Heart myocardium

Heart/myocardium Tumor cellsh Tumor cellsh Tumor cellsh Thyroid Tumor cellsh Normal bone ... 

Digoxin exhibits strong systolic action and slows heart rate. It is removed from the organism faster than digitoxin. It is used from chronic cardiac insufficiency in decompensated valvular disease of the heart, myocardium overload in arterial hypertension, tachycardia, ventricular fibrillation, and other analogous situations. Synonyms of this drug are cedoxin, lanacordin, lanoxin, and others. 

Desflurane is less potent than the other fluorinated anesthetics having MAC values of 5.7 to 8.9% in animals (76,85), and 6% to 7.25% in surgical patients. The respiratory effects are similar to isoflurane. Heart rate is somewhat increased and blood pressure decreased with increasing concentrations. Cardiac output remains fairly stable. Desflurane does not sensitize the myocardium to epinephrine relative to isoflurane (86). EEG effects are similar to isoflurane and muscle relaxation is satisfactory (87). Desflurane is not metabolized to any significant extent (88,89) as levels of fluoride ion in the semm and urine are not increased even after prolonged exposure. Desflurane appears to offer advantages over sevoflurane and other inhaled anesthetics because of its limited solubiHty in blood and other tissues. It is the least metabolized of current agents. 

In addition to its internal blood flow operation, the heart has its own system of blood vessels to keep the muscle wall of the heart, the myocardium, supphed with oxygenated blood (Fig. 3a). The coronary arteries, which branch from the aorta to the right and left sides of the heart, are vital to maintaining that supply. The heart is an extraordinary electromechanical muscle that can be trained to increase blood flow to the body sixfold. It can range from 5 to 30 L /min during exertion. 

The Cardiac Cycle. The heart (Eig. lb) performs its function as a pump as a result of a rhythmical spread of a wave of excitation (depolarization) that excites the atrial and ventricular muscle masses to contract sequentially. Maximum pump efficiency occurs when the atrial or ventricular muscle masses contract synchronously (see Eig. 1). The wave of excitation begins with the generation of electrical impulses within the SA node and spreads through the atria. The SA node is referred to as the pacemaker of the heart and exhibits automaticity, ie, it depolarizes and repolarizes spontaneously. The wave then excites sequentially the AV node the bundle of His, ie, the penetrating portion of the AV node the bundle branches, ie, the branching portions of the AV node the terminal Purkinje fibers and finally the ventricular myocardium. After the wave of excitation depolarizes these various stmetures of the heart, repolarization occurs so that each of the stmetures is ready for the next wave of excitation. Until repolarization occurs the stmetures are said to be refractory to excitation. During repolarization of the atria and ventricles, the muscles relax, allowing the chambers of the heart to fill with blood that is to be expelled with the next wave of excitation and resultant contraction. This process repeats itself 60—100 times or beats per minute... 

Natriuretic peptides are a family of peptide hormones. All of them contain a 17-amino acid long ring that is closed by a disulfide bond between two cysteine residues. ANP (atrial natriuretic peptide) is mainly expressed in the atria of the heart, whereas BNP (B-type natriuretic peptide) is synthesized in the ventricular myocardium. CNP occurs mainly in the endothelium and is thought to have a paracrine function. ANF and BNF lower blood pressure by a direct effect on smooth muscle and on the salt retention in the kidney. Natriuretic peptides bind and activate particulate guanylyl cyclases. 

Cardiotonic drugs increase the force of the contraction of the muscle (myocardium) of the heart. This is called a positive inotropic action. When the force of contraction of the myocardium is increased, the amount of blood leaving the left ventricle at the time of each contraction is increased. When the amount of blood leaving the left ventricle is increased, cardiac output (the amount of blood leaving the left ventricle with each contraction) is increased. 

Flecainide (Tambocor) and propafenone (Rythmol) are examples of class I-C drags. These drugs have a direct stabilizing action on the myocardium, decreasing the height and rate of rise of cardiac action potentials, thus slowing conduction in all parts of the heart. 

Anaphylaxis is the most dramatic and potentially catastrophic manifestation of allergic disorders. It can affect virtually any organ including the cardiovascular system. Cardiovascular collapse and hypotensive shock in anaphylaxis have been attributed to peripheral vasodilation, enhanced vascular permeability and plasma leakage, rather than any direct effect on the myocardium. However, there is increasing experimental and clinical evidence that the human heart is a site and target of anaphylaxis. 

Myocardium is characterized by a predominance of LD-1 (H tetramer) whereas LD-5 (1 tetramer) is the dominant species in liver and skeletal muscle. The heart isoenzyme LD-1 is heat stable whereas liver and skeletal muscle LD-5 is heat labile. 

In diphtheria, the organism C. diphtheriae eonfmes itself to epithelial surfaces of the nose and throat and produces a powerfiil toxin which affects the elongation factor involved in protein biosynthesis. The heart and peripheral nerves are particularly affected resulhng in myocarditis (inflammation of the myocardium) and neuritis (inflammation of a nerve). Little damage is produeed at the infective site. 

In the setting of a sustained loss of myocardium, a number of mechanisms aid the heart when faced with an increased hemodynamic burden and reduced CO. They include the following the Frank-Starling mechanism, tachycardia and increased afterload, and cardiac hypertrophy and remodeling (Table 3-2).5,7... 

Intravenous or oral doses of a P-blocker should be administered early in the care of a patient with STE ACS, and then oral agents should be continued indefinitely. Early administration of a P-blocker to patients lacking a contraindication within the first 24 hours of hospitalization is a quality care indicator.2,3 In ACS the benefit of P-blockers mainly results from the competitive blockade of P,-adrenergic receptors located on the myocardium. Pi-Blockade produces a reduction in heart rate, myocardial contractility, and blood pressure, decreasing myocardial oxygen demand. As a result of these effects, P-blockers reduce the risk for recurrent ischemia, increase in infarct size and risk of reinfarction, and occurrence of ventricular arrhythmias in the hours and days following MI.39... 

Great interest in diphosphino complexes of technetium arose when Deutsch and co-workers found that lipophilic cations are able to be accumulated in heart tissue and can thus be candidates for myocardium perfusion agents [120]. Both the Tc(V) DMPE complex, [Tc02L2]+, and the [TcL2X2] + and [TcL3] + species in oxidation states +3 and +1 have been evaluated. Whereas the [Tc02L2] +... 

Beta-one receptors are the primary adrenergic receptor on the heart (a small percentage of the adrenergic receptors on the myocardium are P2). Both... 

Epinephrine and norepinephrine have equal affinity for Pj-receptors, the predominant adrenergic receptors on the heart. However, the human heart also contains a small percentage of P2-receptors that, like Pj-receptors, are excitatory. Therefore, epinephrine is capable of stimulating a greater number of receptors and causing a greater stimulatory effect on the myocardium. 

Explain why the thickness of the myocardium varies between the different heart chambers... 

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