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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The author describes a family (48 year old mother and 15 year old son) with the muscular variant of glycogenosis-McArde's metabolic myopathy. The mother has been ill since 22 years old, the son--since 7. The disease had a slowly progressive development. The clinical picture was characterized by convulsions of the type of cramps following physical loadings on muscles of the body and extremities. Convulsions were accompanied by pain, an induration and enlargment of the muscles, muscle fatigue and increased significantly in an artifical ischemia of the extremities. A histochemical study of the muscle revealed a pathological accumulation of glycogen. The content of lactic and pyruvic acid in the blood after work in ischemic conditions did not change significantly. A study of the sugar curve in the blood with a loading with glucose and a parallel determination of insulin by a radioimmune method found hyperinsulinemia and a dysfunction of the pancreas.
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PMID:[McArdle's disease (a familial case)]. 106 64

The inflammatory myopathies encompass a group of heterogenous muscle diseases which have in common an acquired myopathy with histological signs of endomysial inflammation. We present evidence based on recently emerged clinical, histologic, immunopathologic, demographic and therapeutic observations that these myopathies comprise three major and distinct groups: polymyositis (PM), dermatomyositis (DM), and inclusion-body myositis (IBM). Immune-mediated mechanisms characteristic for each group appear to play a primary role in the pathogenesis of these diseases. In DM there is an intramuscular microangiopathy mediated by the C5b-9 membranolytic attack complex, leading sequentially to loss of capillaries, muscle ischemia, muscle fiber necrosis and perifascicular atrophy. In contrast, in PM and IBM the muscle fiber injury is initiated by sensitized CD8+ cytotoxic T cells that recognize MHC-I restricted muscle antigens, leading to phagocytosis and fiber necrosis. Among the viruses implicated in the cause of inflammatory myopathies, only the retroviruses, HIV, HTLV-1 and simian retroviruses, have been convincingly associated with PM. Retroviruses, therefore, appear to be the leading group of viruses capable of triggering these diseases. The treatment of inflammatory myopathies has been largely empirical. A detailed therapeutic plan based on our experience with a large number of patients is presented. Patients with bona fide PM or DM respond to steroids to some degree and for some period of time. In contrast, patients with IBM do not respond to any therapy and the disease should be suspected when a patient with presumed PM has failed treatment. Methotrexate and cyclophosphamide are disappointing. Cyclosporine and Azathioprine are commonly used but they are of uncertain benefit. Plasmapheresis is ineffective. High-dose intravenous immunoglobulin is a promising new therapeutic modality.
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PMID:Clinical, immunopathologic, and therapeutic considerations of inflammatory myopathies. 142 35

Relative concentrations of inorganic phosphate [Pi]r, creatine phosphate [CP]r, adenosine triphosphate [ATP]r, and intracellular pH (pHi) were determined by 31P-NMR spectroscopy in the flexores digitorum muscles. The measurements were performed at rest, during bouts of rhythmic exercises at different powers, including one with restricted blood supply, and during recovery. Normal subjects (N) and subjects with previous histories of exercise hyperthermia (EH) were compared. No significant difference was found between N and EH subjects at rest. During exercise [ATP]r was not affected, except in EH subjects exercising under partial muscle ischemia (P less than 0.001); in both N and EH, [CP]r and pHi decreased, and the higher the load the more pronounced the reduction. These changes were significantly larger in EH patients than in N (P less than 0.05), and the differences were dramatically increased by reducing blood supply (P less than 0.001). During recovery, the return to the control values was much slower in EH patients than in N, in particular for pHi after the exercise under partial ischemia. In conclusion, the fact that metabolic disorders are still patent long after the EH occurrence supports the possibility of latent myopathy and of a persistent metabolic disorder. Thus, 31P-NMR spectroscopy could be a useful noninvasive test to detect EH susceptibility in at-risk subjects.
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PMID:Long-term relationship between acute rhabdomyolysis and abnormal high-energy phosphate metabolism potentiated by ischemic exercise. 154 23

The toxic oil syndrome is a multisystemic disease caused by the ingestion of adulterated rapeseed oil. The basic lesion is a peculiar vasculitis that affects mainly the intima, showing the features of an endovasculitis. Vessels of every type and size are involved, affecting practically every organ. The vascular lesions begins with endothelial damage that varies from cellular swelling to cellular necrosis. It then progresses by mixed cellular inflammatory infiltration of the intima and, in some cases, of the media and adventitia. In some cases the infiltrate is rich in eosinophils and a few show foamy histiocytes. Proliferation of myointimal cells and in advanced stages fibroblastic proliferation causes narrowing or obliteration of the vascular lumen. Thromboembolic complications perpetuate the vascular lesion and compound the ischemia and parenchymal atrophy of several organs. The peripheral nerve lesions begin with an inflammatory neuropathy with lymphocytic perineuritis and progress to perineural fibrosis with secondary axonal degeneration. Skeletal muscle lesions exhibit an interstitial inflammatory myopathy at first, followed by a neurogenic muscular atrophy. A direct effect of unidentified toxic substances, possibly free radicals, may cause the endothelial lesion. Other factors, such as immunopathologic mechanisms of delayed hypersensitivity, may contribute to the progression of the vascular lesions.
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PMID:Extracardiac vascular and neural lesions in the toxic oil syndrome. 165 52

In experimental hyperthyroidism, acceleration of lipid peroxidation occurs in heart and slow-oxidative muscles, suggesting the contribution of reactive oxygen species to the muscular injury caused by thyroid hormones. This article reviews various models of oxidative muscular injury and considers the relevance of the accompanying metabolic derangements to thyrotoxic myopathy and cardiomyopathy, which are the major complications of hyperthyroidism. The muscular injury models in which reactive oxygen species are supposed to play a role are ischemia/reperfusion syndrome, exercise-induced myopathy, heart and skeletal muscle diseases related to the nutritional deficiency of selenium and vitamin E and related disorders, and genetic muscular dystrophies. These models provide evidence that mitochondrial function and the glutathione-dependent antioxidant system are important for the maintenance of the structural and functional integrity of muscular tissues. Thyroid hormones have a profound effect on mitochondrial oxidative activity, synthesis and degradation of proteins and vitamin E, the sensitivity of the tissues to catecholamine, the differentiation of muscle fibers, and the levels of antioxidant enzymes. The large volume of circumstantial evidence presented here indicates that hyperthyroid muscular tissues undergo several biochemical changes that predispose them to free radical-mediated injury.
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PMID:Oxidative muscular injury and its relevance to hyperthyroidism. 218 67

Crush injuries are ubiquitous, common sequelae in victims of seismic, industrial and military catastrophes, and were considered to be mainly due to ischemia of the affected limbs. Our clinical experience suggests that early in the crush syndrome, interference with the circulation may occur but is rare. The predominant earliest lesion in the crush syndrome is postulated to be pressure-stretch myopathy, rather than ischemic myopathy. It is proposed that at the membrane level, stretch increases sarcoplasmic influx of Na, Cl, H2O and Ca down their electrochemical gradient. Energy-requiring cationic extrusion pumps work at maximal capacity, but are unable to cope with the increased load. This results in cell swelling and increase in cytosolic and mitochondrial calcium with activation of autolytic destructive processes and interference with cellular respiration. Extensive muscle swelling may cause late muscle tamponade and myoneural ischemic damage (compartmental syndrome). Thus, whereas prevalent theory suggests that the sarcolemmal cationic pump activity is attenuated in the crush syndrome due to early ischemia, we propose that the cationic extrusion pump is maximally activated as in the amphotericin B model. Because the cationic pump is maximally activated in the stretched muscle and in cells exposed to amphotericin, these models rapidly deplete their scarce ATP stores and are susceptible to hypoxia in the face of initially normal circulation.
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PMID:The mechanism of muscle injury in the crush syndrome: ischemic versus pressure-stretch myopathy. 227

Morphologic lesions seen in six 8-month-old Labrador Retrievers with hereditary myopathy were predominantly small- and large-group atrophy of muscle cells of all fiber types. The dogs were intolerant of exercise and fatigued rapidly. An isolated gracilis muscle preparation was used to study the hemodynamic features of the microvasculature. Isogravimetric capillary pressure as well as arterial and venous pressures in the isolated gracilis muscle preparation obtained during maximal vasodilatation were within the range reported for healthy, mixed-breed dogs, as were precapillary, postcapillary, and total vascular resistances. Capillary filtration and osmotic reflection coefficients were not different from those reported in other studies on healthy dogs. All measurements and calculations were repeated during reperfusion, subsequent to a 4-hour period of global ischemia. Postischemic vascular responses were similar to the pattern previously reported in healthy dogs. These studies did not support the hypothesis of a vascular defect as a cause of hereditary myopathy in Labrador Retrievers.
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PMID:Muscle hemodynamics in hereditary myopathy of Labrador retrievers. 245 92

This article describes the ultrastructural study of skeletal muscle biopsy specimens from five patients following envenomization by tropical rattlesnake (Crotalus durissus terrificus). All the patients were bitten in the leg and the biopsy specimens were obtained from the contralateral gastrocnemius muscle in the middle of the lower leg. A wide spectrum of detailed ultrastructural changes involving muscle fibers and microvasculature was demonstrated. Essentially, such lesions included widespread necrotic myofibers intermixed with intact fibers, accompanied by changes in the endothelial lining of the intramuscular blood capillaries and small arterial vessels, reducing their lumens. Since these alterations were observed in biopsy specimens from the limb contralateral to the site of the bite, they clearly demonstrate the systemic myonecrotic action of the venom of a tropical rattlesnake. On the basis of these data, the mechanism of venom-induced myopathy is described. It is postulated that the pathogenesis of systemic myonecrosis due to poisoning by C durissus terrificus is a complex one, probably due to direct damage to cells by the myotoxins of the venom, as well as indirect effects due to ischemia.
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PMID:Electron-microscopic study of systemic myonecrosis due to poisoning by tropical rattlesnake (Crotalus durissus terrificus) in humans. 291 4

Standard methods of echocardiographic analysis permit accurate categorization of cardiomyopathies into dilated, hypertrophic, and restrictive types. However, ascertainment of the cause of a particular cardiomyopathy (e.g., ischemia versus inflammation as the cause of a dilated myopathy) with ultrasound would be greatly facilitated by analysis of myocardial composition with ultrasound tissue characterization techniques. Qualitative observations have identified unusual echocardiographic image texture in hypertrophic cardiomyopathy and in amyloidosis. Quantitative observations have verified these findings and have identified increased ultrasound backscatter in regions of myocardial fibrosis, calcification, and anthracycline-induced cardiomyopathy. Although several technical problems remain unsolved and further research is needed in the mechanisms of normal and abnormal ultrasound/tissue interactions, tissue characterization with ultrasound has the potential to contribute independent information on myocardial composition in patients with cardiomyopathy.
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PMID:Clinical potential of ultrasound tissue characterization in cardiomyopathies. 307 43

Coronary artery disease can have various clinical manifestations, from the presence of "silent" ischemia to the occurrence of an acute myocardial infarction and congestive myopathy. At each point in the clinical manifestation of coronary artery disease, the practitioner has an evolving number of techniques available to guide decisions regarding prognosis and therapy. Guidelines exist for defining which patients with "silent" ischemia need further evaluation. The clinically manifested occurrence of angina pectoris is commonly encountered in the elderly. Prognostic stratification can occur using both invasive and non-invasive techniques. Even patients with unstable angina have different outcomes depending upon clinical presentation and therapeutic management. Finally, a large pool of patients who survive an acute myocardial infarction have a varied prognosis depending upon certain risk markers as documented with widely available non-invasive testing. This article summarizes the evaluations and decisions the physician can make regarding patients who present with the various manifestations of coronary artery disease and provides a summary of recent data supporting decisions regarding prognosis and therapy.
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PMID:Cardiac disorders: a guide to assessing risk in the elderly. 329 56


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