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

During most intracranial procedures, the microscope is used to allow the surgeon to work on structures which are deeply located in the brain. Under these circumstances, brain retraction is required for adequate exposure. It was rapidly suspected and later confirmed that brain retraction causes secondary brain damage. This is due not only to direct effect of the retractor on the cortical surface, but also because a pressure is generated under the retractor, on the brain tissue, which compromises local cerebral blood flow and local cerebral perfusion pressure, thus causing cerebral ischaemia. The need for retraction is increased if the lesion is located deeply and/or if the brain is tensed; thus the risk to generate ischaemic conditions is enhanced. These secondary surgical lesions are promoted and worsened by associated systemic conditions such as hypotension, hypoxaemia, hypercapnia. As an attempt to respond to the problem generated by surgical retraction, the "chemical brain retractor" concept is proposed. By compulsively rendering the brain as relaxed and compliant as possible, the chemical brain retractor should allow the surgeon to operate on without the use of a surgical brain retractor and, if such a retractor is still needed, to reduce the pressure under it. These goals are achieved with an osmotic agent like mannitol to improve brain compliance, and intravenous anaesthetic agents, moderate hypocarbia and a normal or elevated blood pressure, to minimize cerebral blood volume. In conjunction with the chemical brain retractor, two other manoeuvres should be used to enhance cerebral compliance: CSF drainage and moderate head up position during the procedure.
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PMID:[Neuro-anesthetic contribution to the prevention of complications caused by mechanical cerebral retraction: concept of a chemical brain retractor]. 767 88

Fibrin and fibrinogen degradation products in the cerebrospinal fluid (CSF-FDP) were first studied in a group of 29 patients observed during the first and the second week after subarachnoid hemorrhage (SAH), then in a second group of 26 patients for a total of 55 patients. In the latter group only the first FDP value obtained as soon as possible after SAH was taken in consideration. In the whole series of 55 patients several noteworthy factors were found: 1) FDP determination should be performed as soon as possible after SAH; 2) CSF-FDP at or above 40, 80 micrograms/ml was found both in the patients with severe neurological deficits and in those with cerebral ischemia (statistically significant); 3) the significance of CSF-FDP in patients who rebled was also evaluated. In conclusion CSF-FDP could be considered useful in predicting cerebral ischemia.
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PMID:Monitoring of fibrin and fibrinogen degradation products (FDP) in the cerebrospinal fluid of patients with subarachnoid haemorrhage due to ruptured aneurysm. Report of 55 cases. 789 Nov 97

The time course of changes in extracellular glutamic acid levels and their Ca2+ dependency were studied in the rat striatum during focal cerebral ischaemia, using microdialysis. Ischaemia-induced changes were compared with those produced by high K(+)-evoked local depolarization. To optimize time resolution, glutamate was analysed continuously as the dialysate emerged from the microdialysis probe by either enzyme fluorimetry or biosensor. The Ca2+ dependency of glutamate changes was examined by perfusing the probe with Ca(2+)-free medium. With normal artificial CSF, ischaemia produced a biphasic increase in extracellular glutamate, which started from the onset of ischaemia. During the first phase lasting approximately 10 min, dialysate glutamate level increased from 5.8 +/- 0.9 microM.min-1 to 35.8 +/- 6.2 microM where it stabilized for approximately 3 min. During the second phase dialysate glutamate increased progressively to its maximum (82 +/- 8 microM), reached after 55 min of ischaemia, where it remained for as long as it was recorded (3 h). The overall changes in extracellular glutamate were similar when Ca2+ was omitted from the perfusion medium, except that the first phase was no longer detectable and, early in ischaemia, extracellular glutamate increased at a significantly slower rate than in the control group (2.2 +/- 1 microM.min-1; p < 0.05). On the basis of these data, we propose that most of the glutamate released in the extracellular space in severe ischaemia is of metabolic origin, probably originating from both neurons and glia, and caused by altered glutamate uptake mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Extracellular glutamate during focal cerebral ischaemia in rats: time course and calcium dependency. 791 20

The present study was designed to determine the effects of theophylline, an adenosine receptor antagonist, and cyclohexyladenosine (CHA), an adenosine receptor agonist, on ischemic brain injury following normo- and hyperglycemic ischemia and reperfusion in fasted male Wistar rats. Moderate hyperglycemia was achieved by administering 17% D-glucose (3 g/kg i.p.), whereas normoglycemic animals received an equal volume of saline. The animals were further divided into two groups: One group was pretreated with either theophylline (0.20 mumol/g i.p.) or an equal volume of saline; the second group received either intraventricular CHA (6.25 nmol) or mock CSF prior to the onset of ischemia. During ischemia, pericranial temperature was maintained at 36 degrees C and EEG was monitored. Cerebral ischemia was induced for 15 min, after which flow was restored and the animals were allowed to recover completely. There were no significant differences in physiologic parameters among the groups studied. Five days following the ischemic episode, the rats were perfused with formalin and the brains subserially sectioned (8 microns) in the coronal plane and stained with celestine blue/acid fuchsin. Histopathologic analysis was performed in a blinded fashion to determine percentage of dead neurons. Hyperglycemic animals had significantly greater ischemic injury in CA1, cortex, and caudate than the normoglycemic group (p < 0.01). Moreover, rats pretreated with theophylline had a significantly (p < 0.01) higher percentage of dead neurons in CA1, cortex, and caudate than corresponding controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of theophylline and cyclohexyladenosine on brain injury following normo- and hyperglycemic ischemia: a histopathologic study in the rat. 826 53

Alpha-phenyl-tert-butyl-nitrone (PBN) a spin adduct forming agent is believed to have a protective action in ischemia-reperfusion injury of brain by forming adducts of oxygen free radicals including .OH radical. Electron paramagnetic resonance (EPR) has been used to both detect and monitor the time course of oxygen free radical formation in the in vivo rat cerebral cortex. Cortical cups were placed over both cerebral hemispheres of methoxyflurane anesthetized rats prepared for four vessel occlusion-evoked cerebral ischemia. Prior to the onset of sample collection, both cups were perfused with artificial cerebrospinal fluid (aCSF) containing the spin trap agent alpha-(4-pyridyl-1-oxide)-N-tert butylnitrone (POBN 100 mM) for 20 min. In addition 50 mg/kg BW of POBN was administered intraperitoneally (IP) 20 min prior to ischemia in order to improve our ability to detect free radical adducts. Cup fluid was subsequently replaced every 15 min during ischemia and every 10 min during reperfusion with fresh POBN containing CSF and the collected cortical superfusates were analyzed for radical adducts by EPR spectroscopy. After a basal 10 min collection, cerebral ischemia was induced for 15 or 30 min (confirmed by EEG flattening) followed by a 90 min reperfusion. .OH radical adducts (characterized by six line EPR spectra) were detected during ischemia and 90 min reperfusion. No adduct was detected in the basal sample or after 90 min of reperfusion. Similar results were obtained when diethylenetriaminepenta-acetic acid (100 microM; DETAPAC) a chelating agent was included in the artificial CSF. Systemic administration of PBN (100 mg/kg BW) produced a significant attenuation of radical adduct during reperfusion. A combination of systemic and topical PBN (100 mM) was required to suppress .OH radical adduct formation during ischemia as well as reperfusion. PBN free radical adducts were detected in EPR spectra of the lipid extracts of PBN treated rat brains subjected to ischemia/reperfusion. Thus this study suggests that PBN's protective action in cerebral ischemia/reperfusion injury is related to its ability to prevent a cascade of free radical generation by forming spin adducts.
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PMID:alpha-Phenyl-tert-butyl-nitrone (PBN) attenuates hydroxyl radical production during ischemia-reperfusion injury of rat brain: an EPR study. 829 48

Cerebral ischaemia is considered to be the central mechanism leading to secondary brain damage in patients with severe head injury. It would therefore seem appropriate to monitor cerebral oxygenation in these patients. The possibilities of continuous monitoring of brain tissue and CSF oxygen tension as parameters for cerebral oxygenation were evaluated. In experimental studies the influence of changed oxygen offer and decreased cerebral perfusion pressure on CSF and brain tissue pO2 were investigated. Fast changes in CSF pO2 were observed in response to decreasing oxygen offer. Slower changes were noted in response to hypo- and hyperventilation. An autoregulatory mechanism regulating CSF pO2 is postulated. Reducing cerebral perfusion pressure decreased both brain tissue and CSF pO2, but in the reperfusion phase after complete ischaemia a dissociation occurred between brain tissue and CSF pO2, CSF pO2 being restored, but brain tissue pO2 remaining low or even decreasing further. From these studies it is concluded that both CSF pO2 and brain tissue pO2 reflect changes in cerebral oxygenation caused by changes in oxygen offer as well as by changes in cerebral blood flow. Brain tissue pO2 is also sensitive to oxygen demand from the tissue. Preliminary studies of continuous monitoring of brain tissue pO2 in patients with severe head injury are reported.
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PMID:Monitoring cerebral oxygenation: experimental studies and preliminary clinical results of continuous monitoring of cerebrospinal fluid and brain tissue oxygen tension. 831 Aug 63

To determine how vasopressin affects the vascular tone of the smaller cerebral arterioles, we carried out an in vitro study of isolated and cannulated intracerebral arterioles of rats. We found that increasing concentrations of vasopressin induced a triphasic response of vasodilation (10(-12)-10(-11) M), vasoconstriction (10(-10)-10(-8) M), and vasodilation stabilizing to control diameter (10(-7)-10(-6) M) and that the maximum constriction was twice the maximum dilation in these smaller arterioles [21.2 +/- 13.1% (mean +/- SD) decrease in diameter vs. 11.2 +/- 5.7% increased]. Pretreatment of the arterioles with NG-monomethyl-L-arginine (10(-4) M), a specific inhibitor of endothelium-derived relaxing factor, abolished the vasopressin-induced vasodilation and significantly increased the vasoconstriction. These results suggest that these arterioles were maintained in a dilated state by an endothelium-derived relaxing factor activated by vasopressin. Both vasodilation and vasoconstriction were found to be mediated through vasopressin V1 receptors in a study of arterioles pretreated with d(CH2)5Tyr(Me)arginine vasopressin (10(-6) M), a vasopressin V1 receptor antagonist. These results support the hypothesis that vasopressin may constrict smaller cerebral arterioles while simultaneously dilating larger cerebral arteries. Our results also suggest that vasopressin may aggravate cerebral ischemia in pathological conditions, such as subarachnoid hemorrhage, when the arteriolar response to vasopressin shifts from vasodilation to vasoconstriction due to increased vasopressin levels in plasma and CSF and impaired endothelium-derived relaxation.
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PMID:Triphasic response of rat intracerebral arterioles to increasing concentrations of vasopressin in vitro. 843 23

The neuroprotective effect of neurotrophic factors has been demonstrated in experimental cerebral ischaemia recently. These include nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), and basic fibroblast growth factor (basic FGF). The neuroprotective effect of ciliary neurotrophic factor (CNTF), however, has not been studied so far. We have examined the neuroprotective effect of recombinant rat CNTF in a rat forebrain ischaemia model. A continuous infusion of CNTF was started 1 week before the induction of ischaemia and continued until 1 week after the ischaemia. Reversible forebrain ischaemia was induced by 7 minutes of bilateral carotid occlusion with hypotension. Neuronal cell death in the hippocampal CA1 sector was evaluated 1 week after the ischaemia. For the control group artificial CSF (cerebrospinal fluid) was infused instead of CNTF. Per cent neuronal cell death was 83.4 +/- 5.9% (mean +/- SEM, n = 5) in the control group, and 71.1 +/- 10.0% (mean +/- SEM, n = 5) in the CNTF group. Although percentage of neuronal cell death was lower in the CNTF group, the difference was not statistically significant. This result suggests that the protective effect of CNTF in the rat forebrain ischaemia model may be limited compared with other neurotrophic factors. It is considered that the number of neurons protected by CNTF may be small.
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PMID:Effect of CNTF on ischaemic cell damage in rat hippocampus. 880 Mar 34

The excitotoxic hypothesis of neurodegeneration has stimulated much interest in the possibility of using compounds that will block excitotoxic processes to treat neurologic disorders. Riluzole is a neuroprotective drug that blocks glutamatergic neurotransmission in the CNS. Riluzole inhibits the release of glutamic acid from cultured neurons, from brain slices, and from corticostriatal neurons in vivo. It is thought these effects may be partly due to inactivation of voltage-dependent sodium channels on glutamatergic nerve terminals, as well as activation of a G-protein-dependent signal transduction process. Riluzole also blocks some of the postsynaptic effects of glutamic acid by noncompetitive blockade of N-methyl-D-aspartate (NMDA) receptors. In vivo, riluzole has neuroprotective, anticonvulsant, and sedative properties. In a rodent model of transient global cerebral ischemia, a complete suppression of the ischemia-evoked surge in glutamic acid release has been observed. In vitro, riluzole protects cultured neurons from anoxic damage, from the toxic effects of glutamic-acid-uptake inhibitors, and from the toxic factor in the CSF of patients with amyotrophic lateral sclerosis.
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PMID:The pharmacology and mechanism of action of riluzole. 895 95

The actions of Bosentan and PD155080, nonpeptide endothelin receptor antagonists, were examined in feline pial arterioles in situ following middle cerebral artery (MCA) occlusion to gain insight into the cerebrovascular influence of endogenous endothelins in focal cerebral ischaemia. Immediately following permanent MCA occlusion, all pial arterioles overlying the suprsylvian and ectosylvian gyri displayed marked dilatations, which were maintained in a population of vessel but differentiated into sustained constrictions in others. Perivascular subarachnoid microinjections of Bosentan (30 microM), PD155080 (30 microM), and artificial CSF (pH 7.2) were performed between 30 and 210 min following MCA occlusion. The perivascular microapplication of Bosentan (30 microM) and PD155080 (30 microM) around pial vessels overlying the suprasylvian and ectosylvian gyri, which are within the territory of the occluded MCA, elicited in increase in the calibre of postocclusion dilated and constricted pial arterioles. The perivascular microapplication of PD155080 (30 microM) around postocclusion constricted arterioles overlying the ectosylvian and suprasylvian gyri elicited an increase in the calibre of arterioles (69 +/- 49% from preinjection baseline; n = 8). The perivascular microapplication of Bosentan (30 microM) around postocclusion constricted arterioles overlying the ectosylvian and suprasylvian gyri also elicited an increase in the calibre of arterioles (68 +/- 60% from preinjection baseline; n = 13). In contrast, the microapplication of CSF (pH 7.2) elicited small reductions in pial arteriolar calibre of postocclusion constricted arterioles (-8 +/- 13% from preinjection baseline; n = 8). The perivascular microapplication of PD155080 (30 microM) around postocclusion dilated pial arterioles overlying the ectosylvian and suprasylvian gyri elicited an increase in the calibre of arterioles (11 +/- 10% from preinjection baseline; n = 38). The perivascular microapplication of Bosentan (30 microM) around postocclusion dilated arterioles elicited an increase in the calibre of arterioles (16 +/- 15% from preinjection baseline; n = 36). In contrast, the microapplication of CSF (pH 7.2) elicited small reductions in pial arteriolar calibre of postocclusion dilated arterioles (-9 +/- 6% from preinjection baseline; n = 44). Perivascular microapplication of Bosentan or PD155080 had minimal effect on the calibre of pial arterioles on the parasagittal gyrus (anterior cerebral artery territory), although these arterioles had also displayed sustained dilatation following MCA occlusion. These results indicate that contractile factors (whose effects can be reversed with endothelin receptor antagonists) constrict or impair dilatation of cortical resistance arterioles in an acute cerebral ischaemic episode.
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PMID:Endothelin-mediated vascular tone following focal cerebral ischaemia in the cat. 896 8


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