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

In 43 patients suffering from unilateral supratentorial ischaemia the changes over an interval of 3 years in clinical score, quantified EEG (using the neurometric method) and CBF (Xenon inhalation method) were studied. The patients were examined 3 times: shortly after the onset of ischaemia and respectively 3 and 36 months after this first measurement. Three patients died from causes not related to cerebral ischaemia. In the surviving patients the EEG and clinical score improved, often dramatically; the CBF values did not change significantly. Most of the changes occurred in the first 3 months after the stroke. For the evaluation of the prognostic value of the various parameters, 2 sub-groups of patients with different outcome but comparable initial clinical scores were studied. A persistent neurological deficit was predicted by a low CBF at the first measurement. The neurometric parameters obtained from the initial EEG had no value in this respect.
Electroencephalogr Clin Neurophysiol 1988 Sep
PMID:Recovery from cerebral ischaemia. EEG, cerebral blood flow and clinical symptomatology in the first three years after a stroke. 245 26

Colloidal volume expansion during acute cerebral ischaemia was assessed by local cerebral blood flow (CBF) and the power ratio index (PRI) in 8 anaesthetized Macaque monkeys. Focal cerebral ischaemia was produced by right middle cerebral artery occlusion. The animals were then volume expanded (to maximum cardiac output) with 6% hetastarch and then exsanguinated to baseline cardiac output. During volume expansion, local CBF in the ischaemic hemisphere increased from 25 +/- 12 to 39 +/- 23 cc/100 g/min (p less than 0.01) and during exsanguination decreased to 32 +/- 18 cc/100 g/min. Local CBF did not change significantly in the nonischaemic hemisphere. EEG power data, as assessed by PRI [(delta + theta power/alpha + beta power) x 100] changed significantly during blood volume manipulation. The mean PRI value in the right hemisphere deteriorated by increasing from 65 +/- 22 to 94 +/- 25 (p less than 0.01) following vessel occlusion but improved by decreasing to 81 +/- 23 (p less than 0.05) following volume expansion. Following exsanguination, the PRI value increased to 87 +/- 21. These data demonstrate the benefits of volume expansion during acute cerebral ischaemia. Changes in local CBF were consistently associated with changes in the PRI maps and values.
Neurol Res 1988 Sep
PMID:Colloidal volume expansion during acute cerebral ischaemia: assessed by local cerebral blood flow and computerized power ratio index. 246 44

We hypothesize that enhanced activity of capillary Na,K-ATPase promotes Na+ influx into the brain and causes early edema formation in focal cerebral ischemia. The pharmacologic suppression of brain capillary Na,K-ATPase as a means to ameliorate edema formation was examined using the middle cerebral artery occlusion model in 36 cats. With the help of a catheter inserted into the middle cerebral artery, the ischemic brain area was directly perfused with 10(-5) M ouabain. Perfusion was maintained as intermittent 15-second pulse injections given every 5 (n = 6) or 2 (n = 6) minutes. By this method, the naturally occurring circulatory conditions during ischemia were not altered. Four hours after ischemia, the cortical specific gravity at each of six locations over the ischemic area was compared with the corresponding ischemic blood flow measured by the H2 clearance technique. The results show that ouabain perfused every 2 minutes significantly ameliorated edema formation compared with six control cats perfused with Krebs-Ringer solution. In a separate series of experiments, the Na+ flux across the blood-brain barrier was studied by injecting 22NaCl together with an intravascular reference (cobalt-57-labeled microspheres 15 microns in diameter) into the ischemic area. The brain uptake index of 22Na was markedly increased in the ischemic cortex of six control cats; ouabain treatment in six cats suppressed the increase of Na+ influx. The results support our hypothesis that brain capillary Na,K-ATPase activity increases during early focal ischemia, leading to enhanced Na+ together with H2O flux across the blood-brain barrier.
Stroke 1989 Sep
PMID:Effect of enhanced capillary activity on the blood-brain barrier during focal cerebral ischemia in cats. 247 24

We induced brain edema in 72 rats by injecting 5 microliters of 3.0% wt:vol polyvinyl acetate into the left internal carotid artery, producing permanent embolization in the left cerebral hemisphere, which developed ipsilateral brain edema reproducibly. Edema was assessed 24 hours after embolization by determining the brain water content and the sodium and potassium concentrations. In this model, the free radical scavenger MCI-186 at 1.0 and 3.0 mg/kg i.v. prevented brain edema in a dose-dependent manner. At 3.0 mg/kg i.v., MCI-186 significantly reduced water content by 1.5% and improved the sodium-potassium balance to within the normal range in the embolized left hemisphere. Dexamethasone at 1.0 mg/kg i.v. did but at 3.0 mg/kg i.v. did not significantly inhibit the development of brain edema. Indomethacin at 4.0 mg/kg i.p. had no effect on brain edema. We suggest that the cyclooxygenase metabolites of arachidonic acid liberated from neuronal cell membrane phospholipids are not likely to be involved in the pathogenesis of permanent brain edema induced by polyvinyl acetate. Our results suggest that MCI-186 attenuates brain edema by suppressing the production of lipoxygenase metabolites, including free radicals or lipid peroxides, and that it may prove valuable for the treatment of brain edema associated with cerebral ischemia.
Stroke 1989 Sep
PMID:Effect of MCI-186 on brain edema in rats. 250 9

The lupus anticoagulant, an acquired immunoglobulin associated with an increased tendency for thrombosis, has been linked to the occurrence of cerebral ischemia presumably related to in situ thrombosis. Cardioembolic cerebral ischemic events have rarely been reported. We encountered 2 patients with focal cerebral ischemia, substantial mitral valvular masses, and a circulating lupus anticoagulant. In each, diagnostic evaluation supported a cardioembolic etiology. These findings illustrate the need for evaluating patients with cerebral ischemic events for a cardioembolic source when a circulating lupus anticoagulant is present.
Ann Neurol 1989 Sep
PMID:Cardiogenic brain embolism and lupus anticoagulant. 250 37

Xanthine oxidase activity in the rat brain was measured by means of high-performance liquid chromatography with electrochemical detection of uric acid. Cerebral ischemia was produced by a four-vessel occlusion method. In the control rat, the enzyme activity was 0.87 +/- 0.13 nmol/gm wet weight/min at 25 degrees C (mean +/- standard deviation), of which 92.4% was associated with the nicotinamide adenine dinucleotide (NAD)-dependent dehydrogenase form and only 7.6% with the oxygen-dependent superoxide-producing oxidase form. However, the ratio of the latter form increased to 43.7% after 30 minutes of global ischemia, despite the total xanthine oxidase activity remaining the same. Thus, it was revealed that uric acid can be synthesized in the rat brain and that cerebral ischemia induced the conversion of xanthine oxidase from an NAD-dependent dehydrogenase to an oxygen-dependent superoxide-producing oxidase. Although the xanthine oxidase pathway has been proposed as a source of oxygen-derived free radicals in various ischemic organs other than brain, the results of the present study suggest the involvement of the oxygen free radicals generated from this pathway in the pathogenesis of the ischemic injury of the rat brain.
J Neurosurg 1989 Sep
PMID:Changes in xanthine oxidase in ischemic rat brain. 254 24

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.
Brain Res 1989 Sep 25
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

Experimental studies in animal models suggest that the endorphin system may be implicated in the pathogenetic mechanism of cerebral ischemic lesions. Naloxone has been shown to possess a beneficial effect on the neurologic deficit associated with cerebral ischemia in animal experiments, probably because of its endorphin antagonist properties. By contrast, the results of clinical trials are contradictory. Moreover, the true significance of high plasma levels of beta-endorphin in patients with acute focal cerebral infarct (AFCI) has not yet been elucidated. We have evaluated 23 patients with established AFCI, in whom plasma levels of beta-endorphin and corticotropin (ACTH) were simultaneously measured during the first 48 hours after the onset of the disease. The results were compared with those from a control group. In a subgroup of 9 cases new measurements were made after 7 days. In the patients with AFCI, significantly lower levels of beta-endorphin and ACTH than in the control group were found. One week later, a moderate nonsignificant increase in the plasma level of beta-endorphin was found. The localization and estimated size of the infarct area were not relevant. Probably, the plasma levels of beta-endorphin will need to be considered before naloxone therapy is indicated, and only if it is confirmed that the plasma levels of beta-endorphin reflect changes at the cerebral level, as the pathophysiological role of these opioids in AFCI has not yet been established.
Med Clin (Barc) 1989 Sep 16
PMID:[Beta-endorphin in acute focal cerebral infarct]. 255 75

Pharmacologic blockade of excitatory amino acid receptors, especially the N-methyl-D-aspartate-preferring subclass of glutamate receptors, has been shown to reduce neuronal damage in models of global cerebral ischemia followed by reperfusion. The pharmacologic blockade at the NMDA receptor attenuates infarct size following permanent focal vascular occlusion in brain. Functional recovery is improved as well. These effects were seen with treatment begun 15 min following the stroke.
Neurosci Lett 1989 Sep 25
PMID:The specific NMDA receptor antagonist AP-7 attenuates focal ischemic brain injury. 255 20

To assess whether a rigorous clinical classification, based on computerised tomography, of patients with cerebral ischaemia would identify subgroups at higher or lower risk with respect to cigarette smoking habits, a case-control study was carried out on 422 cases of first-episode cerebral ischaemia matched for age and sex with 422 community-based neighbourhood controls. Patients with ischaemic stroke due to extracranial or intracranial vascular disease were at higher risk from smoking than has previously been reported for stroke (relative risk 5.7, 95% confidence interval 2.8, 12.0) whereas those with stroke due to cardiac emboli had no excess risk associated with smoking (relative risk 0.4 [0.1, 1.8]). After cessation of smoking, the relative risk declined gradually over 10 years, at the end of which time a significant risk was still evident. This finding may imply that the risk incurred by smoking is due mainly to atheroma formation, rather than transient haematological effects. Exposure to smoking by a spouse was an independent risk factor for the whole group of cerebral ischaemia patients (relative risk 1.7 [1.1, 2.6]), but this was not so for smoking by either parent (relative risk 1.2 [0.8, 1.8]). These findings suggest that smoking is a more potent risk factor for the most common form of ischaemic stroke than has previously been appreciated. The persistent nature of the risk even after cessation of smoking and the possible risk associated with passive exposure strengthens public health arguments against smoking.
Lancet 1989 Sep 16
PMID:Smoking as a risk factor for cerebral ischaemia. 257 46


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