Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of early ischemia were studied in the anterior tibial muscle of Sprague-Dawley rats after 2--24 hr of tourniquet compression at the thigh. Ragged-red fibers, moth-eaten fibers, cores and targets were seen in tissue examined by enzyme histochemistry and electron microscopy. Giant mitochondria, abnormalities of cristal arrangement, crystalloids, osmiophilic inclusion bodies and myeloid figures were dominant features of the mitochondrial reaction. The results of this experiment indicate that early ischemia induces a variety of changes described in other neuromuscular conditions such as dystrophy and the "mitochondrial myopathies". The pathogenesis of these changes and their relationship to human disease of muscle is discussed.
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PMID:The early effects of ischemia upon skeletal muscle mitochondria. 15 85

Giant mitochondria in kidneys have increasingly been observed since the introduction of Cyclosporin A (CSA) as immunosuppressant in kidney transplants and in patients with autoimmune disorders. In animals treated with CSA, giant mitochondria were also described. In a study of "zero-hour" biopsies taken immediately before or after reperfusion of the renal transplant, giant mitochondria were often unexpectedly found. Retrospective analysis revealed that a significant increase in the number of giant mitochondria is more often associated with CSA therapy than ischemia. Giant mitochondria with sparse cristae seem to prevail in ischemia, whereas those with dense matrix and crystalloid structures predominate in CSA therapy.
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PMID:Giant mitochondria in "zero-hour" transplant biopsies. 158 95

Eight cases of transient reversible segmental asynergy of the left ventricle thought not to be related to coronary artery lesions are reported. Three cases were associated with inflammatory reactions of unknown origin, and one each with lactic acidosis, abdominal surgery, hypoglycemia, tetanus and pneumonia. None of the patients had symptoms suggestive of ischemic heart disease before or after these episodes. Electrocardiograms before these episodes were all normal. Two-dimensional echocardiography was performed to evaluate abnormal electrocardiograms. Coronary angiography was performed in 4 of 8 cases and was normal in all 4 cases; 2 done as emergencies and 2 non-emergencies. Two ergonovine tests were negative. Left ventricular wall motion abnormalities, present mainly at the apex of the left ventricle, returned to normal in 1 to 4 weeks. Giant negative T waves in the chest leads during this recovery period were characteristic electrocardiographic features and normalized in 6 weeks on average. We believe that these episodes were not related to ischemia due to coronary artery disease, but to some metabolic humoral factors. An excellent prognosis can be expected if these abnormal metabolic circumstances can be resolved.
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PMID:Transient segmental asynergy of the left ventricle of patients with various clinical manifestations possibly unrelated to the coronary artery disease. 174 67

Giant fusiform aneurysms of the basilar artery were found in a 6-year-old boy who subsequently died after rupture of the aneurysm, and in a 64-year-old man who showed signs of ischemia and compression of the brain stem. Autopsy disclosed strikingly similar abnormalities of the wall of the basilar artery, consisting of a defect of the internal elastic lamina and absence of the media. A congenital anomaly may play a role in the pathogenesis of this abnormality, in both young and some elderly patients.
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PMID:Basilar artery giant fusiform aneurysms caused by congenital defect of the internal elastic lamina and media. 339 Sep 75

Continuous electrocardiographic recordings during anginal attacks in patients with variant angina were reviewed. Twenty-seven attacks in 15 patients were associated with transient T-wave inversion during recovery periods of angina (type A), while in another 69 attacks in 28 patients there was no T-wave inversion (type B). In none of the patients was there an ischemic T-wave inversion during angina-free periods. Both the maximum elevation (0.79 +/- 0.57 mV) and duration (5.3 +/- 1.2 min) of ST-segment deviation of type A attacks were significantly higher and longer than those of type B (0.44 +/- 0.27 mV, 2.8 +/- 1.4 min). Ten patients who had both type A and type B attacks one time or the other were selected for further evaluation. In these 10, the duration of ST-segment elevation was significantly longer during type A attacks (5.2 +/- 1.2 min, n = 18) than during type B attacks (2.7 +/- 1.2 min, n = 20) but there was no significant difference in the maximum ST-segment elevation. Giant U-wave inversion appeared in 15% of the type A attacks, but never in type B. Therefore, the T-wave abnormality related to ischemic episodes in patients with variant angina seems to be associated with more severe ischemia of longer duration than milder episodes of transient ischemia.
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PMID:Two electrocardiographic patterns with or without transient T-wave inversion during recovery periods of variant anginal attacks. 665 94

Giant-cell arteritis is a polysymptomatic disease of the elderly. Systemic symptomatology includes headaches, arthralgias, myalgias, tender temporal arteries, jaw claudication, low-grade fever, anemia, anorexia, malaise, and weight loss. Visual loss from anterior ischemic optic neuropathy and diplopia resulting from ischemia of the ocular muscles represents the major ocular manifestations of giant cell arteritis. When the diagnosis is suspected, blood for a sedimentation rate should be drawn, and, if it confirms the clinical impression, high dose prednisone should be started immediately and a temporal artery biopsy performed at a later date. Only by asking the proper questions and suspecting the diagnosis will this preventable form of blindness receive the prompt attention it deserves.
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PMID:Giant-cell arteritis. Signs and symptoms. 715 21

The aim of this investigation was to correlate the clinical and histological findings in 85 consecutive patients with temporal arteritis. Particular attention was given to a possible correlation between optic nerve involvement and the presence of giant cells upon histological examination. Severe ischemia as in anterior ischemic optic neuropathy and central retinal arterial occlusion was presented in 37 patients (43%). Giant cells were definitely observed in 32 biopsy specimens (37.6%) and suspected in 11 additional specimens (13%): In 42 specimens (49.3%) no giant cells were present. Our study showed no correlation between the occurrence of severe optic nerve involvement and the histological findings with regard to giant cells. Statistical evaluation also failed to show a significant correlation between the frequency of pain and jaw claudication and the respective histological findings regarding giant cells. In the biopsy specimen of one patient, numerous eosinophilic granulocytes had infiltrated the vessel wall.
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PMID:Temporal arteritis. Comparison of histological and clinical findings. 797 62

Giant negative U waves transiently appeared in a patient with acute myocardial infarction (AMI). During hospitalization, these giant negative U waves (0.3-0.5 mV) were observed in leads V2 through V4 of the electrocardiogram (ECG). The waves disappeared 10 days after hospitalization, but reappeared during a treadmill exercise test 3 weeks after the onset of AMI. The same waves were detected again when the patient was admitted for angina pectoris 3 months later. Since these giant negative U waves appeared concomitant with myocardial ischemia, ischemia seems to be their cause. To our knowledge, there are no previous reports on reproducible U waves like those seen in this patient.
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PMID:Giant negative U waves during acute myocardial infarction and ischemia. 914 4

Giant cell (temporal) arteritis continues to be a sight-threatening, systemic vasculitis with a poorly understood pathogenesis. The characteristic granulomatous inflammation of the vessel wall commonly leads to local ischemia. Recent advances in immunological investigations have characterized the cellular components of the disease process, but the etiology has so far remained unresolved. A reappraisal of the clinical features of giant cell (temporal) arteritis demonstrates the heterogeneity of the manifestations of the disease, including ischemic optic neuropathy. A range of new laboratory investigations and blood flow studies with color Doppler imaging have demonstrated promising roles, with respect to diagnosis and long-term follow-up. Prompt diagnosis and expeditious treatment require a high index of clinical suspicion, particularly for atypical cases. Corticosteroids remain the treatment of choice, other immuno-suppressive agents being used as second line steroid-sparing agents. Giant cell (temporal) arteritis leads to increased vascular and visual morbidity and, if untreated, may prove fatal. To maintain high standards of management of this enigmatic disorder, ophthalmologists need to be aware of the clinical spectrum of giant cell (temporal) arteritis and currently available diagnostic tests and treatment strategies.
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PMID:Current concepts in giant cell (temporal) arteritis. 938 74

Giant aneurysms of the basilar artery are rare. With a diameter of 25 mm or more they are often partially thrombosed and show atheromatous plaques. There are some problems in the treatment especially when the aneurysm is broadbased with bulbous origin encorporating the origin of the posterior cerebral artery (PCA). In many of these cases neither operative clipping alone nor coil embolization alone will be practical without causing an ischemia in the depending brain areas. We will report about two patients with giant aneurysms of the basilar artery involving the origin of the PCA and a combined surgical and interventional neuroradiological approach. Preoperatively both patients showed only mild neurological symptoms (slight left hemiparesis, incomplete hemianopsia). We anastomosed the superficial temporal artery as an extracranial-intracranial bypass end-to-side to the PCA followed by clipping the PCA out of the aneurysm. Next day embolization of the aneurysm with Guglielmi ditachable coils was done. Both patients recovered without complications. An angiographic control showed no more filling of the aneurysm and a free running bypass feeding the PCA. In our opinion this combined approach is an effective method to treat giant aneurysms of the basilar artery which involve the origin of the PCA when clipping alone is impossible.
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PMID:Giant basilar artery aneurysms encorporating the posterior cerebral artery: bypass surgery and coil occlusion--two case reports. 1023 84


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