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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a pilot study, 26 patients with acute completed strokes (48 hours to 5 days after cerebral infarction) were randomly assigned to the prostacyclin (PGI2) or placebo groups. PGI2 sodium salt (Epoprostenol, Wellcome Research Laboratories and Upjohn Company) or its solvent (glycine buffer) were infused into the subclavian vein for six-hour periods in five courses separated by six-hour intervals. Prostacyclin was administered at a rate of 2.5-5.0 ng/kg/min. A significant alleviation of neurological deficits occurred 6 and 54 hours after the treatment in patients receiving prostacyclin. This improvement lost its statistical significance at the end of a two-week observation period. It is concluded that further modified controlled studies are required to evaluate the therapeutic usefulness of PGI2 in the treatment of patients with cerebral ischaemia.
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PMID:Double-blind controlled trial of the therapeutic effects of prostacyclin in patients with completed ischaemic stroke. 390 21

Adult normothermic monkeys were submitted to 1 h of total cerebral ischemia, followed by blood recirculation for 1.5-24 h. During ischemia EEG and evoked potentials were suppressed within 12 s and 3 min, respectively. Upon recirculation, high-voltage EEG bursts began to reappear after 82-125 min, followed by gradual return of continuous background activity and near normalization of EEG frequency pattern within 24 h. Somatically evoked potentials, in contrast, exhibited only partial recovery, and consciousness did not return during the observation period. At the end of the experiments, tissue contents of sodium, potassium, calcium, and magnesium were measured in the gray and white matter of parietal lobe by atomic absorption spectroscopy. Gray matter sodium content gradually increased by approximately 50% from 41.0 to 59.8 mumol/g wet wt during 24 h of recirculation. The other electrolytes including calcium did not change during the observation period. Postischemic recovery reported in this and the accompanying article is attributed to careful control of postischemic general physiological state and prevention or treatment of postischemic complicating side effects such as postischemic brain edema, hypotension, acidosis, pulmonary distress, and anuria. No specific drug treatment such as application of calcium antagonists or metabolic inhibitors was necessary to achieve this effect.
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PMID:Recovery of monkey brain after prolonged ischemia. I. Electrophysiology and brain electrolytes. 394 13

Correlations between T1 and T2 relaxation times and water and electrolyte content in the normal and ischemic rat and gerbil brains were studied by means of both nuclear magnetic resonance (NMR) spectroscopic and imaging methods. In the spectroscopic experiment on excised rat brains, T1 was linearly dependent on tissue water content and T2 was prolonged in edematous tissue to a greater extent than expected by an increase in water content, showing that T2 possesses a greater sensitivity for edema identification and localization. Changes in Na+ and K+ content of the tissue mattered little in the prolongation of relaxation times. Serial NMR imaging of gerbil brains insulted with permanent hemispheric ischemia offered early lesion detection in T1- and especially T2-weighted images (detection as soon as 30 min after insult). The progressive nature of lesions was also imaged. Calculated T1 and T2 relaxation times in regions of interest correlated excellently with tissue water content (r = 0.892 and 0.744 for T1 and T2, respectively). As a result, detection of cerebral ischemia utilizing NMR imaging was strongly dependent on a change in tissue water content. The different nature of T1 and T2 relaxation times was also observed.
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PMID:Characterization of experimental ischemic brain edema utilizing proton nuclear magnetic resonance imaging. 395 65

Simultaneous occlusion of both common carotid arteries in female Sprague-Dawley CFY rats produced characteristic symptoms of global cerebral ischemia, such as staggering, circling, convulsions, followed by coma and death. A close correlation existed among these symptoms and the elevation of water and Na+ content, appearing at the stage of staggering; Evans blue extravasation and diminution of K+ content, detected at circling; and the increase in Ca2+ content in the total brain tissue, manifesting itself at the phase of convulsions, indicating the development of cerebral edema due to ischemia. Dexamethasone given subcutaneously in a single 2.0 mg kg-1 dose 5 hours prior to the induction of global cerebral ischemia reduced considerably the morbidity and mortality, the alterations in water and electrolyte content, and albumin leakage in the brain tissue. Actinomycin D, in a dose of 0.5 mg kg-1 injected intravenously 1 hour before steroid treatment, abolished the beneficial effect. This finding suggests that de novo protein synthesis is involved in the cerebroprotective effect of dexamethasone.
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PMID:Actinomycin D suppresses the protective effect of dexamethasone in rats affected by global cerebral ischemia. 400 66

Sodium-23 magnetic resonance imaging can be used to detect and assess experimental cerebral ischemia in the rat. An imaging technique utilizing a surface coil is described to produce sodium magnetic resonance images of good quality and resolution within 10 min. A novel method of hemispheric occlusion showed edema in the right brain of the rat head within 3 hr after injury. The edema was especially pronounced by 12 hr with effects in the right brain, eye and surrounding muscle evident.
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PMID:In vivo sodium-23 magnetic resonance surface coil imaging: observing experimental cerebral ischemia in the rat. 408 12

Lead encephalopathy was induced in suckling rats by administering lead to the mother. The brains were studied by light and electron microscopy, and the results were compared with observations in the human disease as well as in cases of cerebral ischemia in children. In their severe forms, both human and experimental lead encephalopathies are characterized by exudative extracellular edema and perivascular PAS-positive globules. The latter consist of osmiophilic non-membrane-limited cytoplasmic inclusions located, in the rat exclusively and in the human predominantly, in perivascular astrocytes. Intervascular strands are also found in both forms of the disease. In the rat these consist of basement membrane surrounding endothelial cytoplasm. Chemically, experimental lead encephalopathy with morphologically demonstrable edema is associated with an increase in brain water, sodium and serum albumin. Relative to the serum concentration, the increase in water is disproportionately greater than the sodium or albumin. There were no demonstrable changes in chloride or potassium.
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PMID:Electron microscopic and chemical studies of the vascular changes and edema of lead encephalopathy. A comparative study of the human and experimental disease. 435 30

In this study of the rat hippocampal CA1 stratum radiatum 4 days after 20 min transient cerebral ischaemia, we demonstrated ultrastructural dendritic degeneration and loss, whereas most axons appeared undamaged. Autoradiographs 4 days after ischaemia showed unchanged Na+-dependent glutamate high affinity uptake. The role of glutamate and Ca2+ for this selective postsynaptic vulnerability is discussed.
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PMID:Selective dendrite damage in hippocampal CA1 stratum radiatum with unchanged axon ultrastructure and glutamate uptake after transient cerebral ischaemia in the rat. 614 37

To study the protective effect of phenytoin on postischemic brain damage, total cerebral ischemia was produced for 8-12 min (aortic occlusion balloon catheter method) in 36 adult mongrel dogs. The regional cerebral blood flow (rCBF), sodium:potassium ratio in the cerebral cortex, electroencephalogram (EEG), and plasma electrolytes in the superior sagittal sinus blood were examined before ischemia and during the acute stage up to 120 min after recirculation in the control and phenytoin-treated groups. Measurement of rCBF (microsphere method) indicated easing of postischemic hypoperfusion of the cerebral cortex. The time from total cerebral ischemia to EEG electrical silence was significantly prolonged, and recovery of the electrical activity after recirculation was hastened. The increase in plasma potassium concentration in the superior sagittal sinus tended to be suppressed immediately after recirculation, and the sodium:potassium ratio in the cerebral cortex was lowered. Phenytoin increased the rCBF in the cerebral cortex, hastened the recovery of electrical activity, and stabilized the water and electrolyte balance in the cerebral cortex, suggesting some protecting effect on total cerebral ischemia.
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PMID:Effects of phenytoin on regional cerebral blood flow, electroencephalogram, and electrolyte contents in cerebral blood and cerebral cortex following total cerebral ischemia in dogs. 661 66

We have examined the extracellular pH (pHe) during spreading depression and complete cerebral ischemia in rat parietal cortex utilizing double-barrelled H+ liquid ion exchanger microelectrodes. The baseline pHe of the parietal cortex was 7.33 at a mean arterial PCO2 of 38 mm Hg. Following spreading depression and cerebral ischemia, highly reproducible triphasic changes in pHe occurred, which were intimately related to the negative deflection in tissue potential (Ve). The changes in pHe for spreading depression (n = 23) were a small initial acidic shift, beginning before the rapid change in Ve, followed by a rapid transient alkaline shift of 0.16 pH units, the onset of which coincided with the negative deflection in Ve. A prolonged acidic shift of 0.42 pH units then occurred. The maximal decrease in pHe was to 6.97 and the mean duration of the triphasic pHe change was 7.8 min. The lactate concentration in brain cortex increased from baseline 1.2 mM to 7.0 mM (n = 6) during the maximal acidic change in spreading depression. In addition, lactate levels correlated well with resolution of the pHe changes during spreading depression. The triphasic pHe changes following complete cerebral ischemia were an initial acidic shift of 0.43 pH units which developed over 2 min, then an alkaline shift of 0.10 pH units coincident with the negative deflection in Ve, and a final acidic shift of 0.26 pH units. The terminal pHe was 6.75. Superfusion of the cortex with inhibitors of carbonic anhydrase (acetazolamide), Na+/H+ counter transport (amiloride), and Cl-/HCO-3 countertransport (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid) altered the triphasic pHe changes in a similar fashion for both spreading depression and cerebral ischemia, providing insights into the pHe regulatory mechanisms in mammalian brain.
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PMID:Extracellular pH changes during spreading depression and cerebral ischemia: mechanisms of brain pH regulation. 669 12

A simple-time-series approach for testing the efficacy of an ocular plethysmograph has been developed. This statistical methodology is used to demonstrate the clinical potential of the Buffington ocular plethysmograph for the noninvasive detection of cerebral ischemia. This is done by correlating intraocular pulse amplitude to systemic blood pressure changes during controlled hypotension induced by the intravenous administration of sodium pentobarbital (25 mg/kg) in five dogs.
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PMID:A simple-time-series approach for evaluating an ocular plethysmograph. 672 27


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