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

The gerbil model of unilateral cerebral ischemia has been used to test the temporal and spatial stability of the MRI T2 effects of oxygen-17 water. Following unilateral carotid ligation, symptomatic animals were given a single large intraperitoneal injection of H2(17)O and the distribution and stability of the brain T2 effects were followed with a spin-echo sequence. In contrast to the ischemic areas, the perfused tissue shows a marked and prolonged loss in intensity with little evidence of diffusion of the T2 effect of 17O into the ischemic tissue.
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PMID:The stability of proton T2 effects of oxygen-17 water in experimental cerebral ischemia. 179 91

We examined the effect of atrial natriuretic peptide on cerebral edema in 96 rats. Forty-four rats were given 30 (n = 11), 120 (n = 26), or 150 (n = 7) micrograms/kg of the peptide intravenously over 24 hours after occlusion of the left middle cerebral artery to induce cerebral ischemia. We then measured the brain water content, the brain sodium and potassium contents, the in vitro proton nuclear magnetic resonance longitudinal (T1) and transverse (T2) relaxation times, and the area of the edematous regions. Compared with saline treatment (n = 39), peptide treatment decreased the brain water content in a dose-dependent manner and decreased the brain sodium content significantly (p less than 0.05). Peptide treatment also suppressed the lengthening of both T1 and T2 in edematous tissue (p less than 0.05 and p less than 0.01, respectively) and reduced the area of the edematous regions observed by magnetic resonance imaging (p less than 0.01). Atrial natriuretic peptide appears to have a pharmacological effect on ischemic brain edema, possibly by suppressing the elevation of water content through regulation of electrolyte transport in the brain.
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PMID:Effects of atrial natriuretic peptide on ischemic brain edema in rats evaluated by proton magnetic resonance method. 182 2

Spontaneously hypertensive rats subjected to focal cerebral ischemia develop larger infarcts than normotensive rat strains. To determine whether antihypertensive therapy decreases infarct volume in hypertensive rats, 60 13-week-old animals were treated with 20 mg/kg hydralazine added daily to the drinking water for 1.5, 6, 10, or 16 weeks and then subjected to focal cerebral ischemia by tandem right common carotid artery and middle cerebral artery occlusion. Blood pressure in the treated groups was substantially lower than that in untreated groups after 1 week of hydralazine therapy and remained lower for the entire treatment period in all four experiments. Mean infarct volume in spontaneously hypertensive rats treated for 10 (p = 0.02) or 16 (p = 0.005) weeks, but not 1.5 or 6 weeks, was significantly less than that in the untreated controls. The percentage reduction of infarct volume in animals treated for 10 and 16 weeks was similar. This study demonstrates that antihypertensive therapy decreases infarct volume in hypertensive rats subjected to focal cerebral ischemia. This treatment effect appears to be dependent on the duration of therapy, and the magnitude of the treatment effect seems to plateau by 10 weeks of therapy.
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PMID:Effect of antihypertensive therapy on focal stroke in spontaneously hypertensive rats. 185 7

Hypovolemic patients are more likely to suffer delayed cerebral ischemia and infarction after a subarachnoid hemorrhage (SAH). Prompt recognition and correction of hypovolemia may improve the outcome. We have identified computed tomographic (CT) scan findings that increase the probability of a patient presenting with hypovolemia soon after an SAH. The plasma volume (PV) of 25 patients admitted within 96 hours of an SAH was measured using radioiodinated serum albumin. The normal PVs were measured in an outpatient setting 6 months later or predicted from their total body water. Nine patients (36%) were found to be hypovolemic, defined as a fall in PV exceeding 10% of the normal PV (mean fall, 18 +/- 2%). Sixteen patients were normovolemic or hypervolemic (mean PV, +9 +/- 2%). The basal cisterns were compressed or obliterated on the CT scans of all hypovolemic patients compared with 12.5% of normovolemic patients (chi-square, 14.52; P less than 0.01). The probabilities of a patient being hypovolemic if the CT scan indicated raised intracranial pressure were high: hydrocephalus, P = 0.80; compression of the basal cisterns, P = 0.82; and compression of the basal cisterns associated with intracerebral hematoma or midline shift, P = 1.00. Patients with an SAH and radiological evidence of raised intracranial pressure should be considered at particular risk for systemic hypovolemia.
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PMID:Association of hypovolemia after subarachnoid hemorrhage with computed tomographic scan evidence of raised intracranial pressure. 188 54

The effects of ONO-1016, as an inhibitor of C1-/HCO3-exchange, on the brain edema and circulatory failure following cerebral ischemia were examined in stroke-prone spontaneously hypertensive rats (SHR-SP). SHR-SP were divided into three groups: control (sham-operation), non-treated, ONO-1016 group, respectively. Cerebral ischemia was produced by bilateral carotid artery occlusion (BCAO) for 1 hr and then following reperfusion. The brain water content and local cerebral blood flow (LCBF) were determined by dry-wet method and 14C-iodoantipyrine method 2 hr after start of reperfusion. ONO-1016 was given intravenously at a dose of 100 micrograms/kg/min prior to ischemia. The brain water content increased in septum (SP), amygdala (AM) in both non-treated and ONO-1016 groups compared from those in control group. However, brain water contents in SP and midbrain were lower in ONO-1016 group than those in non-treated group. LCBFs decreased to 50-80% in SP, cerebral cortex (CT), striatum (ST), hippocampus (HC) and AM in non-treated group, while LCBFs decreased to 60-80% in SP, CT, ST, AM in ONO-1016 group when compared from those in control group. Decrease of LCBF in ST and HC in ONO-1016 group were less severe than those in non-treated group. From these results, ONO-1016 may prevent the brain edema formation associated with hypoperfusion during reperfusion period after ischemia in SHR-SP.
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PMID:[Effects of ONO-1016, inhibitor of C1-/HCO3- exchange, on the brain water content and local cerebral blood flow following cerebral ischemia in spontaneously hypertensive rats]. 191 Sep 44

It has been postulated that lipoxygenase metabolites of arachidonic acid play a role in the pathogenesis of cerebral ischaemia. Severe forebrain ischaemia in rats was induced by four-vessel occlusion with mild hypotension. After 30 min of ischaemia, circulation was restored by removing the arterial clamps and increasing blood pressure to preischaemic levels. During 30 min of cerebral ischaemia, free arachidonic acid increased by approximately 8.5 times compared with the preischaemic level. This accumulation was reversed within 60 min of reperfusion. The concentration of leukotriene C4 in brain tissue increased significantly during reperfusion: treatment with a 5-lipoxygenase inhibitor, AA-861, decreased the increase of brain water content associated with reperfusion. This study demonstrated that the increased arachidonic acid resulting from cerebral ischaemia in rats is metabolized to leukotrienes via the lipoxygenase pathway once circulation is restored, and these leukotrienes may play some role in the development of postischaemic cerebral oedema.
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PMID:Role of brain tissue leukotriene in brain oedema following cerebral ischaemia: effect of a 5-lipoxygenase inhibitor, AA-861. 197 46

Potential involvement of neuroexcitatory mechanisms was studied in: 1) repetitive forebrain ischaemia in gerbils, 2) global cerebral ischaemia in rats and 3) cryogenic injury to the cerebral cortex in rats and gerbils. Uptake of 45Ca was used as a marker of injury, whereas ultrastructural localization of calcium was assessed with an oxalate-pyroantimonate method. The blood-brain barrier was evaluated with immunostaining for serum albumin. Changes in extracellular glutamate were estimated by microdialysis and an enzymatic cycling assay. Changes in water content were assessed by specific gravity measurements. Repetitive ischaemia of 3 x 5 min carotid occlusions produced a cumulative effect with regard to development of oedema and neuronal injury. This was associated with several-fold increments in glutamate release after repeated insults, whereas there was no apparent correlation with energy metabolism disturbances. Other studies revealed in all models a development of secondary foci distant to the primary impact of ischaemia or cold lesions, which were characterized by calcium accumulation in swollen dendrites, chronic neuronal changes and intraneuronal uptake of serum proteins, all of these changes being potentially compatible with involvement of neuroexcitatory mechanisms.
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PMID:Role of neuroexcitation in development of blood-brain barrier and oedematous changes following cerebral ischaemia and traumatic brain injury. 198 78

Leukotrienes are powerful metabolites of arachidonic acid which are known to increase the permeability of peripheral blood vessels. These substances are found in brain tissue in association with cerebral ischemia, and in brain tumors. Therefore, it has been proposed that leukotrienes have a mediator function in brain edema. This hypothesis was subjected to further experimental analysis in this study, in which the authors investigated whether: 1) superfusion of the exposed brain surface with leukotrienes increases the permeability of extraparenchymal blood vessels in vivo; 2) intraparenchymal infusion of leukotrienes induces brain edema; and 3) pharmacological inhibition of leukotriene formation by BW755C, an inhibitor of leukotriene synthesis, reduces formation of brain edema from a standardized traumatic insult. The pial vessels of the parietal cortex of cats were examined by fluorescence microscopy during cerebral superfusion with the leukotrienes C4 (LTC4), D4 (LTD4), or E4 (LTE4) by using an open cranial window preparation. Intravenous Na(+)-fluorescein served as an in vivo blood-brain barrier (BBB) indicator. Superfusion of the pia with leukotrienes (up to 2 microM) did not open the barrier to fluorescein, but was associated with a significant constriction (up to 25%) of arterial and venous vessels. In experiments with slow infusion of leukotriene B4 (LTB4) or LTC4 into the white matter of feline brain, the tissue water content was subsequently determined in serial brain slices using the specific gravity method. Tissue water profiles obtained after a 15-microM infusion of either LTB4 or LTC4 were virtually identical with those of control animals infused with mock cerebrospinal fluid. Thus, neither LTB4 nor LTC4 led to an augmentation of infusion-induced brain edema. In a final series, a cold lesion of the left parietal cortex was induced in rabbits. Twenty-four hours later, swelling of the exposed hemisphere was quantified by gravimetrical comparison of its weight with that of the contralateral nontraumatized hemisphere. Eight animals received BW755C intravenously prior to and after trauma to inhibit formation of leukotrienes. Seven rabbits were infused with an equivalent volume of saline as a control study. The resulting hemispheric swelling was 7.7% +/- 0.6% (mean +/- standard error of the mean) 24 hours later in animals receiving BW755C and 7.8% +/- 1.2% in the control group, indicating that inhibition of leukotrienes was ineffective in preventing formation of vasogenic brain edema. The findings demonstrate that leukotrienes administered to the brain in concentrations occurring under pathological conditions do not open the BBB nor do they induce brain edema.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evidence against leukotrienes as mediators of brain edema. 173 Sep 68

The reperfusion of previously ischemic tissue may lead to the formation of highly reactive free radicals that promote tissue injury. Xanthine oxidase has been implicated as one source of these free radicals. We examined the role of xanthine oxidase in brain injury using a cerebrospinal fluid compression model of global cerebral ischemia with 15 minutes of ischemia and 4 hours of reperfusion. Seven dogs were pretreated with the xanthine oxidase inhibitor allopurinol (50 mg/kg for 5 days). Neurophysiological recovery was monitored with cortical somatosensory evoked potentials. As an attempt to correlate brain recovery with the mechanism of protection, free brain malondialdehyde was measured at the end of reperfusion by high-performance liquid chromatography. Brain water content was measured by wet-dry weights. Compared with seven untreated control dogs, allopurinol pretreatment significantly improved recovery of somatosensory evoked potentials after 4 hours of reperfusion. However, the amount of free malondialdehyde in the allopurinol-treated dogs was 32% greater than that in the controls. Brain water content was similar in the two groups. These results suggest that xanthine oxidase contributes to brain injury after ischemia and reperfusion. However, tissue damage caused by xanthine oxidase may be mediated through mechanisms other than free radical production.
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PMID:Allopurinol pretreatment improves evoked response recovery following global cerebral ischemia in dogs. 202 98

A new method of external selective brain cooling is described, showing its effectiveness in reducing neuronal damage following global cerebral ischemia in cat. The cooling apparatus consists of a specially fitted kind of water jacket in which the animal's head was laid. In a preliminary study it was verified that the device effectively reduces brain temperature without the risk of cardiac arrhythmias due to lowering of core temperature. In the main study cardiac arrest was induced in 23 adult cats, followed after 15 min by cardiopulmonary resuscitation (CPR). Eight cats could not be revived; of the 15 remaining animals, 7 were assigned to the control group (normothermia) and 8 to the treatment group (cerebral hypothermia). The latter received external brain cooling for 30 min, starting as soon as CPR was begun. Four hours after cardiac arrest all animals were transcardiacally perfused with glutardialdehyde. The brains were stored in fixative and subsequently processed for histopathological and morphometrical evaluation by light microscopy. Analysis of the resulting data showed that animals in the treatment group had a significantly higher percentage of undamaged neurons than animals in the control group, both in the cingulate gyrus (38% vs 10%) and in the parietal cortex (39% vs 14%). The treatment group also had more undamaged neurons in the hippocampus and fewer severely damaged neurons in all three regions, but these differences, though suggestive, were not statistically significant.
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PMID:Global cerebral ischemia and subsequent selective hypothermia. A neuropathological and morphometrical study on ischemic neuronal damage in cat. 202 47


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