Muscle damage mechanism

Clofibrate causes a necrotizing myopathy, particularly in patients with renal failure, nephrotic syndrome or hypothyroidism. The myopathy is painful and myokymia of unknown origin is sometimes present. The mechanism of damage is not known, but p-chlorophenol is a major metabolite of clofibrate and p-chlorophe-nol is a particularly potent uncoupler of cellular oxidative phosphorylation and disrupts the fluidity of lipid membranes. Muscle damage is repaired rapidly on the cessation of treatment. 

Emetine emetine is still used at high doses for the treatment of patients with severe amebiasis. Muscle damage is uncommon but when it does occur can be a severe generalized necrotizing myopathy. The outcome is, at times, fatal, especially when an emetine-induced cardiomyopathy is also present. Despite the suggestion that there may be neuritic changes, there is no evidence that emetine damages peripheral nerve. The myopathy is usually painful but reversible. The mechanism of action of emetine is unknown. 

A second group of myotoxic toxins, found almost exclusively in the venoms of cobras, are the cytotoxins (often called cobratoxins, cytolysins, cardiotoxins, or direct lytic factors). These, rather than phospholipases, are almost certainly the primary cause of muscle damage following bites by cobras. Their mechanism of action is not properly known, but it is certainly the case that their action is potentiated by the presence of phospholipases in the venom, even if the phospholipases concerned are not, themselves, myotoxic. The cytotoxins of cobra venom possess no hydrolytic activity of any kind. 

Brazeau, GA. and Fung, H.-L. Mechanisms of creatine kinase release from isolated rat skeletal muscles damaged by propylene glycol and ethanblRharm. Sci, 79, 393-397, May 1990. 

Allen, D.G., Whitehead, N.P., and Yeung, E.W., 2005, Mechanisms of stretch-induced muscle damage in normal and dystrophic muscle role of ionic changes, J Physiol, 567, pp 723—735. 

Adenosine triphosphate creatine A-phosphotransferase (EC 2.7.3.2), also creatine phosphokinase. Creatine kinase is found in muscle and is responsible for the formation of creatine phosphate from creatine and adenosine triphosphate creatine phosphate is a higher energy source for muscle contraction. Creatine kinase is elevated in all forms of muscular dystrophy. Creatine kinase is dimer and is present as isozymes (CK-1, BB CK-2, MB CK-3, MM) and Ck-mt (mitochondrial). Creatine kinase is also used to measure cardiac muscle damage in myocardial infarction. See Bais, R. and Edwards, J.B., Creatine kinase, CRC Crit. Rev. Clin. Lab. ScL 16, 291-355, 1982 McLeish, M.J. and Kenyon, G.L., Relating structure to mechanism in creatine kinase, Crit. Rev. Biochem. Mol. Biol 40, 1-20, 2005. 

The mechanism of muscle damage with opiates is most hkely related to profound and prolonged compression of muscle with compromise of the regional vascular supply [107,109,113,118-120]. The presence of hypovolemia and hypotension may further contribute to the ischemic damage. There is a direct correlation between the duration of altered consciousness and the severity of the rhabdomyolysis. Moreover, there is no evidence for any major direct toxic effect of narcotics on muscle in the vast majority of addicts who present without coma or stupor. Trauma, exertion and seizures may contribute to the muscle damage in some patients. 

Sensory nerve endings are found throughout the body in the skin, muscles, joints, blood vessels and internal organs. These nociceptors are sensitive to the effects of potentially damaging mechanical, thermal and chemical stimuli. 

I. Mechanism of toxicity. In plants, the compounds act as growth hormone stimulators. The mechanism of toxicity is unclear, but may involve mitochondrial injury. In animals, cell membrane damage, uncoupling of oxidative phosphorylation, and disruption of acetylcoenzyme A metabolism are found, widespread muscle damage occurs, and the cause of death is usually ventricular fibrillation. Massive rhabdomyolysis has been described in human cases. 

Finally, the ET fraction of pomegranate may improve the recovery of isometric strength 2—3 days after a damaging eccentric exercise, producing delayed-onset muscle soreness. Nonetheless, serum markers of inflammation and muscle damage did not provide insight regarding possible mechanisms behind this fact. ... 

The grain contains besides the hair follicles glands, veins and special muscles. The basic substance of the grain is an interwoven fibrous tissue consisting of the protein collagen. The fibres are very fine and especially the outer layer can be damaged mechanically or by microorganisms easily (Herfeld, 1990). 

ADM may evolve over several years, the extent of fiber atrophy provides an important indication of the chronicity of muscle degeneration. Acute muscle necrosis and phagocytosis give some indication as to how active the disease is at the time of biopsy. In most biopsies from ADM patients, the inflammatory cell foci are perivascular and perimysial rather than endomysial and are dominated by B-lymphocytes. The ratio of T4 lymphocytes (helper cells) to T8 lymphocytes (cytotoxic) generally indicates a predominance of the former. As in JDM, this is consistent with humoral mechanisms of cell damage, and vascular involvement is also apparent in the form of capillary endothelial cell abnormalities (tubular arrays) and duplication of basal lamina. Loss of myofibrillar ATPase from the central portions of fibers is a common prelude to muscle necrosis. 

In broad terms, pain can be divided into two categories, acute and chronic, which differ in their aetiology, mechanisms and pathophysiology. Acute pain and its associated responses are provoked by noxious stimulation and/or disease, or by abnormal function of muscle or viscerae which does not involve actual tissue damage. Although acute pain conditions may last for a length of time if not treated effectively, many cases of acute... 

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