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

The time course of structural change in epilepsy-induced necrosis of the substantia nigra was studied by light and electron microscopy, and was correlated with previous metabolic studies. By light microscopy, tinctorial pallor appeared early, followed by pan-necrosis and macrophage infiltration. Mild lesions showed neuropil vacuolation but sparing of neurons, rather than a selective neuronal vulnerability. Electron microscopy of the evolving necrosis revealed an orderly sequence of structural damage involving first axons, then dendrites, neurons, and glia. No necrotic endothelial cells could be found, even in areas of apparent pan-necrosis by light microscopy. Pericytes near the vascular lumen were spared, whereas those in outer locations were necrotic. Edema, measured densitometrically, was absent. Previous metabolic studies of this lesion have demonstrated a pronounced focal lactic acidosis due to anaerobic hypermetabolism. Although the lesions resemble infarcts, hypermia rather than ischemia has been shown to accompany their development. Structural preservation of endothelial cells and inner pericytes likely stems from proximity to the moving blood stream, away from the site of lactic acid production in the neuropil. The findings indicate that the perfusion of necrotic tissue occurs via a persisting, intact microcirculation. The relative neuronal sparing and the early axonal rather than dendritic lesion show a clear distinction from excitotoxic pathology.
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PMID:Early axonal lesion and preserved microvasculature in epilepsy-induced hypermetabolic necrosis of the substantia nigra. 379 37

Intracellular brain pH, cortical blood flow, and electroencephalograms (EEG's) were recorded in severely and moderately ischemic regions in 10 control and 10 nimodipine-treated rabbits prior to and following major branch occlusion of the middle cerebral artery (MCA). Preocclusion cortical blood flow was 51 ml/100 gm/min and intracellular brain pH was 7.01 in both the control and the treated animals. After MCA occlusion, the severely ischemic regions in the control group showed initial and 4-hour postocclusion flows of 12.7 and 5.2 ml/100 gm/min with a brain pH of 6.64 and 6.08, respectively. In animals given nimodipine after MCA occlusion, blood flow increased from 10.5 to 18.8 ml/100 gm/min, with an associated elevation in intracellular brain pH from 6.57 to 6.91. Comparable findings were observed in areas of moderate ischemia. Improvements in cortical blood flow, intracellular brain pH, and EEG attenuations produced by nimodipine were all statistically significant. Inspection of the cortex revealed reversal of cortical pallor and small-vessel spasm following treatment with nimodipine. It is hypothesized that nimodipine exerts its effects through reversal of ischemia-induced secondary vasoconstriction, and that this drug may be an important adjunctive treatment for patients with focal cerebral ischemia.
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PMID:Effect of nimodipine on intracellular brain pH, cortical blood flow, and EEG in experimental focal cerebral ischemia. 395 Jul 44

Two cases of multiple births were observed in which a twin placenta showed a striking gross and microscopic ischemia of one of its fused components. In both cases death of one or more of the infants occurred. Case 1 was a triplet birth of identical siblings and two of the infants died on the second and third days after birth, respectively. Case 2 was a twin birth in which one of the infants was stillborn. Two other cases are quoted from the literature in which a similar pallor of one-half of the twin placenta was observed, and both these cases were also associated with death of the associated fetus.It is possible that this placental lesion may be due to transfusion of blood from one placental half to the other (twin transfusion syndrome) with harmful effects on one or both fetuses.
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PMID:Unilateral ischemia of the fused twin placenta: a manifestation of the twin transfusion syndrome? 601 55

The pathophysiologic events in optic nerve axons have recently been recognized as crucial to an understanding of clinically significant acquired alterations in the ophthalmoscopic appearance of the optic disc. Stasis and related abnormalities of axonal transport appear to explain most aspects of optic nerve head swelling, including optic disc drusen and retinal cottonwool spots. Loss of axoplasm and axonal death can be invoked to interpret optic disc pallor, thinning and narrowing of rim tissue, changes in the size and outline of the optic cup, laminar dots, atrophy of the retinal nerve fiber layer, and acquired demyelination and myelination of the retinal nerve fiber layer. It is speculated that the axons may also play a role in the mechanical support of the lamina cribrosa in resisting the pressure gradient across the pars scleralis of the optic nerve head. Axons and their associated glial cells may be involved in those cases where "reversibility" of cupping of the optic disc has been reported. The structure, physiology, and experimental pathologic findings of the optic nerve head have been reviewed. Many aspects concerning the final anatomic appearance of the optic nerve head have been explained. However, many questions remain concerning the intermediate mechanisms by which increased intracranial pressure retards the various components of axonal transport in papilledema and by which increased IOP causes axonal loss in glaucoma. Investigation of the molecular biology of axonal constituents and their responses to abnormalities in their physical and chemical milieu could extend our understanding of the events that result from mechanical compression and local ischemia. Moreover, we have identified a need to further explore the role of axons in the pathophysiology of optic disc cupping.
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PMID:Optic nerve axons and acquired alterations in the appearance of the optic disc. 620 9

Thirty-five cases of renal medullary crest necrosis morphologically similar to the renal papillary necrosis of analgesic nephropathy as described in man and rats are reported in horses receiving maintenance dosages of phenylbutazone. The primary lesion is a well-demarcated focal medullary necrosis resulting in sequestration of fragments of the renal crest. Renal cortical lesions are considered secondary to the medullary necrosis and consist of segmental pallor as a result of tubular dilatation, filtrate retention, and interstitial edema. Ischemia in concert with phenylbutazone is suggested as the etiology. Renal medullary crest necrosis is presented as more appropriate morphological terminology for this lesion in the equine species than renal papillary necrosis as is used in man and rats.
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PMID:Renal medullary crest necrosis associated with phenylbutazone therapy in horses. 664 37

A case of arteriosclerotic posterior ischemic optic neuropathy without optic disc edema is described and documented photographically. The development of optic disc cupping and pallor with ischemia in this patient supports the vascular basis for development of similar cupping and pallor in open angle glaucoma and low tension glaucoma.
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PMID:Development of cupping and pallor in posterior ischemic optic neuropathy. 688 56

Fifteen patients with ischemia of the colon are presented. The majority showed a similar clinical presentation with hematochezia, abdominal pain, and diarrhea in an elderly patient population having associated disease. Colonoscopy was abnormal in all patients studied. Three endoscopic stages were recognized; (1) acute stage characterized by petechiae, pallor, and hyperemia; (2) subacute stage consisting of ulceration and exudation; and (3) chronic stage characterized by stricture, decrease in haustrations, and mucosal granularity. Conventional barium enemas were abnormal and suggested ischemic colitis in six of 15 patients. Rigid proctoscopy was normal or demonstrated nonspecific proctitis in 12 of 15 patients studied. Colonoscopic biopsies demonstrated superficial inflammatory changes in all patients. Thirteen patients had complete mucosal healing endoscopically in 2 weeks to 3 months with stricture developing in four patients. Because ischemic colitis is a distinct subtype of ischemic bowel disease most often limited to the superficial mucosa, colonoscopy is an alternative and usually safe modality in the diagnosis of this entity and proved more accurate that conventional x-ray and proctoscopy.
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PMID:Colonoscopy in ischemic colitis. 729 23

Morphologic changes in the subendocardial myocardium that appeared to be caused by severe, chronic subendocardial ischemia were studied in patients with fatal ischemic heart disease admitted to the Specialized Center of Research for Ischemic Heart Disease at the University of Alabama in Birmingham in the period 1970--1977. Thirteen patients were selected for this report on the basis that they had the lesions in the subendocardial myocardium we believe to have been caused by subendocardial ischemia and had no evidence of acute or remote myocardial infarction or other conditions that may have contributed to their terminal illness or death. Clinical findings were unstable angina, congestive heart failure, usually no increase in plasma enzymes indicative of myocardial damage, and electrocardiographic changes consistent with subendocardial ischemia. All 13 patients had 75% or greater stenosis of the three major coronary arteries; none had acute thrombotic or embolic coronary artery occlusion. The left ventricle in all cases was hypertrophied. The subendocardial myocardium showed circumferential pallor, hyperemia, or focal fibrosis without perceptible loss of volume in papillary muscles or trabeculae carneae. Microscopically, acute lesions showed one to two layers of preserved myofibers adjacent to the endocardium, vacuolar change in the deeper fibers, and focal areas of coagulation necrosis of variable size in the myocardium external to the fibers with vacuolar change. Coagulation necrosis was extensive in some cases and usually was not associated with infiltration of neutrophils. The repair reaction involved removal of necrotic sarcoplasm by mononuclear phagocytes, resulting in a reticular-appearing tissue without evidence of stromal collapse. Granulation tissue was not seen. Collagen fibers appeared to be deposited within the area of previous sarcolemmal sheaths. The distribution and morphology of subendocardial myocardial lesions associated with severe coronary atherosclerosis are distinctive and can be distinguished from myocardial necrosis or fibrosis associated with acute total occlusion of a coronary artery.
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PMID:Subendocardial ischemic myocardial lesions associated with severe coronary atherosclerosis. 736 50

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are common diseases in the elderly. The arteritis usually affects medium sized vessels, but large vessel involvement can also occur leading to arm claudication, bruits, loss of pulses and pallor of the upper extremities. The differential diagnosis of large vessel arteritis includes atherosclerosis and Takayasu's disease. Atherosclerosis, which affects patients of similar age to GCA is usually confined to the lower limbs and can be differentiated on the basis of the clinical setting and investigations such as the ESR, arteriography and temporal artery biopsy. Takayasu's arteritis' although histologically and arteriographically indistinguishable from GCA, is predominantly a disease of young women. A patient is described who presented with upper limb ischemia. A clinical examination revealed absence of right radial pulses and presence of murmurs at level of the carotids. The blood pressure was unrecordable in the upper right limb. The ESR was 102 mm/hr and the C-reactive protein was 11.66 mg/dl. A selective arteriography of the aortic arch and its branches revealed a right subclavian artery obstruction with good collateral circulation and a left subclavian artery stenosis. The biopsy of left temporal artery showed a typical GCA in acute stage. Treatment with prednisolone 30 mg/day was started and four weeks later, the ESR had fallen to normal. In addition this case confirms that PMR implies a systemic arteritis.
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PMID:[Giant cell arteritis and polymyalgia rheumatica presenting as subclavian artery obstruction]. 823 15

Central retinal artery occlusion occurs most commonly between the ages of 50 and 70 years, and nearly one-half (45%) of patients also have carotid artery disease. Other causes of vision-threatening vascular disease include atherosclerosis, embolism, hypertension, diabetes mellitus, and valvular disease. Symptoms vary, depending on the ocular structures involved. The patient's symptoms are an important clue to the diagnosis of peripheral or posterior retinal vascular occlusion, macular blood vessel disease, intravitreal hemorrhage, optic nerve ischemia, and ocular ischemic syndrome. The patient's ocular symptoms should lead to investigation for clinical signs of ocular vascular disease (eg, hemorrhage, "hard" or "soft" exudates, neovascularization, retinal edema, pallor, emboli, vessel narrowing, or atriovenous crossing changes).
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PMID:Ocular vascular disease: in-office primary care diagnosis. 843 37


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