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Tissues heart

The structure of heart myocytes is different from that of skeletal muscle fibers. Heart myocytes are approximately 50 to 100 p,m long and 10 to 20 p,m in diameter. The t-tubules found in heart tissue have a fivefold larger diameter than those of skeletal muscle. The number of t-tubules found in cardiac muscle differs from species to species. Terminal cisternae of mammalian cardiac muscle can associate with other cellular elements to form dyads as well as triads. The association of terminal cisternae with the sarcolemma membrane in a dyad structure is called a peripheral coupling. The terminal cisternae may also form dyad structures with t-tubules that are called internal couplings (Figure 17.31). As with skeletal muscle, foot structures form the connection between the terminal cisternae and t-tubule membranes. [Pg.559]

Prenyl amine (66) was long used in the treatment of angina pectoris, in which condition it was believed to act by inhibiting the uptake and storage of catecholamines in heart tissue. Droprenilamine (69), an analogue in which the phenyl ring is reduced, acts as a coronary vasodilator. One of several syntheses involves simple reductive alkylation of 1,1-diphenyl-propylamine (67) with cyclohexyl acetone (68)... [Pg.47]

Reentrant arrhythmia occurs when due to inhomogeneous repolarization or unidirectional block, heart tissue which is no longer refractory is close beside tissue which is still activated. This may result in a circuit propagation of activation serving as a reverberator. [Pg.1063]

Potential Usage oe TMC-Based Copolymers in Tissue Engineering 8.5.4.1 TMC-DLLA Copolymers in Heart Tissue Engineering... [Pg.232]

Pego AP, Siebum SB, Luyn MJAV, et al. Preparation of degradable porous structures based on 1,3-trimethylene carbonate and D,L-lactide(co)polymers for heart tissue engineering. Tissue Eng, 2003, 9, 981 994. [Pg.249]

Only a new land of science could begin to cross the great gulf between knowledge ofwhat one thing does—one water molecule, one cell of heart tissue, one neuron—and what millions of them do. [Pg.157]

Fig.1. Electron micrograph of a mast cell in human heart tissue. The cytoplasm contains numerous secretory granules. The mast cell is adjacent to a coronary blood vessel, surrounded by collagen fibers and close to a myocyte. Uranyl acetate and lead citrate stained. Orig. magnif. lO.OOOx. [Pg.100]

Mast cells are present in the normal human heart and even more abundant in diseased hearts [ 16-18,25,47]. Within heart tissue, mast cells he between myocytes and are in close contact with blood vessels. They are also found in the coronary adventitia and in the shoulder regions of coronary atheroma [20, 21], The density of cardiac mast cells is higher in patients with dilated and ischemic cardiomyopathy than in accident victims without cardiovascular diseases [25], Importantly, in some of these conditions there is in situ evidence of mast cell activation [16,34],... [Pg.106]

Different tissues have different lipid compositions. The most common lipid components of membranes are PC and PE. Lipid extracts from brain and lung are also rich in PS heart tissue is rich in PG, and liver is rich in PI [567]. Human blood cells, as ghost erythrocytes (with cytoplasm contents removed), are often used as membrane models. These have different compositions between the inner and outer leaflets of the bilayer membrane. Phospholipids account for 46% of the outer leaflet membrane constituents, with PC and Sph about equal in amount. The inner leaflet is richer in phospholipids (55%), with the mix 19% PE, 12% PS, 7% PC and 5% Sph [567],... [Pg.132]

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] +... [Pg.100]

However, the reaction of NP with thiols may be a necessary but not sufficient cause for the release of NO from the ion as there are many thiols in frog heart tissue and NP is a vasodilator only under illumination. Furthermore Sogo et al. [50] could not detect NO generation from NP in human plasma containing cysteine, glutathione, homocysteine and reduced cysteine residues. Therefore, there must be a unique component of mammalian tissues which is involved in the release of NO from NP, and this reaction comes after reaction with thiol. Kowaluk et al. [51] report that NP is readily metabolised to NO in subcellular fractions of bovine coronary arterial smooth muscle and that the dominant site of metabolism is in the membrane fraction. This led to the isolation of a small membrane-bound protein or enzyme that can convert NP into NO. The mechanism shown in Scheme 8.2 combines the thiol reaction and that with an enzyme. [Pg.211]

Voss, H.P., Shukrula, S., Wu, T.S., Donnell, D., and Bast, A., A functional beta-2 adrenoceptor-mediated chronotropic response in isolated guinea pig heart tissue selectivity of the potent beta-2 adrenoceptor agonist TA 2005, /. Pharmacol. Exp. Ther., 271, 386-389, 1994. [Pg.282]

In pregnant Alderley-Park rats, whole-body exposure to 1,4-dichlorobenzene at air concentrations of 74.7, 198.6, or 508.4 ppm, 6 hours a day from Gd 6 to 15 produced no adverse clinical or pathological signs in the heart tissues of the dams (Hodge et al. 1977). [Pg.47]

Cardiovascular Effects. Inhalation and oral studies in humans and animals have not revealed any treatment-related histopathological lesions of heart tissue, or impairment of cardiac functions, even at dose levels causing severe liver and kidney damage (Adams et al. 1952 Stewart et al. 1961 Umiker and Pearce 1953). It is possible that high-level carbon tetrachloride exposure may produce cardiac arrhythmias by sensitization of the heart to catecholamines (Reinhardt et al. 1971). Accordingly, there is some concern for cardiovascular toxicity following substantial exposure to carbon tetrachloride. [Pg.77]

The electrocardiographic effects of moricizine include alterations in conduction velocity without an effect on the refractoriness of heart tissue. Moricizine enhances sinus node automaticity and prolongs sinoatrial and His-Purkinje intervals and the QRS. Moricizine prolongs ventricular conduction, thereby widening the QRS complex on the electrocardiogram. It has no significant effects on the QT interval. [Pg.176]

The overview of HPMA copolymer-anticancer drug conjugates and their antitumor activities can be found in Table 1. As with other carrier systems, attachment of an anticancer drug to the HPMA copolymer carrier changes the drug s pharmacokinetics. For example, ADR attached to HPMA copolymers via a Gly-Phe-Leu-Gly sequence showed a 15-times longer intravascular half-life and a 100-fold lower initial peak level in the heart tissue when compared to free... [Pg.105]

Examples of some conditions which are known,or are believed to be, to be autoimmune responses include myasthenia gravis (destruction of acetylcholine receptors), rheumatic fever (a streptococcal infection challenges the immune system and then the immune system mistakes heart tissue for another strep infection), Addison s disease (destruction of the adrenal glands), arthritis (an infection of unknown origin starts the immune response but somehow IgG becomes changed, enough so as to start another IgM response - this time to the body s own IgG), pernicious anemia (inability to process vitamin B12)- insulin-dependent diabetes mellitus (IDDM or type I diabetes), multiple sclerosis, aspermatogenesis, and photosensitivity. [Pg.196]


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See also in sourсe #XX -- [ Pg.832 ]

See also in sourсe #XX -- [ Pg.249 ]




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