Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty patients suffering from post-ischaemic encephalopathy were treated with high doses of barbiturates during the period immediately following resuscitation. The duration of cerebral ischaemia was assessed retrospectively. The degree of ischaemic damage was evaluated on the one hand by the pupillary signs seen 10 minutes after the reestablishment of the circulation and secondly by enzyme levels in the CSF. This barbiturate load was not associated with major complications and the excretion of barbiturate continued for several days. The clinical signs seen 12 hours after ischaemia and continuous observation of the tracing of the cerebral function monitor made it possible to give an early favourable prognosis from a neurological standpoint. In all the patients (apart from one) in whom there was total cerebral ischaemia for less than 10 minutes, neurological recovery was complete.
 ...
PMID:[Clinical use of thiopental in post-ischemic encephalopathy; preliminary report]. 3 55

Eosinophilic granulocytes in the CSF were observed in 94 of approximately 10,000 qualitative cytologic preparations. Those cases of eosinophilia which occurred in the context of a parasitic disease or a puncture-related hemorrhage were excluded. CSF eosinophilia exceeding 1% was found in 57.5% of the cases and 5% in 23.5%. Increased cell counts were observed in 67.7% of the cases; elevated CSF protein values, in 68% to 73%; blood eosinophils, in 10.4%. There was no reason to suspect a relationship between these findings and the number of eosinophils in the CSF.--Fifty-two percent of the cases involved inflammatory diseases of the nervous system; the 18 cases of abacterial inflammation of unknown etiology were particularly striking. In the remaining cases, eosinophils were found in conjunction with cerebral ischemia and hemorrhage, with tumors, and in a relatively high percentage of children (21%). The frequency of occurrence with drained or undrained hydrocephalus was striking. A review of the pathophysiological function of eosinophils indicated that revived or corpuscular antigens were present in all cases of CSF eosinophilia in which an eosinophilic reaction was induced. Nothing can be said at this time, however, concerning the classification of the antigens.
 ...
PMID:Eosinophilic granulocytes in cerebrospinal fluid: analysis of 94 cerebrospinal fluid specimens and review of the literature. 8 Dec 95

Total cerebral ischaemia in rats caused a marked increase in the cisternal CSF potassium concentration but little change in CSF sodium or chloride concentration. The anaesthetic techniques studied (pentobarbitone, halothane/oxygen and nitrous oxide/oxygen/relaxant) did not effect the potassium increase following cerebral ischaemia. We conclude that the mechanism of barbiturate protection following cerebral ischaemia is different from that of hypothermia.
 ...
PMID:Effect of anaesthetic agents on the ionic composition of cerebrospinal fluid following total cerebral ischaemia. 62 2

We investigated the ability of N6-cyclohexyladenosine (CHA), a potent and selective agonist of the adenosine A1 receptor, to attenuate elevations of levels of extracellular hippocampal glutamate and glycine that result from episodes of transient global cerebral ischemia (TGCI). A total of 30 New Zealand white rabbits were randomly assigned to receive 0 (n = 5), 0.1 (n = 8), 1.0 (n = 6), 10 (n = 6), or 100 (n = 5) microM CHA. The drug was dissolved in artificial CSF (vehicle) and administered via a microdialysis probe placed stereotactically into the dorsal hippocampus. A second microdialysis probe placed into the contralateral hippocampus of each animal was perfused with vehicle alone. Ten minutes of TGCI was induced by neck tourniquet inflation and deliberate hypotension from 0 to 10 min. Microdialysis samples were collected as follows: every 20 min preischemia (at -80, -60, -40, -20, and 0 min); every 5 min during ischemia and in the immediate reperfusion period (at 5, 10, 15, and 20 min); and every 20 min for the remainder of the reperfusion period (at 40, 60, and 80 min). Samples were then analyzed for their concentration of glutamate and glycine by HPLC. Following 10 min of ischemia, glutamate levels increased to a peak of 3.28 +/- 0.55 times baseline and returned to preischemic levels by 40 min, i.e., during reperfusion. Glycine concentrations increased to 5.41 +/- 0.91 times over baseline and remained elevated for the duration of the study.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The effect of cyclohexyladenosine on the periischemic increases of hippocampal glutamate and glycine in the rabbit. 135 2

Clinical studies have demonstrated the prognostic importance of increased intracranial pressure in central nervous system infections. To delineate development of intracranial pressure in meningitis experiments were carried out in rabbits. Meningitis was induced by injecting streptococcus pneumoniae bacteria into the cisterna magna and blood, and intracranial pressures were continuously recorded. In the experimental model, three stages were seen: incubation period (0-8 h)--in which CSF becomes positive for the infecting organism and biochemical changes occur, but there are no hemodynamic or intracranial pressure changes; stage of slowly increasing intracranial pressure - because blood pressure remains normal, cerebral perfusion pressure is maintained adequate for cerebral metabolic need (9-24 h); terminal stage (greater than 25 h)--with hemodynamic collapse, critical reduction of cerebral perfusion pressure, cerebral ischemia, and death of the experimental animals. It is suggested that a similar sequence occurs in human disease. The clinical implication stresses the need for early recognition and treatment of intracranial hypertension as an important adjunct to antibiotic treatment of the infecting organism.
 ...
PMID:Intracranial pressure and cerebral perfusion pressure in experimental streptococcus pneumoniae meningitis. 157 Apr 13

For understanding of the role of monoamines in cerebral ischemia, 3-methoxy-4-hydroxyphenylglycol (MHPG), hydroxyindoleacetic acid (5HIAA) homovanillic acid (HVA) the three major monoamine metabolites in CSF of 33 patients and 18 controls were measured with high-performance liquid chromatography. Results showed MHPG was more sensitive to cerebral ischemia than the two others. All three metabolites were elevated in patients with severe ischemia but only MHPG and 5-HIAA were significantly elevated. A positive correlation between any two of metabolites was found in controls and in patients in the first week after stroke but altered at the end of the second week. Computer assisted multivariate analysis indicated 5-HIAA might contribute more to the state of illness in the acute stage while HVA the least. Clinically, MHPG appeared to be the most significant element on reflecting the degree of the damage and the prognosis of the disease among the metabolites.
 ...
PMID:[The changes of monoamine metabolites in CSF of patients with cerebral stroke]. 171 95

Elevated intracranial pressure (ICP) is undoubtedly a determinant factor of outcome in severe head injured patient. Until now, medical treatment of elevated ICP in diffuse brain lesions consisted of hyperventilation, CSF drainage, mannitol and barbiturates without accurate selection criteria. In fact, in comatose patients, the cerebral blood flow (CBF) can vary independently of the cerebral metabolic rate of oxygen (CMRO2) which is typically reduced. The venous oxygen saturation (SjO2) measured in the jugular bulb and the arterial-jugular oxygen difference (ajDO2) can be used for more appropriately selecting therapeutic measures. According to the following equation: CMRO2 = CBF x ajDO2, the measurement of the changes in ajDO2 might serve as an indicator of CBF adequacy, out of the presence of cerebral ischemia. A decreased ajDO2 suggests that CBF is excessive for cerebral metabolic requirements and an elevated ajDO2 indicates a decreased CBF. Consequently, treatment of elevated ICP in the presence of a low ajDO2 should be more oriented towards moderate hyperventilation and administration of metabolic depressive agents with maintenance of normal arterial blood pressure. Conversely, in case of high ajDO2, ICP control should aim to increase CBF by maintaining normocapnia, improving hemodynamic status or reducing extravascular volume accordingly.
 ...
PMID:[Value of arteriovenous oxygen difference in the therapeutic approach of post-traumatic intracranial hypertension]. 184 41

Recent advances in high-resolution MR imaging and multinuclear spectroscopy have stimulated studies of the functional relationships between tissue hypoperfusion, cellular energy depletion, and brain edema associated with cerebral ischemia. The very slow (microns/sec) random translational motion of water protons in various brain tissues and intracranial fluid compartments can now be assessed with MR diffusion imaging. More slowly diffusing protons in ischemic tissues can be differentiated from normal parenchyma, CSF, and flowing blood, enabling the detection and localization of ischemic regions within minutes of the onset of stroke. Perfusion imaging "snapshots," obtained in as little as 25 msec with echoplanar MR methods, permit the evaluation of tissue washin/washout kinetics of contrast agents in the microvasculature, and thus the quantification of brain perfusion on a regional basis. Also, delineation of major intra- and extracranial arterial and venous structures with MR angiography, acquired with two- or three-dimensional Fourier transformation techniques, has enabled accurate noninvasive assessments of vascular occlusive disease. Finally, improvements in MR spectroscopic techniques have facilitated investigations of metabolic regulation and bioenergetics in experimental animal models of cerebral ischemia, as well as in stroke patients. Combined MR imaging and spectroscopy will likely play an important role in differentiating reversibly from irreversibly ischemic brain tissues and in the investigation of various neuroprotective pharmaceuticals.
 ...
PMID:Recent advances in MR imaging/spectroscopy of cerebral ischemia. 202 55

Following complete global cerebral ischemia and reperfusion, a brief period of reactive hyperemia is followed by a prolonged period of low flow commonly referred to as the delayed postischemic hypoperfusion state. It is generally assumed that this low-flow state may be injurious because of inadequate substrate delivery, thus implying that flow is no longer coupled to metabolic needs. This relationship of CBF to CMRO2 was examined in six anesthetized dogs that were subjected to 12 min of complete ischemia induced either by CSF compression or aortic occlusion. Following reperfusion and onset of the low-flow state, which stabilized at 45 min postischemia, control normothermic (37 degrees C) measurements of CBF and CMRO2 were determined. Thereafter, femoral arterial blood was circulated through a heat exchanger (42.5 degrees C), and brain temperature was increased to 40 degrees C and measurements were repeated. The brain was then cooled back to 37 degrees C for a final set of normothermic measurements. Thereafter, brain biopsies were taken to determine the energy state of the brain. CMRO2 changed approximately 6%/degrees C. CBF paralleled the change in CMRO2. Accordingly, the ratio of CBF to CMRO2 remained constant throughout at a value of 8 to 9, demonstrating maintained coupling. The brain energy state was normal at the end of the study. The authors conclude that postischemic CBF is modulated by the brain's metabolic needs.
 ...
PMID:Postischemic canine cerebral blood flow is coupled to cerebral metabolic rate. 205 Jul 48

Ischemic cerebral edema frequently develops after aneurysm surgery and may lead to severe intracranial hypertension. Of prime importance are reducing the level of ICP and preserving oligemic areas from becoming infarcted. Besides correction of factors known to worsen intracranial hypertension, several therapeutics may be of value: external CSF drainage, perfusion of mannitol, induced arterial hypertension and use of anesthetic agents with cerebral vasoconstricting capability. Hyperventilation is not recommended. Arterial hypotension and hypovolemia certainly contribute to aggravate cerebral ischemia and must be corrected. Cerebral ischemia may be reduced by two specific approaches: by improving cerebral oxygen transport in ischemic areas using arterial hypertension and calcium blockers rather than hemodilution or hypervolemia; by reducing cerebral metabolic rates with heavy anesthesia under the cover of a complete cardiovascular monitoring. In view of the large heterogenicity in cerebral lesions and physiopathological stages, a therapeutical trial appears suitable in each individual case. Criteria allowing to know if any therapeutic, used alone or in association, is beneficial include increase in blood flow in ischemic areas, reduction of ICP level and normalizing of indices like CSF or venous jugular blood lactate.
 ...
PMID:[Treatment of ischemic cerebral edema with intracranial hypertension after neurosurgery of intracranial aneurysms]. 212 75


1 2 3 4 5 6 7 8 9 Next >>