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

Intracranial pressure (ICP) changes and the development of cerebral edema during the first 24 hours after middle cerebral artery (MCA) occlusion in a rat were studied. ICP was measured via a catheter implanted into cisterna magna and the dynamics of cerebral edema was observed using serial T2 magnetic resonance (MR) measurements. Two T2 components were separated, fast (30-120 ms) and slow (120-240 ms). The first IPC increase was noted within first 2 hours after MCA occlusion and thereafter ICP started to rise 6 hours after stroke. These findings correlated with the development of edema, especially with the increase in extracellular water seen in T2 images. The highest ICP and the largest edema was noted in rats with largest infarcts. An experiment forms a basis for further studies on ICP and edema in a rat model of focal cerebral ischemia.
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PMID:The effects of brain edema on intracranial pressure in focal cerebral ischemia. An experimental study in a rat using magnetic resonance imaging. 262 22

We investigated the ability of postischemic insulin administration to modify the structural and neurobehavioral consequences of cerebral ischemia in rats. Forebrain ischemia was induced in fed rats by combining controlled systemic hypotension with bilateral carotid artery clamping for 10 1/2 minutes. Following clamp release, one group of six rats [corrected] was given insulin (2 IU/kg s.c. b.i.d.) for 1 week. An ischemic-control group of five rats [corrected] received no postischemic treatment. A sham-ischemia group of rats was used as a behavioral control. Throughout the recovery period until sacrifice, the drinking water of all rats was supplemented with 25% glucose. Rats were trained on two water maze place navigation tasks 1-2 months after ischemia. Escape latencies and swim patterns were recorded. Performance in the insulin-treated group was better than that in the ischemic-control group (p less than 0.05) on both tasks and did not differ significantly from that of the sham-ischemia group. Improvement in behavior correlated with a significant reduction in CA1 hippocampal necrosis in the insulin-treated group (p less than 0.05). Our findings demonstrate that postischemic treatment with insulin improves neurobehavioral performance in addition to lessening ischemic neuronal necrosis.
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PMID:Postischemic insulin reduces spatial learning deficit following transient forebrain ischemia in rats. 265 86

Hypothermia protects tissue function in ischemia. This study determined if selective brain cooling inhibits cerebral cortical lactate accumulation and thus accounts for imporved neurologic outcome after complete cerebral ischemia in dogs. The brain was selectively cooled (hippocampal temperature 33 degrees C) by nasal lavage with water at 5 degrees C. Control dogs received nasal lavage with water at 39 degrees C. Mean +/- SEM rectal temperature in both groups was 39 +/- 1 degree C prior to ischemia. Selective brain cooling before and during 10 minutes of cardiac arrest was associated with significantly improved neurologic function and 100% survival, whereas normothermic cardiac arrest produced marked neurologic dysfunction and 100% mortality. Cerebral cortical lactate accumulation was measured in a complementary series of dogs exposed to the same two treatments but with the addition of six cerebral cortical brain biopsies taken before, during, and immediately after cardiac arrest. Brain and rectal temperatures of dogs in the brain biopsy protocol were similar to those of dogs in the recovery protocol. There was no difference detected in cerebral lactate accumulation during ischemia between brain-cooled and control dogs. Thus, reduction in cortical brain lactate during ischemia cannot account for the postischemic functional protection afforded by preischemic selective brain cooling.
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PMID:Protection from cerebral ischemia by brain cooling without reduced lactate accumulation in dogs. 272 44

Effects of S-adenosyl-L-methionine (SAM) on the metabolism in ischemic brain were investigated. The ischemic model employed was an incomplete cerebral ischemia of the spontaneously hypertensive rat (SHR) produced by the occlusion of both common carotid arteries. One hundred mg/kg of SAM was administered (i.p.) 6 times from the beginning of occlusion at 30 min intervals. At 3 hr after the onset of occlusion, animals were killed by microwave irradiation and creatine phosphate (CrP), ATP, glucose, lactate and gamma-aminobutyric acid (GABA) contents in the brain were measured. SAM significantly mitigated both the reductions in CrP, ATP and glucose levels and the increase in GABA level due to the cerebral ischemia. In another set of experiments with the same experimental schedule, water content in the brain was examined. SAM significantly suppressed the increase in water content due to the cerebral ischemia. These results indicate ameliorating effects of SAM on the metabolism in ischemic brain.
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PMID:S-adenosyl-L-methionine ameliorates ischemic brain metabolism in spontaneously hypertensive rats. 273 57

The use of a water-suppressing spin-echo pulse sequence reported recently (V. Sklenar and A. Bax, J. Magn. Reson. 74, 469 (1987); M. von Kienlin, M. DeCorps, J. P. Albrand, M. F. Foray, and P. Blondet, J. Magn. Reson. 76, 169 (1987)) was evaluated for in vivo brain proton surface coil NMR spectroscopy. The studies were performed on cat brain using surface coils at 4.7 T. The sequence produced brain spectra with adequate water suppression, and a broader excitation profile than sequences which form spin echoes using 1331 pulses (P. J. Hore, J. Magn. Reson. 54, 539 (1983); H. P. Hetherington, M. J. Avison, and R. G. Shulman, Proc. Natl. Acad. Sci. USA 82, 3115 (1985)). The phase artifacts were smaller than those produced in 1331 methods, but theoretical analysis showed they should not be completely absent. The effectiveness of lengthening the spin-echo delay in the new sequence for suppression of unwanted lipid resonances was demonstrated. The sequence was shown to be capable of detecting lactate formation and clearance in a global cerebral ischemia experiment.
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PMID:Evaluation of a newly discovered water suppression pulse sequence for high-field in vivo 1H surface coil NMR spectroscopy. 274 18

A modified method of occluding the middle cerebral artery (MCA) by inserting a tiny copper wire into the lumen of the vessel to make a model for cerebral ischemia in the cat is described. Of 22 rats, 4 were controls and the remaining 18 were divided into two groups. Bipolar electrocoagulation was used in 9 cats and copper wire insertion was used in the other 9 to occlude the MCA through a transorbital approach. Two cats died after surgery and were excluded from this study. Of the 16 cats in two experimental groups, 13 of 14 showed hemiplegia and the other 2 were killed under anesthesia. Typical ischemic changes can be seen in the territory of the occluded MCA. Increased water content and decreased amplitude of somatosensory evoked potentials can be found in the ischemic hemisphere. Histochemical fluorescence study demonstrated that the sympathetic nerve fibers normally existing on the MCA can be completely destroyed by electrocoagulation but may remain intact with the copper wire method. This new method may have less influence on the vascular regulative function of the autonomic nervous system and be more similar to the pathological changes of cerebral infarction in man. We think our method can be useful for further research in cerebral ischemic disease and the regulative effects of the nervous system on brain vessels.
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PMID:Modification of a model for cerebral ischemia in the cat: a new method to occlude the middle cerebral artery. 275 79

To verify whether lipid peroxidation is associated with focal cerebral ischemia, a unilateral middle cerebral artery occlusion was carried out in rats. The concentrations of various endogenous antioxidants in the ischemic center were measured, including alpha-tocopherol and ubiquinones as lipid-soluble antioxidants and ascorbate as a water-soluble antioxidant. At 30 minutes after ischemia, alpha-tocopherol decreased to 79% of baseline, reduced ubiquinone-9 to 73%, ubiquinone-10 to 66%, and reduced ascorbate to 76%. Six hours after ischemia, alpha-tocopherol decreased to 63% and reached a plateau, whereas reduced ubiquinones and reduced ascorbate declined further to 16% and 10%, respectively, 12 hours after ischemia and then reached plateau levels. These results suggest functional and durational differences between antioxidants and lipid peroxidation in this ischemic model. Although the reciprocal increase in oxidized ubiquinones during ischemia was not observed, that of oxidized ascorbate was noted. The complementary antioxidant system between cytoplasmic and membranous components, the combination alpha-tocopherol/ascorbate, was estimated from the calculated consumption ratio of these antioxidants on the basis that the loss of these reduced antioxidants is due to neutralization of free radicals. This system is suggested to play an important role in the early ischemic period. Urate also increased during ischemia. The possible involvement of the xanthine-xanthine oxidase system in initiating free radical reactions in cerebral ischemia is also discussed.
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PMID:Lipid peroxidation in focal cerebral ischemia. 276 92

Sodium derived from the blood is known to accumulate in brain tissue during the early stages of incomplete ischemia. Our present studies were undertaken to determine the relation between blood-brain barrier sodium transport and the development of ischemic brain edema. Incomplete cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. Following recovery from the anesthetic, the gerbis were evaluated for the presence of neurologic symptoms and were divided into symptomatic (n = 77) and asymptomatic (n = 94) groups. Tissue water, sodium, and potassium contents, tissue plasma volume, and brain uptake of 22Na were measured in both groups 1.5, 3, 6, 12, and 24 hours after carotid ligation. There was a progressive accumulation of sodium and water in the ipsilateral cerebral cortex of the symptomatic group compared with either the corresponding contralateral cortex of the same gerbils or with the asymptomatic group. Net changes in brain sodium and potassium concentrations appeared to be the main determinants of fluid accumulation. Brain edema was not due to opening of the blood-brain barrier because the unidirectional transport of 22Na remained low and was even reduced by 35-55% in the ischemic cortex. Nevertheless, this sodium transport activity appeared to be rate-limiting in the development of brain edema during the first 3 hours of ischemia because the rate of sodium accumulation in the tissue was the same as the rate of 22Na transport from the blood to the brain. We conclude that blood-brain barrier sodium transport is an important factor in the formation of ischemic brain edema.
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PMID:Blood-brain barrier sodium transport limits development of brain edema during partial ischemia in gerbils. 277 85

To verify the lipid peroxidation in the focal cerebral ischemia, the levels of alpha-tocopherol, ubiquinone and ascorbate were measured in the ischemic center in rats. The former two were endogeneous lipid soluble antioxidants and the last was a water soluble antioxidant. alpha-Tocopherol, reduced ubiquinone-9 and -10, and reduced ascorbate decreased to 79%, 73%, 66%, and 76% 0.5 hour after ischemia, respectively. alpha-Tocopherol decreased to 63% 6 hours after ischemia, and then reached a plateau, while reduced ubiquinones and reduced ascorbate declined further to 16% and 10% 12 hours after ischemia, respectively, and then reached plateau levels. These results suggest their functional and durational differences as antioxidants against lipid peroxidation in this ischemic model. Although the reciprocal increase in oxidized ubiquinones during ischemia was not observed, that in oxidized ascorbate was noted. The complementary antioxidant system between cytoplasmic and membranous components, the combination alpha-tocopherol/ascorbate, was estimated from the calculated consumption ratio of these antioxidants, assuming that the loss of these reduced antioxidants is due to neutralization of free radicals. This system was suggested to play an important role in an early ischemic period. Urate also markedly increased during ischemia. Therefore, xanthine oxidase activity was measured in rats both in normal brain and in ischemic brain induced by four-vessel occlusion method. In the control rat, the enzyme activity was 0.87 +/- 0.13 nmol/g wet brain/min at 25 degrees C (mean +/- S.D.): 92.4% was associated with the 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 0.5 hour of global ischemia despite the same level in total xanthine oxidase activity. This result suggests the involvement of the oxygen free radicals generated from the xanthine oxidase pathway in the pathogenesis of the ischemic injury of the rat brain.
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PMID:[Lipid peroxidation and changes in xanthine oxidase in cerebral ischemia]. 280 15

Cerebral ischemia is known to be accompanied by brain edema. This increase in brain tissue water content probably influences the final outcome of an ischemic insult negatively. Despite extensive investigations on different aspects of brain edema, information on edema development during the early recirculation period following ischemia is sparse. We assessed changes in brain water content, as reflected by changes in tissue density, during the early recirculation period following severe forebrain ischemia. Fasted rats were subjected to 5, 15, or 30 minutes of ischemia and 5 to 180 minutes of recirculation. The specific gravity of specimens from the caudoputamen, frontoparietal cortex, hippocampus, and mesencephalon were measured with a Percoll linear density gradient. Five minutes of ischemia followed by recirculation did not produce any significant regional brain edema. However, following 15 minutes of ischemia, transient edema developed in the caudoputamen, frontoparietal cortex, and hippocampus. This edema was maximal after 30 minutes of reperfusion and was normalized after 180 minutes of reperfusion. Similar edema was seen following 30 minutes of ischemia. In the mesencephalon (where blood flow is approximately 50% of control during the ischemic insult) no brain edema was noted following 5, 15, or 30 minutes of ischemia. We discuss to what extent this transient regional brain edema may influence the selective neuronal vulnerability and cell damage observed in rats subjected to reversible forebrain ischemia and how these findings may correlate with neurochemical alterations observed during the early recirculation period.
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PMID:Time course of early brain edema following reversible forebrain ischemia in rats. 281 92


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