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

Serum and CSF calcium, magnesium, potassium and sodium were analyzed in 14 patients suffering from subarachnoid haemorrhage and in 10 healthy controls. The calcium and potassium concentrations in serum and CSF were decreased while magnesium unchanged and sodium were unchanged. A deranged electrolyte homeostasis was thus detectable in the CSF following subarachnoid haemorrhage. It could not be established whether symptoms of delayed cerebral ischemia were related to CSF calcium and/or potassium levels.
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PMID:Electrolyte concentrations in serum and CSF following subarachnoid haemorrhage. 235 81

The effect of the N-methyl-D-aspartate (NMDA) receptor antagonist dizociplipine maleate (MK-801) on cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRO2), intracranial pressure and systemic variables was examined in 6 normal dogs (Group I). In 6 additional dogs (Group II), the effects of a prior 11 min episode of complete cerebral ischemia on the response to dizocilipine was studied. CBF was measured with a sagittal sinus outflow technique and CMRO2 was calculated as the product of CBF and the arterial to sagittal sinus O2 content difference. Dizocilipine was administered as a 150 micrograms/kg i.v. bolus followed by a 75 micrograms.kg-1.h-1 infusion for 90 min. Plasma dizocilipine levels were greater than 25 ng/ml for the duration of the infusion. The CSF levels were approximately half the plasma levels. Five minutes after initiation of dizocilipine treatment, Group I dogs experienced a 63% increase in heart rate (P less than 0.01) and an 8% decrease in the mean arterial blood pressure (P less than 0.05). Over the same time interval. CBF increased by 85% (P less than 0.01) and intracranial pressure nearly doubled (P less than 0.05). In addition, dizocilipine treatment in all Group I animals resulted in EEG quasiperiodic bursts of delta-waves and polyspikes on a background of beta-activity. With the exception of the intracranial pressure, the above changes in systemic and cerebral variables persisted for the duration of the drug infusion. Intracranial pressure was no longer significantly elevated after 80 min of drug infusion. Hemispheric CMRO2 was unchanged by dizocilipine in Group I dogs. There was a decrease in the cortical glucose level at the end of the study, but no significant change in phosphocreatine, ATP, lactate, or energy charge when compared with 6 laboratory normals. An identical dose of dizocilipine administered after an 11 min episode of complete cerebral ischemia resulted in no significant changes in either cerebral or systemic variables. The absence of systemic effects in Group II dogs suggests that dizocilipine administration in normal dogs results in a centrally mediated activation of the peripheral sympathetic nervous system. The uncoupling of CBF and CMRO2 observed following dizocilipine treatment is similar to that reported for two other known NMDA antagonists, ketamine and phencyclidine. If administration of dizocilipine results in improved histopathological and neurological outcome following an episode of complete cerebral ischemia, this improvement is unrelated to changes in postischemic CBF or hemispheric CMRO2.
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PMID:The effect of the excitatory amino acid receptor antagonist dizocilipine maleate (MK-801) on hemispheric cerebral blood flow and metabolism in dogs: modification by prior complete cerebral ischemia. 255 56

In the ventricular cerebrospinal fluid (vCSF) of 10 hydrocephalic patients the mean (+/- S.D.) concentrations of glutamate and asparate were 2.9 +/- 0.2 and 0.2 +/- 0.2 microM, respectively. Significantly higher concentrations of these amino acids were found in two patients (glutamate 37.8 and 22.4 microM, aspartate 2.2 and 0.6 microM) with symptoms of impaired brain tissue perfusion, i.e. relative ischemia due to severely increased intraventricular CSF pressure. Our results are consistent with recent experiments in rats showing increased extracellular concentrations of glutamate and aspartate during transient cerebral ischemia.
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PMID:Elevated concentrations of glutamate and aspartate in human ventricular cerebrospinal fluid (vCSF) during episodes of increased CSF pressure and clinical signs of impaired brain circulation. 286 76

To investigate the role of endogenous opioid peptides in the pathophysiology of cerebral ischaemia, the CSF levels of immunoreactive beta-endorphin and leu-enkephalin in 16 patients with cerebral infarction were measured. Both the CSF beta-endorphin and leu-enkephalin levels in the acute stage of cerebral infarction were significantly higher than the values in the chronic stage. The CSF concentrations of the two peptides revealed a positive correlation in the acute but not the chronic stage. The increased endogenous opioid peptides in the CSF in the acute stage may modify the evolution of cerebral infarction.
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PMID:CSF beta-endorphin and leu-enkephalin levels in the acute and chronic stages of cerebral infarction. 295 70

Experimental focal cerebral ischemia was produced in monkeys (Macaca radiata) by occlusion of the right middle cerebral artery (MCA). The release of the lysosomal glycosidases, beta-D-hexosaminidase, alpha-L-fucosidase and alpha-D-mannosidase into the soluble fraction in the right basal ganglia of the experimental animals was measured at different periods from 30 min to 12 hr after occlusion and compared with the corresponding sham operated control animals. There was a significant increase in the released lysosomal enzymes in the MCA occluded animals at all periods and particularly at 4 hr after occlusion. The CSF from the experimental animals also showed elevated levels of hexosaminidase and fucosidase. The free fatty acids (FFA) measured in the basal ganglia at 30 min and 2 hr after occlusion showed a 100 fold increase in the experimental animals. The predominant fatty acid released was linoleic acid (18:2) followed by arachidonic acid (20:4). Lipid peroxidation in the basal ganglia measured by the thiobarbituric acid (TBA) reaction in the presence or absence of ascorbic acid also showed a significant increase in the experimental animals at all periods with a maximum at 30 min to 2 hr after occlusion. In order to assess whether lipid peroxidation causes damage to the lysosomes and release of the enzymes, a lysosome enriched P2 fraction from the normal monkey basal ganglia was prepared and the effect of peroxidation studied. Maximum peroxidation in the P2 fraction was observed in the presence of arachidonic acid, ascorbic acid and Fe2+.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Free fatty acids, lipid peroxidation, and lysosomal enzymes in experimental focal cerebral ischemia in primates: loss of lysosomal latency by lipid peroxidation. 296 24

A review of 15 cases of pancreas transplantation at the Presbyterian University Hospital in Pittsburgh showed that all of the neurologic complications occurred outside of the pancreas transplantation surgery itself. Major CNS complications included hypoxic encephalopathy (20 per cent), cerebral and spinal-cord infarction (7 per cent), and seizures (13 per cent). These appeared to be closely associated with cardiovascular collapse or cardiac arrest that often occurred following septic, hemorrhagic, or additional surgical-anesthetic stresses, removed in time from the transplantation. When patients who died of sudden cardiorespiratory arrest were included, the overall frequency of global cerebral ischemia was 33 per cent. The occurrence of herpes zoster neuritis (13 per cent) was contrasted with the lack of CNS infections. The possible associations of visual hallucinations with cyclosporine therapy (7 per cent), CSF pleocytosis with OKT3 therapy (7 per cent), and compressive neuropathy with operative-anesthetic monitoring (7 per cent) were discussed in relation to previous reports in the literature. Randomized controlled clinical studies were suggested to distinguish more clearly the complications due to pancreas transplantation from those due to the natural history of the underlying diabetes and to distinguish the beneficial and adverse effects of pancreas transplants from those of coexisting renal transplants.
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PMID:Neurologic complications of pancreas transplants. 304 46

The response of cerebrospinal fluid (CFS) pressure to increased arterial carbon dioxide tension (PCO2) was evaluated in 5 control animals and 7 animals with experimentally induced communicating hydrocephalus. The CSF pressure in control dogs increased moderately in response to PCO2; in dogs with hydrocephalus, an increase in PCO2 produced a pronounced increase in CSF pressure accompanied by a simultaneous decrease in cerebral perfusion pressure. Progression of hydrocephalus can be explained by increased intracranial pressure, periventricular edema and cerebral ischemia.
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PMID:Cerebrospinal fluid pressure alterations in experimental communicating hydrocephalus. Response of cerebrospinal fluid pressure to increase in arterial carbon dioxide tension. 308 49

Recently there has been a renewed interest in the neurosurgical treatment of large cerebral aneurysms and AV malformations utilising cardiopulmonary bypass (CPB) and total circulatory arrest (TCA). However, the differing tolerance limits of coagulation and bleeding, pH control and fluid constraint are difficult to reconcile. Although clinical assessment, electro encephalogram (EEG) and intracranial pressure-monitoring assist in identification of cerebral damage, CPB and TCA inflict their own penalties with resultant uncertainty in post-operative neurological evaluation, and producing difficulties in interpretation and management. Additionally, an unanswered question is, to what extent the known cardiac and cerebral effects of circulating histamine might influence the post-circulatory arrest recovery in these patients, and whether this would further compromise the neurological result. We report our experience of 9 such cases who underwent this procedure, and were able to achieve a satisfactory neurological result in 7 patients with differing lesions. During the operation both CSF (from the open cranium) and blood (from the right internal jugular vein) were sampled at intervals for subsequent plasma histamine estimation. Despite markedly elevated histamine levels during CPB and TCA, this was not associated with an unfavourable neurological outcome. These early findings have given us encouragement to the useful role of CPB and TCA in these complex neurosurgical presentations, and raise interesting questions about the clinical importance of histamine-evoked cerebral ischaemia that has been demonstrated in experimental models.
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PMID:The clinical significance of elevated CSF and plasma histamine in cerebral aneurysm surgery utilizing cardiopulmonary bypass with total circulatory arrest. 339 87

The calcium antagonist nimodipine blocks the effects of many vasoconstrictors of cerebrovascular smooth muscle and may reduce the incidence of delayed cerebral ischaemia following subarachnoid haemorrhage though not necessarily by inhibiting the development of angiographic cerebral vasospasm. Post-haemorrhagic CSF contains abnormally large quantities of various eicosanoids that partly reflect enhanced production by cerebral arteries. Does nimodipine affect this process? The extra-arterial and intra-arterial production of PG6 keto-F1 alpha, PGE2, PGF2 alpha and TXB2 were measured in perfused common carotid arteries taken from rabbits in which the arteries had been ensheathed by blood clot in vivo for 7 days. All rabbits were given the antifibrinolytic agent tranexamic acid to retard resolution of the clot, and half were given oral nimodipine (2 mg/kg/day) for 10 days. Nimodipine significantly reduced the extra-arterial production of TXB2 during the third and fourth hours of perfusion and, less consistently, the production of PGF2 alpha, PGE2 and PG6 keto-F1 alpha. Lutrol, the solvent for nimodipine, had no such effect.
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PMID:Oral nimodipine reduces prostaglandin and thromboxane production by arteries chronically exposed to a periarterial haematoma and the antifibrinolytic agent tranexamic acid. 347 5

Clinical and neuroradiological evaluation of 40 adult patients, suffering from migraine-type headache, produced evidence of a relationship between migraine, increased CSF pressure in the posterior fossa and cerebellar herniation. These findings have led to an alternative pathophysiological concept of migraine. A disturbance of CSF circulation is thought to be the underlying factor, which causes increased pressure in the basal cisterns and posterior fossa. This results in headache, acquired cerebellar herniation and, in severe cases, spasm of the vertebral arteries with subsequent cerebral ischemia. There seems to be no essential difference in pathophysiology between common and classic migraine.
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PMID:Migraine, a result of increased CSF pressure: a new pathophysiological concept (preliminary report). 373 95


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