Cardiac tissues

The Class I agents decrease excitability, slow conduction velocity, inhibit diastoHc depolarization (decrease automaticity), and prolong the refractory period of cardiac tissues (1,2). These agents have anticholinergic effects that may contribute to the observed electrophysiologic effects. Heart rates may become faster by increasing phase 4 diastoHc depolarization in SA and AV nodal cells. This results from inhibition of the action of vagaHy released acetylcholine [S1-84-3] which, allows sympathetically released norepinephrine [51-41-2] (NE) to act on these stmctures (1,2). 

The Class III antiarrhythmic agents markedly prolong action potential duration and effective refractory period of cardiac tissue. The QT interval of the ECG is markedly prolonged. 

Kenakin, T. P., and Beek, D. (1984). The measurement of the relative efficacy of agonists by selective potentiation of tissue responses Studies with isoprenaline and prenalterol in cardiac tissue. J. Auton. Pharmacol. 4 153—159. 

The histamine H2-receptor (359 amino acids) is best known for its effect on gastric acid secretion. Histamine H2-receptor activation, in conjunction with gastrin and acetylcholine from the vagus, potently stimulate acid secretion from parietal cells. High concentrations of histamine are also present in cardiac tissues and can stimulate positive chronotropic and inotropic effects via H2-receptor stimulation and activation of adenylyl... 

Microscopic examination of the heart revealed edematous separation of myofibrils that had resulted in compression thinning and fragmentation of myofibres. Myofibre outlines were less distinct, and there was loss of acidophilic staining. Mitotic figures were rare, indicating that growth of the cardiac tissue was suppressed. The incidence of cardiac lesions is given (Table VI). 

Analytical models of the heart are a reality. They are based on detailed descriptions of cardiac tissue architecture and anatomy, including the coronary vasculature. In sihco cardiac tissues possess realistic passive mechanical properties, and both electrical and mechanical activity can be simulated with high accuracy. Descriptions of key components of cellular metabolism have been introduced, as have models of drug-receptor interactions. 

If cellular redox state, determined by the glutathione status of the heart, plays a role in the modulation of ion transporter activity in cardiac tissue, it is important to identify possible mechanisms by which these effects are mediated. Protein S-,thiolation is a process that was originally used to describe the formation of adducts of proteins with low molecular thiols such as glutathione (Miller etal., 1990). In view of the significant alterations of cardiac glutathione status (GSH and GSSG) and ion-transporter activity during oxidant stress, the process of S-thiolation may be responsible for modifications of protein structure and function. 

Nakaya, H., Tohse, N. and Kanno, M. (1987). Electrophysio-logical derangements induced by lipid peroxidation in cardiac tissue. Am. J. Physiol 253, H1089-H1097. 

Ischemic heart disease (IHD) is also called coronary heart disease (CHD) or coronary artery disease. The term ischemic refers to a decreased supply of oxygenated blood, in this case to the heart muscle. Ischemic heart disease is caused by the narrowing of one or more of the major coronary arteries that supply blood to the heart, most commonly by atherosclerotic plaques. Atherosclerotic plaques may impede coronary blood flow to the extent that cardiac tissue distal to the site of the coronary artery narrowing is deprived of sufficient oxygen in the face of increased oxygen demand. Ischemic heart disease results from... 

CXCR4 AMD-3100 AnorMED Phase II Phase I Stem cell transplantation Repair cardiac tissue after myocardial infarction 111, 112 111, 112... 

Hydrogen sulfide inhibits mitochondrial cytochrome oxidase, resulting in disruption of the electron transport chain and impairing oxidative metabolism. Nervous and cardiac tissues, which have the highest oxygen demand (e.g., brain and heart), are especially sensitive to disruption of oxidative metabolism (Ammann 1986 Hall 1996). 

Of the following diuretic agents, which would be least likely to indirectly cause an increased binding of digoxin to cardiac tissue sodium-potassium-adenosine triphosphatase (Na K ATPase) ... 

Lu, H.R., Vlaminckx, E., Teisman, A., and Gallacher, D.J., Choice of cardiac tissue plays an important role in the evaluation of drug-induced prolongation of the QT interval in vitro in rabbit, /. Pharmacol. Toxicol. Methods, 52, 90-105, 2005. 

Class III agents increase the refractoriness of cardiac tissue, thus preventing an aberrant impulse from propagating. A selective Class III agent has little or no effect on simple PVC s. At the cellular level, the increased refractoriness is manifest by a delay in the repolarization phase (Phase 3) of the cardiac action potential Figure 2.1), thereby increasing action potential duration. During the action potential cycle a complex series of ionic currents. 

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