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

Adult normothermic rhesus monkeys were submitted to one hour's complete cerebral ischemia, followed by periods of blood recirculation varying from 45 min to 24 h. The functional impact of ischemia and the subsequent recovery was monitored by electrophysiological recording and a distinction was made between animals with signs of functional recovery and animals without recovery. Prior to ischemia the water content of the gray matter was 81.1 plus or minus 0.3% (mean plus or minus S.D.) and of the white matter 68.9 plus or minus 0.8%. The sodium-potassium ratio in the gray matter was 0.43 plus or minus 0.02 and in the white matter 0.62 plus or minus 0.06. During one hour's ischemia brain water did not change significantly, but the differences in the sodium-potassium ratio in white and gray matter were reduced. Blood recirculation of the brain after ischemia caused a considerable increase in brain water content and a shift in the sodium-potassium ratio up to 1.0. Calculated brain swelling was maximal after 45 min when it reached 11.1% of the total brain volume in an animal with recovery and 12.2% in another one without recovery. In animals with signs of functional recovery brain swelling rapidly diminished, followed by a more gradual normalization of brain electrolytes within 24 h. In animals without functional recovery electrolyte shifts were irreversible or even progressed further. It is concluded that brain swelling and electrolyte derangements following one hour's cerebral ischemia are fully reversible when signs of functional recovery appear and brain metabolism returns.
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PMID:Resuscitation of the monkey brain after one hour's complete ischemia. II. Brain water and electrolytes. 16 36

The effects of severe cerebral ischemia on postischemic brain perfusion were examined in a series of pentobarbital-anesthetized cats. Ischemia of 15 or 30 minutes' duration was produced by occlusion of both common carotid arteries and the basilar artery and was coupled with mild systemic hypotension. A 90-minute period of normotensive postischemic recirculation was permitted in some animals. In 9 of 10 animals studied at the end of the ischemic insult and not allowed to recover, blood flow in the cerebral hemispheres was greatly reduced, with minimal flow (0.01 to 0.11 ml gm-1 min-1) persisting only in scattered perisulcal regions in 4 animals. Following 15 minutes of ischemia, blood flow was restored uniformly during recirculation, though at subnormal levels (31 to 35% of control). In contrast, 30 minutes of prior ischemia led to marked heterogeneities of local cerebral perfusion during recirculation, with multiple zones of persistent severe ischemia. Thus, while recirculation was suboptimal following both 15 and 30 minutes of ischemia, the 30-minute insult led to focal postischemic perfusion abnormalities that were sufficiently severe to make the possibility of functional recovery appear unlikely.
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PMID:Diffuse cerebral ischemia in the cat: I. Local blood flow during severe ischemia and recirculation. 67 14

In adult normothermic cats cerebral blood flow was interrupted for 1 hour by clamping the innominate and subclavian arteries. Following ischemia the brains were recirculated with blood, and the coagulation system was investigated by measuring coagulation times and blood content of fibrinogen and platelets. Ischemia induced progressive consumption coagulopathy with an increase in coagulation times and a decrease of platelets and fibrinogen by more than 40%. Coagulopathy was accompanied by a respiratory distress syndrome with a significant increase in the alveolar-arterial carbon dioxide gradient from --3.3 to --13.5 mm Hg. A correlation was found between plasma fibrinogen concentration, cerebral blood flow and electrophysiological function, indicating that a relationship exists between the severity of postischemic coagulopathy and functional recovery following prolonged cerebral ischemia.
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PMID:Coagulopathy following experimental cerebral ischemia. 84 91

Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 +/- 4.2 ml/100 gm/min to 26.3 +/- 4.4 (p less than .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.
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PMID:Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 1: Pathophysiology, electroencephalography, cerebral blood flow, blood-brain barrier, and neurological function. 115 66

Adult rhesus monkeys were subjected to complete cerebral ischemia for one hour and subsequent recirculation for up to 24 h. Animals with signs of functional recovery (e.g. spontaneous EEG activity) exhibited a partial replenishment of cellular energy sources (ATP, phosphocreatine) and a progressive normalization of cerebral lactate levels. Glucose and pyruvate concentrations showed a transient increase over control values during the early stages of postischemic recirculation. Monkeys without functional recovery lacked a significant resynthesis of energy-rich compounds; adenine nucleotides continued to decrease and lactate concentrations were higher than in animals subjected to ischemia without recirculation. Cerebral polysome profiles remained unaltered during the ischemic period but in all animals a marked disaggregation of polyribosomes with a concomitant increase in ribosomal subunits occurred after the onset of recirculation. In monkeys with indications of functional recovery these changes were reversible but a normal polysome profile was only observed after 24 h of recirculation. The results obtained indicate a postischemic depression of protein synthesis due to an inhibition of peptide chain initiation. After recirculation of the brain for 3-6 h there was evidence for an induction of enzymes involved in polyamine synthesis (ornithine decarboxylase and S-adenosylmethionine decarboxylase). No changes in the activity of these enzymes were observed at the end of the ischemic period, indicating that during complete cerebral ischemia not only the synthesis but also the catabolism of proteins is inhibited.
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PMID:Resuscitation of the monkey brain after one hour complete ischemia. III. Indications of metabolic recovery. 115 69

Twelve rabbits were submitted to 20-min global cerebral ischemia. Half of them were treated continuously with prostacyclin (PGI2) for 3 min before and during ischemia, and for 15 min after it. Untreated animals were not given PGI2 medication. The cases treated with PGI2 were found to have recovered bioelectric activity of the brain in half the time that its return took in the untreated cases. In the group that received PGI2, the ischemic ultrastructural changes in the cytoplasm of neuroglial cells were abolished, however, PGI2 did numerous vesicular structures, nuclear inclusions and chromatin clumping and margination. The vesicular structures were enclosed in a single smooth membrane without contact with the nuclear envelope. It is suggested that the vesicular structures may form as the result of disturbances in the water-electrolyte exchange between the cytoplasm and karyoplasm of neuroglial cells. The inclusions consisted of filaments and/or membranes. The amassing in the karyoplasm of vesicular structures and intranuclear inclusions with chromatin clumping and margination probably leads later to the death of the neuroglial cells after total cerebral ischemia. Hence, the described data indicate that the curative effects of PGI2 are directed only to early changes in the neuroglial cells cytoplasm and reflect a transient facilitation of functional recovery and/or metabolism rather then permanent brain protection after complete cerebral ischemia.
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PMID:The effects of prostacyclin on early ultrastructural changes in the cytoplasm and nuclei of neuroglial cells following complete cerebral ischemia. 179 Dec 98

The effects of NC-1100 on the central nervous system were analyzed behaviorally and electroencephalographically in mice, rabbits and mongolian gerbils, using ifenprodil as a control material. NC-1100 showed potentiating effects on spontaneous locomotor activities and excitatory motor activities induced by methamphetamine, but did not affect the rotarod test, traction test, sleeping time induced by pentobarbital, analgesic test, anticonvulsant test (MES and pentetrazol test), body temperature and group toxicity induced by methamphetamine. Following i.v. injection of NC-1100 to rabbits with chronically implanted electrodes, electroencephalographic properties in spontaneous EEGs such as fast waves with low voltages in the neocortex became distinguished slightly. Seizure discharges produced by stimulation of the dorsal hippocampus were slightly inhibited, but arousal responses produced by stimulation of the midbrain reticular formation or the posterior hypothalamic area were not inhibited. Furthermore, the effects of NC-1100 on functional recovery after transient cerebral ischemia in gerbils were not distinct. Based on these results, NC-1100 was considered to be an agent that improves cerebral metabolism and selectively increases cerebrovascular blood flow with few central nervous actions.
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PMID:[Effects of 1-(3,4-dimethoxyphenyl)-2-(4-diphenylmethylpiperazinyl)ethanol dihydrochloride (NC-1100) on the central nervous system]. 181 67

The aetiology of strokes was studied in a hospital based series of patients aged up to 40 years with precise clinical and radiological criteria. One hundred and forty five patients (75 males and 73 females) aged five to 40 years with cerebral ischaemia were evaluated. Aetiology was heterogeneous and could be classified into seven groups. Cerebral arteriograms were performed in all cases and indicated the aetiological diagnosis in most patients. Embolism was the most frequent recognised abnormality (38.4%). There were no complications of arteriography. Arterial dissections discovered by arteriography were the cause of the stroke in 10.1% of the patients. Atherosclerosis was diagnosed in 32 cases and was the commonest cause (21.6%). In one fifth of cases no cause was found. Contraceptive drugs were considered as potential cause of ischaemic stroke in 11.5%, cardiac diseases in 12.8% and haematological disorders in 8.1%. Other potential causes included migraine, inflammatory diseases, pregnancy and lacunas. Follow up in 126 cases showed that many patients had good functional recovery.
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PMID:Cerebral infarction in young people. A study of 148 patients with early cerebral angiography. 189 19

Increasing evidence is available indicating that systemically administered GM1 is able to provide for functional recovery in different experimental models of CNS injury, including cerebral ischemia. Current evidence indicates that the GM1 effects are associated, in the acute phase, with attenuation of secondary neuronal damage due to its capability to antagonize excitatory amino acid-related neurotoxicity in vivo as in vitro. Furthermore, the ganglioside is able to facilitate occurrence of long-term reparative processes, an effect most likely reflecting the potentiation of the action of neuronotrophic factors. This bifaceted action of GM1 makes the ganglioside ideally suited for clinical treatment of patients afflicted by cerebrovascular insufficiencies.
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PMID:Monosialoganglioside effects following cerebral ischemia: relationship with anti-neuronotoxic and pro-neuronotrophic effects. 213 Jun 63

To test the effect of flunarizine on cerebral ischaemia, 15 dogs were subjected to ischaemia, using the 'canine model of the completely ischaemic brain regulated with a perfusion method' in which the cerebral blood flow (CBF) can be fully regulated. Five animals served as untreated controls, 10 received flunarizine, a calcium antagonist (1 mg/kg in 5 dogs and 3 mg/kg in 5 dogs), before the ischaemic period. After 1 h CBF was restored and recovery of the electrical activity of the brain and the degree of brain swelling were observed for 3 h. At the end of the experiments, the degree of extravasation of Evans blue was examined. Remarkable recovery of EEG was found in the groups given flunarizine when compared with untreated controls. However, no significant difference was found between untreated controls and flunarizine treated groups for the degree of brain swelling and the degree of extravasation of Evans blue. These results suggest that the treatment of flunarizine is of benefit for functional recovery against cerebral ischaemia, but does not suppress ischaemic brain oedema.
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PMID:Cerebral protective effect of flunarizine in a canine model of cerebral ischaemia. 290 77


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