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)

To evaluate the concordance between elevated plasma MB CPK and irreversible myocardial ischemic injury, coronary occlusion was induced for 10 minutes to 48 hours in 21 open chest dogs and 13 conscious animals. Results of plasma CPK and MB CPK assayed in samples obtained serially ofr 24 hours were compared to microscopic changes in hearts from the same animals examined 48 hours after occlusion. Twelve of the 34 dogs died within two hours after coronary occlusion. Among the surviving 22 dogs, one failed to exhibit gross of electrocardiographic evidence of ischemia and was therefore excluded. Twelve had coronary occlusion maintained for 30 minutes or longer and in 11 of these peak plasma MB CPK activity exceeded thenormal range (mean +/- 2 SD) and baseline values by at least 100%. Necrosis was present in the hearts from each manifested by nuclear pyknosis, eosinophilia, shrinkage of cytoplasm, and leukocytic infiltration. In the remaining nine dogs with occlusion for less than 30 minutes, peak plasma MB CPK activity was not elevated and necrosis was not detected. The close concordance between plasma MB CPK elevations and myocardial necrosis was significant (chi2 = 14.5, P less than 0.001), and thus, increased plasma MB CPK activity reflected irreversible myocardial ischemic injury.
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PMID:The association of increased plasma MB CPK activity and irreversible ischemic myocardial injury in the dog. 93 19

The eosinophilia-myalgia syndrome associated with the ingestion of L-tryptophan was recognized in late 1989. We describe our pathologic study of skin, fascial, and muscle biopsies from 21 patients evaluated by light microscopy, histochemistry, and electron microscopy. A perivascular, lymphocytic infiltrate with eosinophils was present in the dermis, fascia, and skeletal muscle. Lymphocytic infiltration of arteries and arterioles was seen. Ultrastructurally, capillary and arteriolar endothelial cell thickening and necrosis was present. This microangiopathy suggests that ischemia may be a contributing factor to the findings in this syndrome.
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PMID:Microangiopathy in the eosinophilia-myalgia syndrome. 227

A 47-year-old male smoker with chronic eosinophilia developed progressive ischemia in his extremities. Pathologic examination of vessels in amputated limbs revealed changes of thromboangiitis obliterans. Focal segments of some arteries, however, revealed infiltration of thrombus and vessel wall by eosinophils. Furthermore, the patient developed a totally occluded right temporal artery, which on biopsy specimen showed marked infiltration by eosinophils within the vessel wall. In contrast to most patients with the hypereosinophilic syndrome, however, this patient had no evidence of endomyocardial thrombosis or fibrosis. In view of recent evidence that eosinophil granule proteins are toxic to endothelial cells, the findings in this patient suggest the possibility that eosinophils may be involved in the pathogenesis of thromboangiitis obliterans.
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PMID:Thromboangiitis obliterans associated with idiopathic hypereosinophilia. 402 3

A young Protugese man, who had never travelled outside of Europe, was found to have a bacterial complication of a fibroplastic endocarditis. The onset was by a spontaneous chest pain, associated with a posterolatero-apical subepicardial ischemia and giant T waves in V3, V4, and calcification in the apex of the heart on radiography. Diagnosis was confirmed by intracardiac explorations: ventricular telediastolic pressures were increased; the lower border of the right ventricle was smooth, the left ventricle had a globular appearance with a smooth anterior border, the apex appearing to be completely excluded; coronarography was normal. Histological examination confirmed the presence of fibrosis. Anticoagulant treatment was started. Four months after the onset of the disease, a high fever, an apical systolic murmur, and nine positive blood cultures for a streptococcus mitis, suggested the development of a bacterial endocarditis, though no direct evidence was discovered. Improvement occurred after appropriate antibiotic therapy, and the anticoagulants were continued. Cardiac ultrasonography recordings were normal following this episode. This case-report is of two-fold interest: on the one hand it represents an early form of fibroplastic endocarditis, diagnosed by intracardiac exploration, and on the other hand it emphasizes the rare nature of bacterial complications of this affection. Authors differ in their evaluation of the frequency of chest pain, but their inaugural and isolated nature are rarely described. In most cases the presence of the disease is revealed by a progressive cardiac insufficiency. A very positive factor is the presence of calcifications, and the absence of an eosinophilia does not exclude the diagnosis. Electrical anomalies of the ischemic type are possible, but are rarely isolated findings, and the giant appearance of the T waves in this case is rather atypical. Bacterial complications are rare, and are only reported in 12 of the 218 cases described in the published literature. They are rarely diagnosed during the life of the patient (1 case only). The infection affects the cords, the valves, the thrombus, or the fibrosis itself.
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PMID:[Bacterial endocardiitis complicating fibroplastic endocarditis: a case report (author's transl)]. 746 43

Atheromatous plaque material containing cholesterol crystals may dislodge and cause distal ischemia. To characterize atheroembolic renal failure, we retrospectively evaluated all patients at the Massachusetts General Hospital from 1981 to 1990 with both renal failure and histologically proven atheroembolism after angiography or cardiovascular surgery. Over the 10-year period, 52 patients were identified. They tended to be elderly men with a history of hypertension (81%), coronary artery disease (73%), peripheral vascular disease (69%), and current smoking (50%). Within 30 days of their procedure, only 50% of patients had cutaneous signs of atheroembolism, and 14% had documented blood eosinophilia. Urinalysis was often abnormal. Hemodynamically unstable patients died shortly after their procedure, yet renal function in the remainder continued to decline over 3 to 8 weeks. Patients who received dialysis had a higher baseline serum creatinine than those who did not (168 +/- 44 mumol/L versus 133 +/- 18 mumol/L, p = 0.02), with dialysis starting a median of 29 days after the procedure. Patients with renal failure due to atheroembolism alone, as opposed to multiple renal insults, were more likely to recover renal function (24% versus 3%, p = 0.03) and had a lower risk of death during the 6 months after their procedure (log-rank p = 0.002). Renal failure due to procedure-induced AE is characterized by a decline in renal function over 3 to 8 weeks. This time course is not consistent with most other iatrogenic causes of renal failure, such as radiocontrast or nephrotoxic medications, which present earlier and often resolve within 2 to 3 weeks after appropriate intervention.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atheroembolic renal failure after invasive procedures. Natural history based on 52 histologically proven cases. 750 Aug 98

There are several indications for an involvement of neuroexcitatory mechanisms in ischemic neuron damage. Since we forwarded the hypothesis in 1982 that the transmitter glutamate is playing a key role, several lines of evidence have substantiated this: there is a pronounced transmitter release induced by ischemia and there is uptake of Ca++ via NMDA-operated calcium channels. Under certain circumstances postischemic neuron death can be impaired by administration of either NMDA-antagonists or calcium blockers. Further proof for the induction of harmful excitatory mechanisms by ischemia has been obtained by preischemic denervation of the vulnerable nerve cells. After transient cerebral ischemia in rats or gerbils, there are signs of irreversible damage (eosinophilia) of neurons in the dentate hilus (somatostatin-positive cells) after 2-3 hours and of hippocampal pyramidal neurons after 2-3 days (delayed neuron death). In the first case, removal of the (main) input to hilus cells by degranulation (colchicine selectively eliminates granule cells) protects these. In the case of pyramidal neurons removal of Schaffer collaterals/commisurals or input from the entorhinal cortex have a protective effect. Recently, we have measured glutamate and calcium in CA1 of denervated rats during 10 min of ischemia, and it turns out that there is almost no extracellular glutamate release or lowering of calcium in contrast to ischemic animals with intact innervation. Also in the postischemic period there are indications of a continuation of the damaging processes induced by ischemia. Besides the well known postischemic hypoperfusion, a prolonged release of glutamate has been reported, as well as burst firing in some models.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ischemia as an excitotoxic lesion: protection against hippocampal nerve cell loss by denervation. 838 Jun 75

Traumatic spinal cord injury occurs in two phases: biomechanical injury, followed by ischemia and reperfusion injury. Biomechanical injury to the spinal cord, preceded or followed by various pharmaceutical manipulations or interventions, has been studied, but the ischemia/reperfusion aspect of spinal cord injury isolated from the biomechanical injury has not been previously evaluated. In the current study, ischemia to the lumbar spinal cord was induced in albino rabbits via infrarenal aortic occlusion, and two interventions were analyzed: the use of U74006F (Tirilazad mesylate), a 21-aminosteroid, and cerebrospinal fluid (CSF) drainage. These treatment modalities were tested alone or in combination. In Phase 1 of this study, the rabbits received 1.0 mg/kg of Tirilazad or an equal volume of vehicle (controls) prior to the actual occlusion, three doses of Tirilazad (1 mg/kg each) during the occlusion, then several doses after the occlusion. Of the Tirilazad-treated animals, 30% became paraplegic while 70% of the control animals became paraplegic. Phase 2 involved the same doses of Tirilazad as in Phase 1 and, in addition, CSF pressure monitoring and drainage were performed. The paraplegia rate was 79% in the control animals, 36% in the group receiving Tirilazad alone, 25% in the group with CSF drainage alone, and 20% in the Tirilazad plus CSF drainage group. This rate also correlated with changes noted in CSF pressure; both Tirilazad administration alone and CSF drainage alone induced a decrease in CSF pressure and the two combined produced a further decrease. There was marked improvement in the perfusion pressure when using Tirilazad alone, CSF drainage alone, and Tirilazad therapy in combination with CSF drainage, with the last group producing the largest increase. This change in CSF pressure and perfusion pressure correlated with improved functional neurological outcome. Pathological examination revealed that Tirilazad therapy reduced the extensive and diffuse neuronal, glial, and endothelial damage to (in its most severe form) a more patchy focal region of damage in the gray matter. Cerebrospinal fluid drainage resulted in pyknosis of some motor neurons, and some eosinophilia. The combination of CSF drainage and Tirilazad administration resulted in the least abnormality, with either normal or near-normal spinal cords. It is concluded that Tirilazad administration decreased CSF pressure during spinal cord ischemia and reperfusion and, like CSF drainage, increased and improved the perfusion pressure to the spinal cord, decreased spinal cord damage, and improved functional outcome.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Limiting ischemic spinal cord injury using a free radical scavenger 21-aminosteroid and/or cerebrospinal fluid drainage. 841 Feb 54

Focal brain ischemia induced in rats by occlusion of an intracranial artery is a widely used paradigm of human brain infarct. Details of the structural changes that develop in either the human or the rat brain at various times after occlusion of an intracranial artery are incompletely characterized. We studied, in 48 adult Wistar rats, structural alterations involving the cerebral hemisphere ipsilateral to an arterial occlusion, at intervals ranging from 30 min to 7 days. Microscopic changes developed over time in separate areas of the corresponding cerebral hemisphere in a predictable pattern, appearing as small lesions in the preoptic area (30 minutes), enlarging to involve the striatum, and finally involving the cerebral cortex. Two types of neuronal responses were noted according to the time elapsed; acute changes (up to 6 hours) included scalloping, shrinkage, and swelling, whereas delayed changes (eosinophilia and karyolysis) appeared later (> or = 12 hours). Three types of astrocytic responses were noted. 1) Cytoplasmic disintegration occurred in the preoptic area at a time and in a place where neurons appeared minimally injured. 2) Nuclear and cytoplasmic swelling were prominent responses in the caudoputamen and cerebral cortex at a time when neurons showed minimal alterations. 3) Increased astrocytic glial fibrillary acidic protein reactivity was noted at the interface between the lesion and the surrounding brain tissue after 4 to 6 hours. The gross pattern of the brain lesion and the maturation of neuronal changes typical of a brain infarct have a predictable progression. Focal brain ischemia of up to 6-hour duration does not induce coagulation necrosis.
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PMID:Progression from ischemic injury to infarct following middle cerebral artery occlusion in the rat. 843 52

Significant morbidity and mortality occur during the acute phase of the eosinophilia-myalgia syndrome (EMS), and many patients still have chronic manifestations of the disease. Although the precise etiologic agent or agents within implicated batches of L-tryptophan remain uncertain, histopathologic studies support a role for a cell mediated immune response underlying the pathophysiology of EMS. The cellular immune response seems to lead to a microangiopathy and release of cytokines that can induce eosinophilia and fibrosis. Such responses are most marked within the dermis, subcutis, fascia, and connective tissue in and around muscles, nerves, and other tissues. The pathophysiology of the chronic symptoms is poorly understood but may involve ischemia, neuropathy, and metabolic abnormalities.
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PMID:Pathophysiology of the eosinophilia-myalgia syndrome. 889 79

We examined the characteristics of neuronal death induced by ischemia in the spinal cord. Spinal cord ischemia was induced in Long-Evans rats by occlusion of the descending aorta with a 2F Fogarty catheter for 20 min (model 1) or more limited aortic occlusion (15 min) coupled with blood volume reduction (model 2); rats were sacrificed 6 h-7 days later. The animals developed variable paraparesis in model 1 and reliable paraplegia in model 2. The extent of histopathological spinal cord damage, being maximal in the lumbar cord, correlated well with the severity of paraparesis. Two distinct types of spinal cord neuronal death were observed, consistent with necrosis and apoptosis. Neuronal necrosis was seen in gray matter laminae 3-7, characterized by the rapid (6 h) onset of eosinophilia on hematoxylin/eosin-stained sections, and gradual (1-7 days) development of eosinophilic ghosting. Although TUNEL positivity was present, disintegration of membranes and cytoplasmic organelles was seen under electron microscopy. Neuronal apoptosis was seen after 1-2 days in dorsal horn laminae 1-3, characterized by both TUNEL positivity and electron microscopic appearance of nuclear chromatin aggregation and the formation of apoptotic bodies. DNA extracted from the ischemic lumbar cord showed internucleosomal fragmentation (laddering) on gel electrophoresis. These data suggest that distinct spinal cord neuronal populations may undergo necrosis and apoptosis following transient ischemic insults.
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PMID:Neuronal apoptosis and necrosis following spinal cord ischemia in the rat. 941 26


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