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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pharmacological inhibition of excitatory neurotransmission attenuates cell death in models of global and focal ischemia and hypoglycemia, and improves neurological outcome after experimental spinal cord injury. The present study examined the effects of the noncompetitive N-methyl-D-aspartate receptor blocker MK-801 on neurochemical sequelae following experimental fluid-percussion brain injury in the rat. Fifteen minutes after fluid-percussion brain injury (2.8 atmospheres), animals received either MK-801 (1 mg/kg, i.v.) or saline. MK-801 treatment significantly attenuated the development of focal brain edema at the site of injury 48 h after brain injury, significantly reduced the increase in tissue sodium, and prevented the localized decline in total tissue magnesium that was observed in injured tissue of saline-treated animals. Using phosphorus nuclear magnetic resonance spectroscopy, we also observed that MK-801 treatment improved brain metabolic status and promoted a significant recovery of intracellular free magnesium concentrations that fell precipitously after brain injury. These results suggest that excitatory amino acid neurotransmitters may be involved in the pathophysiological sequelae of traumatic brain injury and that noncompetitive N-methyl-D-aspartate receptor antagonists may effectively attenuate some of the potentially deleterious neurochemical sequelae of brain injury.
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PMID:Effect of noncompetitive blockade of N-methyl-D-aspartate receptors on the neurochemical sequelae of experimental brain injury. 216 32

The effect of nimodipine pretreatment on CBF and brain edema was studied in conscious rats subjected to 2.5 h of focal cortical ischemia. An infusion of nimodipine (2 micrograms/kg/min i.v.) or its vehicle, polyethylene glycol 400, was begun 2 h before the ischemic interval and was continued throughout the survival period. Under brief halothane anesthesia, the animals' right middle cerebral and common carotid arteries were permanently occluded, and 2.5 h later, they underwent a quantitative CBF study ([14C]iodoantipyrine autoradiography followed by Quantimet 970 image analysis). Nimodipine treatment improved blood flow to the middle cerebral artery territory without evidence of a "vascular steal" and reduced the volume of the ischemic core (cortex with CBF of less than 25 ml/100 g/min) and accompanying edema by approximately 50% when compared with controls (p = 0.006 and 0.0004, respectively). Mild hypotension induced by nimodipine did not aggravate the ischemic insult. The ischemic core volumes, however, were 50-75% smaller than the 24-h infarct volumes generated in a similar paradigm that demonstrated 20-30% infarct reduction with continuous nimodipine treatment. These results suggest that nimodipine pretreatment attenuates the severity of early focal cerebral ischemia, but that with persistent ischemia, cortex surrounding the ischemic core undergoes progressive infarction and the early benefit of nimodipine treatment is only partly preserved.
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PMID:Nimodipine pretreatment improves cerebral blood flow and reduces brain edema in conscious rats subjected to focal cerebral ischemia. 221 83

To clarify whether astrocyte-derived factors may protect cerebral tissue from ischemia, we examined brain edema, demyelination and astrocyte proliferation in brains with focal ischemia and treated with astrocyte-cultured medium. We occluded the left middle cerebral artery of rats and implanted the Osmotic Minipump, which continuously infused the glial-cultured medium or control medium into the left lateral ventricle. Animals were sacrificed at 3 days or 7 days after occlusion. Brains of both groups were compared by several markers, i.e. extravasation of Evans blue, demyelination by Woelcke's staining and glial proliferation by GFAP staining. We found the astrocyte-cultured medium reduced leakage of Evans blue-plasma protein complex from ischemic lesions and reduced the size of demyelinated lesions. However, the degree of astrocyte proliferation was similar in both groups. From these data, we speculate that humoral factors derived from cultured astrocytes lessened the brain edema by modifying the blood-brain barrier. These factors might also induce proliferation of the microglia, and may protect the neurons from secondary injury by oxygen-free radicals.
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PMID:Effect of astrocyte-derived factors on ischemic brain edema induced by rat MCA occlusion. 222 39

It is well known that epidural pulse pressure (PP) increases with rising intracranial pressure (ICP). However, PP at the same ICP is not always identical in various intracranial pathologies. Many authors have investigated PP at increased states of ICP, but few studies related to brain edema have been done. This study was carried out in order to clarify the changes of PP in brain edema following focal ischemia. ICP and PP were measured in two groups of anesthetized dogs; 1) increased volume of CSF by cisternal saline injection (control, n = 5), 2) brain edema caused by focal ischemia (edema, n = 11). Ischemia was induced by electro-coagulation of the right anterior cerebral artery and by clipping the right middle cerebral artery and right internal carotid artery transorbitaly. The brain was recirculated for 6 hours after 2 hours of ischemia. The ischemic areas were identified by Evans blue, triphenyl tetrazolium chloride (TTC) or histological examination. Water content of the brain was measured by the wet-dry weight method. The canine focal ischemic model showed consistent ischemic damage in the caudate nucleus and produced brain edema successfully. PP increased linearly with rising ICP to 35 mmHg, and PP in the edema group was significantly smaller than that in the control group at the same ICP value. The slopes of the regression equation of ICP and PP were significantly different between the edema and control group (edema: 0.061 +/- 0.030, control: 0.107 +/- 0.015, mean +/- SD, p less than 0.01). These results suggest that PP is easily affected by ischemic brain edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in epidural pulse pressure in brain edema following experimental focal ischemia]. 222 60

The correlation between protective effect of ginsenosides Rb + R0 and brain endogenously-derived prostacyclin synthesis, thromboxane A2 formation and lipid peroxidation were estimated in rats. Ginsenosides Rb + R0 100 mg/kg iv 30 min before 4-vessel occlusion elevated 6-keto-PGF1 alpha level, declined thromboxane B2 and brain edema formation, reduced the rise of lipid peroxides and suppressed the reduction in both creatine phosphokinase (CK) and superoxide dismutase (SOD) activities in brain tissue after 40-min ischemia followed by 1-h reperfusion. Furthermore, these improvements were partially abolished by pretreating with iv indomethacin. It is concluded that ginsenosides possess protective effect on cerebral ischemia-reperfusion injury of rats and ginsenosides Rb + R0 are the active principles. The underlying mechanism of protection is ascribed partially or mainly to the facilitated synthesis and release of prostacyclin, reduced formation of thromboxane A2 and inhibited generation of free radicals and subsequent lipid peroxidation.
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PMID:Anti-lipid peroxidation and protection of ginsenosides against cerebral ischemia-reperfusion injuries in rats. 227 84

Brain damage after transient cerebral ischemia may be related to changes in postischemic cerebral blood flow and brain edema. In this study, the relationship between postischemic cerebral blood flow and edema was evaluated in the gerbil. Bilateral carotid occlusion (for 1, 1.5, 5, 15, or 30 min) was carried out in 110 female gerbils (50-70 g) under anesthesia with 2% halothane in 30% O2 and 70% NO2. Cerebral blood flow was measured by a [14C]-iodoantipyrine method modified slightly for use in small animals, and brain edema was evaluated by a specific gravity method. The threshold duration of ischemia which gives rise to subsequent hypoperfusion or edema was also established. In another 52 female gerbils under the same anesthesia, we investigated the effect of ischemia of variable duration on postischemic blood pressure and blood gas. Throughout all experiments, rectal temperature was maintained at 37-38 degrees C with a heating pad. Student's t test was used to calculate statistical significance. Neither blood pressure nor blood gas did vary significantly at any time following recirculation. Each brain region showed the same pattern of blood flow change, one almost independent of duration of occlusion. Namely, after the release of occlusion, transient recovery of blood flow was observed. But the flow then fell to 30-40% of the normal value at 1 h, after which it returned up to normal at 6 h. The severity of postischemic hypoperfusion was also independent of occlusion time. Interestingly, we did not observe postischemic hyperemia in any experimental groups except mild hyperemia in hippocampus after 5 and 15 min ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in RCBF and edema after transient cerebral ischemia--ischemic threshold of postischemic hypoperfusion]. 228 74

Since hydrogen peroxide (H2O2) can react with ferrous iron (FE++) to form the more toxic hydroxyl radical (OH) in vitro, and since H2O2 is generated brain xanthine oxidase (XO) during ischemia/reperfusion (I/R), we hypothesized that gerbils depleted of iron by dietary restriction or treated with iron chelators would be less susceptible to I/R injury. We found that gerbils fed a low iron diet for 8 weeks had decreased brain and serum iron levels, less neurologic deficits, and decreased brain edema after temporary unilateral carotid ligation (ischemia) and then reperfusion than gerbils fed a control standard iron diet. In addition, brains from gerbils treated with iron-free deferoxamine (an iron chelator), but not iron-loaded deferoxamine, had decreased (P less than .05) brain edema following ischemia and reperfusion. The results indicate that iron may contribute to cerebral ischemia/reperfusion damage.
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PMID:Iron depletion or chelation reduces ischemia/reperfusion-induced edema in gerbil brains. 230 92

It has been postulated that oxygen-derived free radicals are produced in significant quantities upon reperfusion of ischemic brain and could cause brain edema and cell death. This study was undertaken in an attempt to examine the effect of recombinant human superoxide dismutase, a scavenger of superoxide radicals, on survival outcome and brain edema in gerbils undergoing 1-hour bilateral carotid occlusion and reperfusion. Superoxide dismutase was continuously infused over either 1 or 3 h of reperfusion. Neither low dose (100,000 U/kg bolus followed by 100,000 U/kg/h continuous infusion) nor high dose (100,000 U/kg bolus followed by 800,000 U/kg/h) recombinant human superoxide dismutase had an effect upon water and sodium content of whole brain at 1 h of reperfusion following 1 h of ischemia, but high-dose treatment effectively reduced brain water content at 3 h of reperfusion. All gerbils receiving high-dose treatment survived the 3 h of reperfusion, while 4 of the 7 gerbils in the control group died between 2 and 3 h of reperfusion (p less than 0.05). From this study, we conclude that prophylactic administration of superoxide dismutase can reduce the delayed vasogenic edema developing at 3 h of reperfusion and afford significant cerebroprotection in these models of transient global ischemia.
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PMID:Protective effects of superoxide dismutase on acute reperfusion injury of gerbil brain. 234 Oct 56

The relationship between cerebral blood flow (CBF) and the evolution of brain edema was investigated in an experimental model of perinatal hypoxic-ischemic brain damage. Seven-d postnatal rats were subjected to unilateral common carotid artery ligation followed by 3 h of hypoxia with 8% oxygen at 37 degrees C. This insult produces neuronal necrosis and/or infarction only in the cerebral hemisphere ipsilateral to the arterial occlusion in the majority of animals; hypoxia alone produces no damage. CBF, measured by the indicator diffusion technique using iodo[14C]-antipyrine, and tissue water content were determined concurrently in both cerebral hemispheres at specific intervals during recovery from cerebral hypoxia-ischemia. Water contents in the ipsilateral cerebral hemisphere were 89.1, 89.6, 89.7, 91.0, and 88.3% at 30 min, 4 h, 24 h, 3 d, and 6 d, respectively (p less than 0.001); whereas the percent tissue water in the contralateral hemisphere was unchanged from values in nonligated, hypoxic control rats (87.7%). CBF was similar in both cerebral hemispheres at 30 min, 4 h, and 24 h of recovery (50-65 mL/100 g/min) and not different from age-matched controls. At 3 and 6 d, CBF in the ipsilateral cerebral hemisphere was 30 and 26% of the contralateral hemisphere and 23 and 29% of the control animals, respectively (p less than 0.001). No inverse correlation existed between the changes in brain water content and CBF at any interval until 6 d of recovery. Thus, an early hypoperfusion does not follow perinatal cerebral hypoxia-ischemia, as occurs in adults.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral blood flow and edema in perinatal hypoxic-ischemic brain damage. 234 70

We examined the effect of dilazep dihydrochloride (dilazep) on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats (SHRs). Ataxia and loss of the righting reflex were noted in some SHR after 4 hr occlusion of the bilateral common carotid arteries; and 11 of 15 animals died within 72 hr after reperfusion. One hour after reperfusion, the cerebral water content increased significantly. The chemiluminescence value in the brain homogenate increased slightly during occlusion; and following reperfusion, there was a transient but marked further increase, indicating the acceleration of lipid peroxidation that resulted from free radical reactions. The i.v. infusion of dilazep (0.3-3 mg/kg/hr for 4 hr) during occlusion dose-dependently reduced the appearances of neurological symptoms and mortality during occlusion and after reperfusion. The increase in cerebral water content and chemiluminescence value were clearly prevented by dilazep (3 mg/kg/hr). It is concluded that dilazep possesses the ability to prevent the appearances of neurological symptoms and brain edema induced by ischemia and reperfusion. The suppression of lipid peroxidation may be involved in the mechanism of the preventive effect of dilazep on cerebral injury.
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PMID:[Effect of dilazep dihydrochloride on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats]. 235 33


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