosphate salts. One millimole of potassium phosphate provides 1.47 mEq of elemental potassium. Generally, the concentration of potassium in peripheral PN (PPN) admixtures should not exceed 80 mEq/L (80 mmol/L). While it is safer to also stick to the 80 mEq/L (80 mmol/L) limit for administration through a central vein, the maximum recommended potassium concentration for infusion via a central vein is 150 mEq/L (150 mmol/L).14 Patients with abnormal potassium losses (e.g., loop or thiazide diuretic therapy) may have higher requirements, and patients with renal failure may require potassium restriction. 

An internodal conduction pathway also extends from the SA node and transmits the impulse directly to the atrioventricular (AV) node. This node is located at the base of the right atrium near the interventricular septum, which is the wall of myocardium separating the two ventricles. Because the atria and ventricles are separated from each other by fibrous connective tissue, the electrical impulse cannot spread directly to the ventricles. Instead, the AV node serves as the only pathway through which the impulse can be transmitted to the ventricles. The speed of conduction through the AV node is slowed, resulting in a slight delay (0.1 sec). The cause of this AV nodal delay is partly due to the smaller fibers of the AV node. More importantly, however, fewer gap junctions exist between the cells of the node, which... 

Sodium reabsorption is also influenced by ANP. The original decrease in plasma volume leads to a decrease in atrial filling and a decrease in the release of ANP from the myocardium. Atrial natriuretic peptide, which acts on vascular smooth muscle, granular cells of the kidney, and the adrenal cortex, normally causes the following ... 

Communication between neurons involves neurotransmitters. Up until the beginning of the last century, synaptic transmission was regarded as probably electrical. It was suggested that the close apposition of two neurons allowed the current to jump the synaptic cleft, rather like an electrical spark between two closely positioned wires. There is indeed evidence for electrical synapses in animal species where the synaptic cleft is particularly narrow (2 nm, or nanometres), as well as in the myocardium where the close coupling of cells allows electrical current to flow from one cell to the next,... 

Two forms of xanthine oxidoreductase namely XO and XDH are present in many human and animal cells and plasma, XDH and XO are the predominant species in cytoplasma and serum, respectively [39]. Damaging effects of XO-catalyzed superoxide production in post-ischemic tissues were demonstrated by many authors. For example, Chambers et al. [40] and Hearse et al. [41] have shown that the suppression of superoxide production by the administration of XO inhibitor allopurinol or SOD resulted in the reduction of infarct size in the dog and of the incidence of reperfusion-induced arrhythmia in the rat. Similarly, Charlat et al. [42] has also shown that allopurinol improved the recovery of the contractile function of reperfused myocardium in the dog. However, the use of allopurinol as the XO inhibitor has been questioned because this compound may affect oxygen radical formation not only as a XO inhibitor but as well as free radical scavenger [43]. Smith et al. [44] also showed that gastric mucosal injury depends on the oxygen radical production catalyzed by XO and iron. 

Myocardial infarction, 3 710-711 and blood coagulation, 4 81 Myocardial pacemaker cells, 5 81 Myocardium, 5 79—80 Myoglobin, properties of standard, 3 836t Myosin, role in heart excitation and contraction coupling, 5 81 Myrac aldehyde, 2 278 24 485 Myrascone, 24 571... 

Interestingly, counting of the microvessels revealed no difference between MSC-transplanted animals and cell culture medium-injected controls (p>0.05, not shown). However, the amount of vessels in both groups was about twice as high in the area of injection compared to normal non ischemic myocardium (p<0,001) of the same animal pointing towards an influence of the injection procedure in neovascularization events. 

In in vitro experiments, MSC developed an early myogenic phenotype (Jaquet et al, 2005), however we did not succeed in generating self-contracting or even twitching (cardio-) myoc54es (not shown). Our results reveal that MSC are able to survive at least 10 weeks within the rat myocardium. When paramagnetic iron oxide nanoparticles were incorporated into rMSC prior to transplantation, cells within the myocardial scar area could be detected in our study. This could be some evidence that rMSC are able to migrate into the scar from the site of injection. 

Additionally, we could neither find any evidence that MSCs are able to differentiate into vascular endothelial cells nor did we find more vessels within the transplantation areas as compared to the control group. But, in contrast to normal myocardium the amount of vessels was twice as high in the injection areas. This might indicate that the injury (puncture) of the myocardium caused by the syringe needle alone can be an adequate stimulus for the induction of angiogenesis. Therefore, rather the paracrine effects of implanted MSCs than the incorporation of these cells into the vessel walls may be required for vascular growth in the adult (Kinnaird et al., 2004). 

Balsam, L.B., Wagers A.J., Christensen, J.L., Kofidis, T., Weissman, l.L. and Robbins R.C. (2004) Haematopoietic stem cells adopt mature haematopoietic fates in ischaemic myocardium. Nature 428, 668-673. 

Orlic, D. (2003). Adult bone marrow stem cells regenerate myocardium in ischemic heart disease. Ann N Y Acad Sci. 996, 152-157. 

The activity of this enzyme is regulated by changes in the concentrations of ATP and phosphate the former inhibits whereas the latter activates it. These are the signals that increase the concentration of adenosine. It is transported out of the cell, so that the extracellular concentration also increases. This then stimulates relaxation of the smooth muscle in the arterioles which results in vasodilation and increased blood flow and consequently a greater supply of oxygen to the cardiomyocytes. The blood flow will be increased to those parts of the myocardium that are not totally occluded by the clot, so that more mitochondrial generation of ATP can occur. Provided the portion of the myocardium that is totally occluded is not too large, the heart can then continue to function as a pump. 

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