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 non-invasive continuous inhalation technique of C15O2 and 15O2 coupled with positron emission tomography (PET) provides brain images that are thought to represent local cerebral blood flow (CBF) and oxygen extraction fraction (OEF). Experimental studies in baboons have confirmed that C15O2 inhalation allows tomographic measurement of CBF. The numerous difficulties involved in PET absolute quantitation are stressed, as well as some limitations inherent to the 15O inhalation model. However, the values for local CBF, OEF and CMRO2 obtained in normal young subjects are satisfactory in view of the above-mentioned limitations. The clinical application to recent cerebral infarction has allowed two opposite types of flow-metabolism uncoupling to be identified, which appear to be often predictive if tissue prognosis. The time course of spontaneous changes in CBF and OEF within the infarct is also described. Our studies have, in addition, revealed the previously unknown phenomenon of "crossed cerebellar diaschisis" in supratentorial infarction. Lastly, a state of chronic watershed ischemia, potentially reversible by surgical revascularization, has been identified as presumably involved in the progression of watershed necrosis. The clinical potentials of this method appear considerable.
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PMID:Noninvasive tomographic study of cerebral blood flow and oxygen metabolism in vivo. Potentials, limitations, and clinical applications in cerebral ischemic disorders. 697 68

Six cases of arterial insufficiency of the arm secondary to giant cell arteritis are described, all in elderly white women. The clinical presentation of the occlusive disease ranged from an asymptomatic incidental physical finding to an alarming picture of severe ischemia. All patients were treated with steroids and had subsequent stabilization or improvement of extremity symptoms. Vascular reconstruction was also performed in two patients, one of whom developed rest pain after graft occlusion. Another patient had a cerebral infarction while taking prednisone, despite control of large vessel vasculitis. This study indicates that giant cell arteritis should be considered in cases of occlusive disease of the arms, especially in elderly women. Giant cell arteritis is a seriously morbid and potentially fatal disease which justifies a thorough evaluation when sufficient evidence is present to suggest the diagnosis. The response to steroids is usually adequate to eliminate the need for early surgical intervention.
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PMID:Arm ischemia secondary to giant cell arteritis. 708 59

The object of this investigation was to study the effects of dimethyl sulfoxide (DMSO) upon the evolution of cerebral infarction. Twenty adult cats anesthetized lightly with ketamine hydrochloride underwent right middle cerebral artery occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. Regional cerebral blood flow (rCBF) changes in the right sylvian region were similar in the untreated and treated groups. The mean rCBF before occlusion was 46 +/- 10 ml/100 g/minute in the untreated group and 45 +/- 10 ml/100 g/minute in the treated group. Eight cats in both groups had rCBF measurements consistently below 18 ml/100 g/minute during the 6-hour period after occlusion. An index of erythrocyte flow was determined by measuring the transit of technetium-99 (99Tc)-labeled erythrocytes in the right sylvian region. The period of erythrocyte transit before occlusion was 10 +/- 1 seconds in the untreated group and 10 +/- 2 seconds in the treated group. After 6 hours of occlusion, the erythrocyte transit time was 18 +/- 3 seconds in the untreated group and 19 +/- 3 seconds in the treated group. Increasing delay in erythrocyte transit during the 6-hour occlusion period was seen in 5 untreated cats and 6 treated cats and was thought to represent a progressive increase in microvascular resistance. The complete washout of erythrocytes indicated the absence of microcirculatory obstruction. Electroencephalography (EEG) showed a reduced amplitude of activity in the right cerebral hemisphere after occlusion in cats with an rCBF consistently below 18 ml/100 g/minute. No significant EEG differences were found between the untreated and treated groups. Treatment with DMSO failed to modify the developing ischemia edema, neuronal alterations, or the changes in blood-brain barrier permeability to Evans blue dye and fluorescein. In this study DMSO was ineffective in preventing ischemic damage or acted when irreversible injury had already taken place.
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PMID:Treatment of acute focal cerebral ischemia with dimethyl sulfoxide. 727 70

Because of the demonstrated suitability of the guinea pig (Cuvis cobaya) for a large variety of laboratory investigations, we sought to develop a stroke model in this animal. Many ingenious stroke models in other animals exist; some depend on anomalous anatomy, others utilize methods of intracranial or extracranial vascular occlusion and yet others combine ischemia and anoxic damage (1-14). As one proposed application for this work was to study immune responses following experimental stroke, survival of several days after cerebral infarction was a requirement. Three to five days elapse before detection of a hymoral and cellular immune response is possible. The guinea pig is especially suited to immunological studies because of the enormous amount of accumulated data on the immunology of this animal. However, the guinea pig has proved relatively invulnerable to existing small animal techniques. Moreover the unacceptably short postoperative survival associated with the use of existing techniques necessitated the development of a new procedure. We have successfully pursued the development of an embolic stroke procedure applicable to this animal.
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PMID:Experimental embolic stroke in the guinea pig (Cuvis cobaya). 735 74

Cerebral infarct (stroke) causes striatal damage with subsequent deterioration of sensorimotor and cognitive functions that may be mediated by the dopamine receptor system. In the present study, transient, focal ischemia was induced in Sprague-Dawley rats by middle cerebral artery occlusion. Ischemic animals exhibited significantly less dopamine antagonist (haloperidol)-induced catalepsy and more dopamine agonist (amphetamine)-induced hyperactivity than sham-operated animals. Younger ischemic animals showed more profound behavioral alteration but also displayed greater recovery over time than older ischemic animals. Histologic data revealed a lateral striatal lesion in all ischemic animals. These results place the striatal dopaminergic system as a possible strategic venue for the treatment of cerebral ischemia. In addition, aging is found to be a risk factor for stroke as noted in humans.
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PMID:Striatal dopamine-mediated motor behavior is altered following occlusion of the middle cerebral artery. 750 69

This study investigated the correlation between in vivo serial T2-weighted magnetic resonance (MR) imaging and changes in superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, and water, sodium ion (Na+), and potassium ion (K+) contents measured in vitro using rat brain following right middle cerebral artery occlusion in conjunction with bilateral common carotid artery (CCA) occlusion. One hour later the left CCA was released. Serial MR images showed edema developed from the outer cortex towards the center. The T2 signal intensity of the injured right cortex increased with time compared to that of the contralateral cortex. Increased Na+ and water and decreased K+ contents occurred in the injured cortex, indicating that serial T2-weighted MR imaging reflects the changes in water content and Na+ and K+ concentrations determined by biochemical techniques. GSH-Px activity was little changed. Total SOD in the injured cortex decreased 1 hour after ischemia and remained low throughout the experiment. In contrast, SOD activity in the noninfarcted left cortex also decreased after 1 hour but returned to normal after 2 hours of ischemia. Our results suggest that oxygen free radicals are important in developing ischemic brain edema and cerebral infarction.
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PMID:Reduction of superoxide dismutase activity correlates with visualization of edema by T2-weighted MR imaging in focal ischemic rat brain. 751 45

Long-term evaluation of patients with aneurysms of the internal carotid artery (ICA) treated by intravascular balloon occlusion has not been reported. From 1977 to 1992, 58 patients (age 14 to 81 years) with ICA aneurysms were treated at our institution by this technique. The aneurysms included 40 intracavernous carotid, 5 petrous carotid, 3 cervical carotid, and 10 ophthalmic segment aneurysms. Presenting symptoms were caused by mass effect in 45 patients, transient ischemia or cerebral infarction as a result of emboli in 6, subarachnoid hemorrhage in 4, and epistaxis in 3. Preoperative temporary balloon occlusion of the ICA combined with cerebral blood flow monitoring and induced hypotension were used to determine tolerance for occlusion. Two patients not tolerating test occlusion required an extracranial-intracranial bypass procedure, and another patient underwent extracranial-intracranial bypass prior to test occlusion because of contralateral ICA stenosis. In 55 patients, aneurysms were excluded from the circulation by either occluding the proximal ICA or trapping the aneurysm neck. In three patients, the aneurysm was directly obliterated with intravascular balloons with preservation of the parent ICA. Three patients died during treatment, one from subarachnoid hemorrhage and two from cerebral infarction. Mean follow-up was 76 months (range, 6 months to 15 years). Six patients who developed transient ischemia caused by emboli responded to volume expansion and anticoagulation treatment. Two patients developed a delayed infarction, and one patient developed aneurysm enlargement that required surgical clipping and obliteration. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of aneurysms of the internal carotid artery by intravascular balloon occlusion: long-term follow-up of 58 patients. 770 64

This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study was interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. Patient outcome and the occurrence of hypodense lesions consistent with cerebral infarction on follow-up computerized tomography (CT) were studied prospectively up to 1 year after hemorrhage. Of 291 patients, 31 (11%) died because of the initial hemorrhage and 18 (6%) died due to rebleeding within 4 days after hemorrhage. Of the remaining 242 patients, 90 (37%) had delayed cerebral ischemia, which caused a permanent neurological deficit or death in 54 patients (22%). Of 195 patients undergoing follow-up CT, 85 (44%) had cerebral infarction that was not seen on the CT scan obtained on admission. Those who had salicylates in the urine on admission had a relative risk of 0.40 (95% confidence interval (CI), 0.15 to 1.10) of delayed ischemia with fixed deficit and a risk of 0.40 (95% CI, 0.18 to 0.93) of cerebral infarction compared with patients who did not have salicylates in their urine. This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.
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PMID:Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. 776 Jan 96

To develop an easy, reproducible experimental model of cerebral infarction (CI) without craniotomy in New Zealand white rabbits, a silicone rubber cylinder embedded in a nylon suture was delivered to the middle cerebral arteries through the internal carotid artery in anesthetized animals. Rabbits were sacrificed 0.5-5 h after embolization. CI size and location were ascertained by the triphenyl-2H-tetrazolium chloride (TTC) staining method; cerebral blood flow (CBF) was measured prior to and after embolization. PCO2, temperature and blood pressure were monitored and kept constant. CI occurred in all rabbits after 4 h of ischemia, in 50% after 3 h and only in 33% after 2.5 h. CI did not occur within less than 2.5 h of ischemia. No correlation was found between size and location of CI and occlusion time. CBF was maximally reduced in the right MCA territory but was also reduced in both anterior cerebral arteries and left MCA territories. This model is technically easy and the retrievable embolus allows the study of reperfusion by pulling on the nylon suture. It is suitable for studying chemical and molecular changes of the ischemic cells and/or for studying neuroimage changes after ischemic stroke.
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PMID:A new model of experimental cerebral infarction in New Zealand white rabbits. 778 65

Although a number of studies have demonstrated the neuroprotective effects of antagonists of postsynaptic N-methyl-D-aspartate (NMDA) and non-NMDA receptors in cerebral ischemia, little is known about the treatment of cerebral infarction through presynaptic blocking of extracellular glutamate release. We evaluated the effects of a presynaptic selective N-type calcium channel antagonist (SNX-111, given intravenously by continuous infusion at 5 mg/kg/h from 20 min prior to occlusion until 2 h postocclusion) on blood flow, extracellular glutamate, and infarct volume in rats with permanent occlusions of the right middle cerebral and right common carotid arteries plus 1-h transient occlusion of the left common carotid artery. There was no significant difference in CBF in the occluded cortex during the experiment between the treated and vehicle groups. SNX-111 significantly reduced total amount of extracellular glutamate during the experiment and the peak value of the glutamate after occlusion from 44.2 +/- 15.8 microM (mean +/- SD) to 21.4 +/- 11.4 microM (p < 0.01). Infusion of SNX-111 also significantly reduced the cortical volume of infarction from 47.2 +/- 5.8 to 19.9 +/- 7.3% (p < 0.0001). These results suggest that SNX-111 has a protective effect against focal ischemia through the inhibition of glutamate release from presynaptic sites, although SNX-111 may also affect the release of other neurotransmitters.
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PMID:A selective N-type calcium channel antagonist reduces extracellular glutamate release and infarct volume in focal cerebral ischemia. 779 Apr 9


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