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Myocardium energy metabolism

Fig. 1. Energy metabolism in the normal myocardium (ATP adenosine-5 -triphosphate, ADP adenosine-5 -diphosphate, P phosphate, PDH pyruvate dehydrogenase complex, acetyl-CoA acetyl-coenzyme A, NADH and NAD" nicotinamide adenine dinucleotide (reduced and oxidized), FADH2 and FAD flavin adenine dinucleotide (reduced and oxidized). Fig. 1. Energy metabolism in the normal myocardium (ATP adenosine-5 -triphosphate, ADP adenosine-5 -diphosphate, P phosphate, PDH pyruvate dehydrogenase complex, acetyl-CoA acetyl-coenzyme A, NADH and NAD" nicotinamide adenine dinucleotide (reduced and oxidized), FADH2 and FAD flavin adenine dinucleotide (reduced and oxidized).
The effects of L-arginine on energy metabolism and coronary vessel function of ischaemic and reperfused rabbit myocardium have been investigated with P NMR. Langendorff-perfused rabbit hearts were subjected to 180 min of ischaemia at 15° and then reperfused for 60 min at 37°. When L-arginine was added to the cardioplegia solution, coronary flow rate during reperfusion, ATP and PCr were improved. [Pg.406]

The toxicity of papaverine has been studied,36 as have its effects on energy processes in myocardial mitochondria,37 on the release and metabolism of dopamine,38 on contractile force and C-nucleotide levels in dog myocardium,39 on serum-induced spasms in cerebral arterioles,40 and on production of PGE2 by rabbit gastric mucosa,41 and the biological effects of drotaverine,42 N-benzoylpapaverinium chloride,43 and norlaudanosoline44 have been studied. A rapid method for the determination of papaverine in plasma by h.p.l.c. has been described.45... [Pg.82]

Liposomal ATP protected human endothelial cells from energy failure in a cell culture model of sepsis (21). ATP-L increased the number of ischemic episodes tolerated before electrical silence and brain death in the rat (22,23). In a hypovolemic shock-reperfusion model in rats, the administration of ATP-L increased hepatic blood flow during shock and reperfusion of the liver (24). The addition of the ATP-L during cold storage preservation of rat liver improved its energy state and metabolism (25,26). Co-incubation of ATP-L with sperm cells improved their motility (27). Finally, biodistribution studies demonstrated significant accumulation of ATP-L in ischemia-damaged canine myocardium (28). [Pg.363]

Tracers used for assessment of myocardial metabolism are selected based on the type of metabolism of interest EDO traces glucose metabolism, ["Cjpalmitate traces mitochondrial fatty acid metabolism, and ["Cjacetate is an indirect marker for myocardial oxygen consumption, allowing assessment of ventricular performance. [ CjPalmitate is a useful marker for normal myocardial oxygen consumption because baseline energy needs of the myocardium... [Pg.163]

Since free fatty acids are the major source of metabolic energy under aerobic conditions in the myocardium, it is not surprising that this class of compoimds has received considerable attention for use as tracers in heart... [Pg.441]

The heart is a muscular pump that provides energy to circulate blood to and from the metabolizing tissues. The pumping characteristic of each ventricle, or the relation between its pressure, volume and flow is a complex function of the contractile state of the myocardium and the mechanical interaction that takes... [Pg.64]

The contraction of the left ventricle (LV) is a complex phenomenon which depends on the interrelationships between the mechanics of the myocardium, the energy demand of the metabolic processes within the myocardium and the energy supply to the myocardium via the coronary arteries. Hormonal and neurogenic autoregulatory mechanisms play a major role in controlling these interrelationships. [Pg.331]

Table 15-1], Amphetamines and caffeine (a melhylxanthine alkaloid) stimulate catecholamine release, and tricyclic antidepressants and cocaine inhibit the uptake of released catecholamine neurotransmitters. Fluoroacetate is a metabolic inhibitor of aconitase in the tricarboxylic acid (TCA) cycle and its cardiac effects are the result of acute severe energy deficit in the myocardium. Table 15-1], Amphetamines and caffeine (a melhylxanthine alkaloid) stimulate catecholamine release, and tricyclic antidepressants and cocaine inhibit the uptake of released catecholamine neurotransmitters. Fluoroacetate is a metabolic inhibitor of aconitase in the tricarboxylic acid (TCA) cycle and its cardiac effects are the result of acute severe energy deficit in the myocardium.

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See also in sourсe #XX -- [ Pg.86 ]




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