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

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

Changes in the concentrations of carnitine, long-chain acylcoenzyme A, and long-chain acylcarnitine in ischemic myocardium parallel those in ischemic brain. Since carnitine treatment reverses these changes and improves function in ischemic hearts, we examined whether carnitine given to rats before focal cerebral ischemia (produced by tandem right common carotid artery and middle cerebral artery occlusion) alters infarct volume in four separate experiments. Mannitol was used to control for the osmotic effect of carnitine on brain edema in one experiment. While carnitine was found to significantly decrease infarct volume compared with saline in one experiment (p less than 0.05, Student's t test), this result could not be replicated in the subsequent three experiments. Because the positive treatment effect was not reproducible despite similar experimental conditions, the result of the first experiment was attributed to a type I error. Mannitol also showed no significant effect on infarct volume. This study emphasizes the need for concurrent controls with each group of treated animals and the need for replicating the results of a single experiment when testing for drug efficacy in animal models of focal cerebral ischemia.
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PMID:Carnitine treatment for stroke in rats. 233 61

The effects of a platelet-activating factor (PAF) antagonist on brain edema, cortical microcirculation, blood-brain barrier (BBB) disruption, and neuronal death following focal brain injury are reported. A neodymium:yttrium-aluminum-garnet (Nd:YAG) laser was used to induce highly reproducible focal cortical lesions in anesthetized rats. Secondary brain damage in this model was characterized by progressive cortical hypoperfusion, edema, and BBB disruption in the vicinity of the hemispheroid lesion occurring acutely after injury. The histopathological evolution was followed for up to 4 days. Neuronal damage in the cortex and the hippocampus (CA-1) was assessed quantitatively, revealing secondary and progressive loss of neuronal tissue within the first 24 hours following injury. Pretreatment with the PAF antagonist BN 50739 ameliorated the severe hypoperfusion in 12 rats (increasing local cerebral blood flow from a mean +/- standard error of the mean of 40.5% +/- 8.3% to 80.2% +/- 7.8%, p less than 0.01) and reduced edema by 70% in 10 rats (p less than 0.05) acutely after injury. The PAF antagonist also reduced the progression of neuronal damage in the cortex and the CA-1 hippocampal neurons (decrease of neuronal death from 88.0% +/- 3.9% to 49.8% +/- 4.2% at 24 hours in the cortex and from 40.2 +/- 5.0% to 13.2% +/- 2.1% in the hippocampus in 30 rats; p less than 0.05). This study provides evidence to support progressive brain damage following focal brain injury, associated with secondary loss of neuronal cells. In this latter process, PAF antagonists may provide significant therapeutic protection in arresting secondary brain damage following cerebral ischemia and neurological trauma.
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PMID:Platelet-activating factor and progressive brain damage following focal brain injury. 236 79

The effects of hyperbaric oxygenation on acute focal cerebral ischemia in rats were investigated. All rats suffered 4-hour middle cerebral artery occlusion. Nontreated controls had a 27.9% +/- 5.5% infarct volume, and a left/right hemispheric volume ratio of 109% +/- 3%. Animals treated between 2.5 and 3.5 hours following occlusion had an 18.1% +/- 9.7% infarct volume (p less than 0.01), and a 105% +/- 3% left/right hemispheric volume ratio (p less than 0.001). In conclusion, at least until 4 hours following an ischemic insult, hyperbaric oxygenation reduces ischemic neuronal injury and brain edema following middle cerebral artery occlusion in rats treated between 2.5 and 3.5 hours following occlusion.
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PMID:Therapeutic effects of hyperbaric oxygenation on acute focal cerebral ischemia in rats. 236 29

The effect of reversible cerebral ischemia on brain edema development was studied with a gravimetric method. CBF changes after ischemia were correlated with alterations in brain SG. Forebrain ischemia (15 min) was induced in rats by reversible bilateral ligation of both carotid arteries plus induction of controlled hypotension to 50 mm Hg. The SG of different brain structures was determined in a Percoll column up to 24 hr after ischemia. In addition, rCBF was measured by [14C]iodoantipyrine autoradiography. Cerebral ischemia resulted in reduction of CBF to less than 1% of normal in cortical structures and the caudatoputamen. One hour after the end of ischemia, blood flows were still reduced to 30% to 50% of the control level indicative of DPH. SG in cortex and hypothalamus reached a maximal decrease 10 min after the end of the ischemia and was still significantly reduced at 1 hr, although it was normal again 6 hr later. Regression analysis revealed a significant correlation between CBF obtained during ischemia and the corresponding SG found at 10-min recirculation, which could also be established at 1-hr recirculation. Therefore, a causal relation between the development of the DPH and the formation of ischemia might be considered.
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PMID:Is postischemic hypoperfusion related to brain edema? 239 11

We studied how changes in BBB function are related to the development of ischemic brain edema. Focal cerebral ischemia was produced by left MCA occlusion in rats. The permeability of the BB to small or large molecules was evaluated qualitatively by the extravasation of EB or NaFl dyes and quantitatively by the uptake index of 125I-BSA or 14C-sucrose. Brain water content was determined by specific gravity. Measurements were made from the cortical core of the MCA territory within 14 days of occlusion. Water content progressively increased within 2 days of occlusion and then gradually decreased up to 14 days. Lightly stained EB areas were located only in the proximal portion of the ischemic core. The incidence of NaFl extravasation was similar to that of EB within 2 days of occlusion but was greater than that of EB 3 days after occlusion. NaFl staining diffusely extended into the ischemic core. Although the index of 125I-BSA increased only slightly within 2 days of occlusion, a marked increase in 125I-BSA was found after 3 days. The index of 14C-sucrose increased gradually after occlusion, reaching a peak at 8 days. These findings indicate that the change in BBB permeability is minimal in ischemic brain tissue when the accumulation of edema fluid is maximal and suggest that BBB alteration in ischemic brain tissue may be associated with the stabilization or resolution of the ischemic lesion.
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PMID:Role of blood-brain barrier permeability in focal ischemic brain edema. 239 29

We studied how the osmotic pressure gradient between blood and the brain is related to the development of ischemic brain edema. Focal cerebral ischemia was produced by left MCA occlusion in rats. Brain osmolality was determined with a vapor pressure osmometer, water content of the brain tissue was measured by wet and dry weight, and the tissue sodium and potassium contents were assayed by flame photometry. Permeability of BBB was tested by EB. These measurements were made from the cortical core of MCA territory at various intervals from 1 hr to 14 days after occlusion. Brain osmolality increased from 311 +/- 2 mOsm/kg (M +/- SE) to 329 +/- 2 mOsm/kg (n = 7, p less than 0.01) by 6 hrs after occlusion. Serum osmolality did not significantly change. The osmotic gradient between blood and the brain was about 26 mOsm/kg. Brain osmolality then decreased to 310 +/- 2 mOsm/kg by 12 hr after occlusion and remained about the same level for up to 14 days. Water content progressively increased within 1 day, then gradually decreased by 14 days. Sodium plus potassium content of the brain tissue did not increase and EB extravasation was not seen within 6 hr of occlusion. These findings indicate that an osmotic pressure gradient contributes to the formation of edema only during the early stage of cerebral ischemia. Brain osmolality is not related to tissue electrolyte change and BBB disruption to protein.
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PMID:An osmotic gradient in ischemic brain edema. 239 67

Brain ischemia induces an original form of edema associating a "cytotoxic" component and a "vasogenic" component which is more inconstant. The authors set out a synthesis of fundamental research concerning the different factors of ischemic brain edema. Although anti-edematous drugs (steroids, barbiturates, diuretics) are widely used, there is no serious evidence of their efficacity. New therapies are based on a specific approach of the different disturbances of cerebral ischemia. However, controlled studies are necessary to evaluate the effects of these new drugs.
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PMID:[The role of edema in cerebral ischemia. From physiopathology to therapeutics]. 245 Dec 78


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