Muscles, effect

HMG-CoA REDUCTASE INHIBITORS AND FlBRIC ACID DERIVATIVES. The antihyperlipidemic drugp, particularly die HMG-CoA reductase inhibitors, have been associated with skeletal muscle effects leading to rhab-domyolysis. Rhabdomyolysis is a very rare condition in which muscle damage results in die release of muscle cell contents into die bloodstream. Rhabdomyolysis may precipitate renal dysfunction or acute renal failure The nurse is alert for unexplained muscle pain, muscle tenderness, or weakness, especially if tiiey are accompanied by malaise or fever. These symptoms should be reported to die primary health care provider because the drug may be discontinued. 

Vagal neuropathy in diabetes mellitus [145, 146] and truncal vagotomy [147] may markedly change intestinal motility, as do heart-lung transplantation [148]. Spinal cord lesions also alter gut function, but the outlet obstruction due to failure of the striated muscles involved in defecation is more important than the enteric smooth muscle effects [149]. 

Smooth muscles Receptor interactions and smooth muscle effects... 

Smooth muscle effects. The opposing effects on smooth muscle (A) of a-and p-adrenoceptor activation are due to differences in signal transduction (p. 66). This is exemplified by vascular smooth muscle (A). ai-Receptor stimulation leads to intracellular release of Ca + via activation of the inositol tris-phosphate (IP3) pathway. In concert with the protein calmodulin, Ca + can activate myosin kinase, leading to a rise in tonus via phosphorylation of the contractile protein myosin. cAMP inhibits activation of myosin kinase. Via the former effector pathway, stimulation of a-receptors results in vasoconstriction via the latter, P2-receptors mediate vasodilation, particularly in skeletal muscle - an effect that has little therapeutic use. 

With severe intoxication by all routes, an excess of acetylcholine at the neuromuscular junctions of skeletal muscle causes weakness aggravated by exertion, involuntary twitchings, fasciculations, and eventually paralysis. The most serious consequence is paralysis of the respiratory muscles. Effects on the central nervous system include giddiness, confusion, ataxia, slurred speech, Cheyne-Stokes respiration, convulsions, coma, and loss of reflexes. The blood pressure may fall to low levels, and cardiac irregularities, including complete heart block, may occur. ... 

Skeletal muscle effects All statins have been associated with myalgia, myopathy (ie, muscle pain, tenderness, or weakness with creatine phosphokinase [CPK] values above 10 times the ULN), and rhabdomyolysis. Factors that may predispose patients... 

Skeletal muscle effects The use of fibrates alone, including fenofibrate, may occasionally be associated with myopathy. Treatment with drugs of the fibrate class has been associated on rare occasions with rhabdomyolysis, usually in patients with impaired renal function. Consider myopathy in any patient with diffuse myalgias, muscle tenderness or weakness, or marked elevations of creatine phosphokinase levels. 

Skeletal muscle effects In clinical trials, there was no excess of myopathy or rhabdomyolysis associated with ezetimibe compared with the relevant control arm (placebo or HMG-CoA reductase inhibitor alone). However, myopathy and rhabdomyolysis are known adverse reactions to HMG-CoA reductase inhibitors and other lipid-lowering drugs. 

Excess selenium intake can occur in both animals and humans living in areas with elevated selenium in the soil. Most grass and grains do not accumulate selenium, but when an animal consumes plants that do accumulate selenium (some up to 10,000 mg/kg) they can develop a condition called the blind staggers . Symptoms include depressed appetite, impaired vision, and staggering in circles and can ultimately lead to paralysis and death. Humans are susceptible to similar effects as well as additional neurological effects. Selenium deficiency results in heart disorders, skeletal muscle effects, and liver damage. 

The postsynaptic physiological effects of serotonin are varied and widespread. The administration of serotonin leads to powerful smooth-muscle effects in the cardiovascular and gastrointestinal systems. Vasodilation and hypotension may result, partly through central effects, if the serotonin concentration in the CNS is increased by administration of the serotonin precursor 5-hydroxytryptophan. Unlike serotonin, this precursor can cross the blood-brain barrier. Intestinal mobility is also influenced by serotonin. 

Important differences in vascular selectivity exist among the calcium channel blockers. In general, the dihydropyridines have a greater ratio of vascular smooth muscle effects relative to cardiac effects than do diltiazem and verapamil. Furthermore, the dihydropyridines may differ in their potency in different vascular beds. For example, nimodipine is claimed to be particularly selective for cerebral blood vessels. Splice variants in the structure of the cq channel subunit appear to account for these differences. 

Cyproheptadine resembles the phenothiazine antihistaminic agents in chemical structure and has potent H receptor-blocking as well as 5-HT2-blocking actions. The actions of cyproheptadine are predictable from its histamine and 5-HT receptor affinities. It prevents the smooth muscle effects of both amines but has no effect on the gastric secretion stimulated by histamine. It also has significant antimuscarinic effects and causes sedation. 

The methylxanthines have effects on the central nervous system, kidney, and cardiac and skeletal muscle as well as smooth muscle. Of the three agents, theophylline is most selective in its smooth muscle effects, whereas caffeine has the most marked central nervous system effects. 

Dekker LRC, Fiolet JWT, VanBavel E, Coronel R, Opthof T, Spaan JAE, Janse MJ Intracellular Ca2+, intercellular electrical coupling and mechanical activity in ischemic rabbit papillary muscle. Effects of preconditioning and metabolic blockade. Circ Res 1996 79 237-246. 

Wang, X.-L. Akhtar, R.A. Abdel-Latif, A.A. Purification and properties of D-myo-inositol 1,4,5-trisphosphate 3-kinase from bovine iris sphincter smooth muscle effect,s of protein phosphorylation in vitro and in intact muscle. Biochem. J., 308 (Pt 3), 1009-1016 (1995)... 

Zakaria, E.R., Lofthouse, J. and Flessner, M.F. (1997) In vivo hydraulic conductivity of muscle effects of hydrostatic... 

C13. Cooper, J. M., Mann, V. M., and Schapira, A. H., Analyses of mitochondrial respiratory chain function and mitochondrial DNA deletion in human skeletal muscle Effect of ageing. J. Neurol. Sci. 113,91-98 (1992). 

Salmons, S. and Henrlksson, J. (1981) The adaptive response of skeletal muscle to Increased use. Muscle Nerve 4 94-105. Holloszy, J. 0. (1967) Biochemical adaptations In muscle. Effects of exercise on mitochondrial oxygen uptake and respiratory enzyme activity In skeletal muscle. J. Biol. Chem. 242 2278-82. 

Soussi, B., Idstrom, J.P., Schersten, T., Bylund-Fellenius, A.C. (1989). Kinetic parameters of cytochrome c oxidase in rat skeletal muscle effect of endurance training. Acta Physiol. Scand. 135 373-9. 

In general, when morphine is used and the smooth muscle effects are objectionable, atropine may be given simultaneously to antagonise spasm. Unfortunately this does not always effectively oppose the rise of pressure induced in the biliary system, nor does it restore bowel peristalsis. Glyceryl trinitrate will relax morphine-induced spasm. 

Turinsky J., and Long, C. L. (1990). Free amino acids in muscle Effect of muscle fiber population and denervation. A i. /. Physiol 258, E4S5-E491. 

The authors concluded that beta2-adrenoceptor agonist activity had been responsible for the deleterious muscle effects and they proposed that beta2-adrenoceptor... 

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