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

Steroids reduce permeability of the blood-brain barrier and inhibit active sodium transport by brain capillaries in vitro. Since the rate of edema formation during the early stages of ischemia is related to the rate of sodium transport from blood to brain, this study was designed to determine whether steroids reduce ischemic edema formation by inhibiting blood-brain barrier sodium transport. Dexamethasone was compared with progesterone since the latter is a more potent inhibitor of sodium transport in isolated capillaries. Sprague-Dawley rats were treated with vehicle (n = 22) or 2 mg/kg of either dexamethasone (n = 22) or progesterone (n = 17) 1 hour before occlusion of the middle cerebral artery. After 4 hours of ischemia, brain water content and blood-brain barrier permeability to [3H] alpha-aminoisobutyric acid and sodium-22 were determined. In controls, mean +/- SEM water content of tissue in the center of the ischemic zone was 82.4 +/- 0.2%. Brain edema was significantly reduced following pretreatment with either dexamethasone (80.6 +/- 0.1%, p less than 0.001) or progesterone (81.5 +/- 0.3%, p less than 0.05). There was also a significant reduction in blood-brain barrier permeability to alpha-aminoisobutyric acid in normal brain following either treatment (e.g., 2.21 +/- 0.19 and 1.37 +/- 0.10 microliters/g/min, p less than 0.001, for control and dexamethasone treatments, respectively), but no effect on the permeability to sodium (e.g., 1.19 +/- 0.05 and 1.12 +/- 0.11 microliters/g/min for control and dexamethasone treatments, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of steroids on edema and sodium uptake of the brain during focal ischemia in rats. 238 1

Using cerebral cortical and thalamic ischemia models produced in mongrel dogs, the reversibility of short-latency somatosensory-evoked potentials (SSEPs) and the effects of ischemic brain edema on reversibility were compared. The mean systemic blood pressure (MSBP) of animals was reduced by exsanguination until cortical SSEPs disappeared, and was held constant at that level. The MSBP was recovered by autogenous blood transfusion at 30 minutes (subgroup A), 60 minutes (subgroup B) and 90 minutes (subgroup C) after SSEP disappearance in the cortical ischemia group; and at 15 minutes (subgroup D) and 30 minutes (subgroup E) after SSEP disappearance in the thalamic ischemia group. Local cerebral blood flows (lCBF) were measured and SSEPs were monitored serially up to 2 hours after blood transfusion. At the end of measurement, the leakage of Evans blue was evaluated and brain tissue water content was measured. Cortical SSEPs disappeared when lCBF in the right cerebral cortex, measured by hydrogen clearance method decreased to 18.4 +/- 5.4 ml/100 g/min (mean +/- SD) and neuronal transmission failure in thalamus occurred when thalamic blood flow decreased to 10.0 +/- 3.3 ml/100 g/min. After blood transfusion. SSEP reappeared in all 12 animals in subgroup A, but did not appear in 2 of 9 animals in subgroup B and in all of 7 animals in subgroup C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A comparison of the functional vulnerability of the cerebral cortex and thalamus to acute ischemia]. 239 Mar 69

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

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

Postischemic recovery from brain edema and of protein synthesis was examined following 1 h of middle cerebral artery (MCA) occlusion in rats. Recovery from brain edema and of protein synthesis showed a good correlation until 7 days after reperfusion in each area (cerebral cortex or lateral caudate) in the occluded MCA side. However, regional differences in the above types of recovery in the cortex and in the lateral caudate were found for the first time in this experiment. A profound inhibition of protein synthesis and formation of brain edema began sooner in the lateral caudate than in the cortex and continued long after reperfusion. Grades of cerebral blood flow during ischemia and the early period of reperfusion were almost the same in the two regions. Therefore, the regional differences in the above recoveries may not be due to the difference in the blood flow during ischemia and reperfusion, but may be partly attributable to the imbalance of excitatory and inhibitory innervation in the above two areas of the brain, may be due to a distinctive response to ischemic stress, and may be caused also by the potentiative effect of free arachidonate on the excitotoxic mechanism.
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PMID:Recovery from edema and of protein synthesis differs between the cortex and caudate following transient focal cerebral ischemia in rats. 245 10

A possible role of Ca2+ -activated potassium efflux in brain ischemia was studied using a rat focal cortical infarction model. Three days after ischemic insult, tissue contents of water, sodium, potassium and calcium ions were measured. Charybdotoxin, a specific inhibitor of Ca2+ -activated potassium efflux, was found to reduce the formation of ischemic brain edema when a dosage of 0.15 mg/kg was given by i.v. 20-30 min prior to the onset of ischemic insult.
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PMID:Is Ca2+ -activated potassium efflux involved in the formation of ischemic brain edema? 246 63

This study tested the hypothesis that ischemia-reperfusion injury initiated by the superoxide anion radical is a major component of postdecompression hypoperfusion and cerebral edema, and could be attenuated by superoxide dismutase (SOD). A supratentorial extradural balloon was placed in 20 fasting, lightly anesthetized, mechanically ventilated dogs and inflated in 0.5-ml increments (0.07 ml/sec) at 15-minute intervals. The end-point of balloon expansion was the onset of an isoelectric electroencephalogram, near-arrest of hemispheric cerebral blood flow (CBF) (measured by H2 clearance), and the appearance of a suprainfratentorial intracranial pressure gradient, which was held for 15 minutes. The in vivo development of brain edema was detected by measuring brain elastic response (BER) extradurally, and was correlated with postmortem measurement of brain water content (gravimetry); blood-brain barrier integrity was tested by Evans blue dye given after the insult. After decompression, the dogs were randomly assigned to one of four treatment groups: Group I received hyperventilation (PaCO2 28 +/- 1 mm Hg, mean +/- standard deviation); Group II received furosemide (2.4 mg/kg) and pentobarbital (10 mg/kg) every 8 hours; Group III received 20% mannitol in a 1.4-gm/kg bolus plus furosemide, 0.5 mg/kg; and Group IV received SOD, 15,000 U/kg every 15 minutes for 3 hours. At 4 hours of decompression Group IV had significantly greater recovery in local CBF and BER than Groups I, II, and III (p less than 0.05). The 24-hour survival rate was 20% for Group I, 60% for Group II, 80% for Group III, and 100% for Group IV. The survival rate appeared to correlate with a variable degree of postmortem intraparenchymal hemorrhages, blood-brain barrier disruption, and moderate to severe brain edema for Groups I, II, and III. In contrast, Group IV had the least brain edema (p less than 0.05) and Evans blue dye extravasation (p less than 0.05) and the fewest intraparenchymal hemorrhages. These data support the hypothesis that, under the experimental conditions described here, the superoxide anion plays a major role in the pathophysiology of postdecompression ischemic edema.
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PMID:Attenuation of decompressive hypoperfusion and cerebral edema by superoxide dismutase. 255 47

Nimodipine, a Ca2+ antagonist with cerebrovasodilatory and anti-ischemic effects, binds to rat, guinea pig, and human brain membranes with high affinity (less than 1 nM). Only at higher concentrations has nimodipine been reported to block the release of some neurotransmitters and hormones from neuronal tissue. Nimodipine has no consistent effect on brain oxygen consumption or cortical ATP or phosphocreatine levels, although the ischemia-induced fall of brain ATP levels in gerbils or the lowering of intracellular brain pH in rabbits with focal cerebral ischemia were antagonized by the drug. In rats and baboons with middle cerebral artery occlusion, nimodipine was found to reduce neurological deficits without an increase in intracranial pressure or brain edema. Electrophysiological studies with nimodipine suggested a direct neuronal action. In rabbit dorsal root ganglion cells, concentrations as low as 20 nM were reported to block inward Ca2+ currents. Recent studies have suggested that nimodipine may also improve memory in brain-damaged or old rats, restore sensorimotor function and abnormal walking patterns of old rats, and accelerate acquisition of associative learning in aging rabbits. Blockade of age-related changes in Ca2+ fluxes in rat hippocampal neurones by nimodipine in vitro pointed to neuronal plasma membrane as the site of nimodipine action. The therapeutic usefulness of nimodipine appears not to be limited to cerebral ischemia, but may include dementia, age-related degenerative diseases, epilepsy, and ethanol intoxication.
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PMID:Pharmacological basis for the use of nimodipine in central nervous system disorders. 256 39

Cerebral blood volume (CBV) was calculated in gerbils from specific-gravity (SG) changes between normal and saline-perfused brains. Furthermore, changes in CBV were investigated during ischemia using carbon-14-labeled dextran (MW 70,000) as an intravascular marker. Both data were used to evaluate the possible error due to a change in CBV on the measurement of ischemic brain edema by the SG method. The methodological error found was 0.0004 for a 100% CBV change. This error is insignificant, being less than the standard deviation in the SG measured for the gerbil cortex (SG 1.0494 +/- 0.0006). Thus, CBV changes are not responsible for the SG variations observed during the first phase of ischemia. These variations are better explained as an increase of brain water content during ischemia.
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PMID:The role of cerebral blood volume changes in brain specific-gravity measurements. 258 Sep 60

The paper comprises 70 cases of extensive supratentorial infarctions. The topography and structure of secondary lesions occurring in the region of herniation and displacements caused by the coexisting brain edema were analysed. The extent of edema served as criterion in the division of the material into three groups in dependence on the occurrence of herniations and displacements. Most frequent was herniation of hippocampal uncus and most rare that of the cerebellar vermis. In group I showing no herniations selective necrosis was noted of neurons particularly sensitive to ischemia and anoxia, especially in Sommer's sector of the hippocampus. In group II secondary necrosis was visible in the regions of herniae, and in the group III also in the translocated deep brain structures in the hemisphere contralateral to the infarct and in the brain stem where, moreover, secondary hemorrhages were present. Supratentorial secondary hemorrhages were less frequent. They were noted in the thalamus both on the side of the infarct and in the contralateral hemisphere. Supratentorial necroses were more frequent. Their intensity varied from selective necrosis to Jacob's edematous necrosis. Severe displacement of deep structures and of the brain stem was associated with development of secondary internal hydrocephalus, especially in the hemisphere contralateral to the herniation. To the most important pathogenetic factors causing development of secondary morphological lesions belong disturbances of blood supply occurring as the result of pressure differences between the supra- and infratentorial space, resulting from pressure and displacement of arterial vessels, damage of their walls and distrubances of venous flow and also development of secondary internal hydrocephalus. Extensive necroses and hemorrhages increase the area of primary necrosis. Lesions resulting from herniation, displacement and compression of vessels were superposed on the picture of brain edema both present or passed. Secondary necroses damaging bilaterally structures belonging to the limbic system and reticular formation may be an additional factor in the development of edematous encephalopathy and the development of a psychoorganic syndrome after stroke.
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PMID:[Topography and structure of secondary brain damage in edema associated with supratentorial foci of encephalomalacia]. 262 77


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