Brain Edema

Chan, Pak H.; Fishman, Robert A.

doi:10.1007/978-1-4757-0797-7_9

Cited by 8 publications

(8 citation statements)

References 132 publications

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“…Our data are in agreement with the results of Chan et al [49,50,58,61,69]. The results demonstrate the absence of BE development at the injection of C 20:4 , as well as at the influence of cold-injure factor at preliminary or simultaneous administration of superoxide dismuthase (SOD) in liposomes.…”

supporting

confidence: 93%

“…These experimental lesions are associated with relatively stable levels of PS and PE and are characterized by increased content of PC in the brain during ischemia development and especially after acute BE; in reperfusion, PC content is lowered. On the other hand, the intracerebral injection of C 20:4 inhibits the membrane ATPases [49], thus promoting the accumulation of sodium ions and water in the cells increasing permeability of the BBB, and causing acute BE. (2).…”

Section: Phospholipid Pool Lipid Peroxidation and Superoxide Disimimentioning

confidence: 99%

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Oxidative Stress in the Molecular Mechanism of Pathogenesis at Different Diseased States of Organism in Clinics and Experiment

Karageuzyan

2005

CDTIA

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According to modern images and results of our observations the oxidative stress (OS) is a non-specific though certain component of pathogenesis at numerous diseased states of organism having in the basis the thoroughness of pathogenic disturbances of phospholipids (PL) metabolism and processes of their free radical oxidation (FRO), which takes place in the membrane formations of as the whole cell, as well as the mitochondrial and microsomal fractions (MCF and MSF) of the white rat brain, liver mitochondria, lung shadows, at the same time erythrocyte and lymphocyte shadows at brain acute edema, ischemia, reperfusion and desympathization, infarction of myocardium, tuberculosis of lungs, diabetes, Familial Mediterranean Fever (FMF), intoxications under halothane anaesthesia (HA) and with micotoxin zearalenon. The regularities observed promote to understand from the point of view of modern approaches the molecular mechanisms of initiation, development and generalization of factors for OS formation under pathologic conditions. It is more obvious at zearalenon intoxication with intensification of lipids FRO processes and failures in PL-PL ratio phenomena. The lymphocytes membranes of the white rats spleen subjected OS induced by zearalenon intoxication permit us conclude that the general immune status of the organism decreases. It is generally peculiar to the states under conditions of generalized intoxication. The observed increase of phospholipase A(2) activity induces the release of high concentrations of lysophosphatidylcholines (LPC) and non-etherified fatty acids (NEFA) of polyenic range with prevail of arachidonic acid as a pathogenic factor, namely, at modelling brain acute edema by tetraethylolovo to white rats. Formation of the above mentioned disturbances to some extent depends on hydrophobic properties of toxins, particularly, zearalenon. The latter gives certain tropism to dopamine-beta-monooxygenase (DBM), and ability to stimulate functional activity of the enzyme. Striking haemolytic properties of phospholipase A(2) induced by existence of LPC and NEFA high concentrations, and products of their peroxidation, promote elimination of separate protein fractions of erythrocyte membranes (EM) responsible for OS formation and decrease of erythrocytes resistance to peroxide hemolysis. Increase of DBM activity under the effect of relatively moderate doses of zearalenon (1-15 microg/ml) is accompanied with extra intensification of catecholamine synthesizing function of the organism with lethal result. Data of publications represented testify exceptional efficiency of sodium thiosulfate (STS) as a powerful synergist for endogenous factors of antioxidant effect, particularly alpha-tocopherol (alpha-T), which is the main component for the system of cell antiradical defence. Detoxicating effect of STS can be demonstrated indeed on the example of zearalenon intoxication during the first two hours with the reduction of metabolism disturbances of PL and products of its peroxidation. Comparative evaluation of molecular me...

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supporting

confidence: 93%

Section: Phospholipid Pool Lipid Peroxidation and Superoxide Disimimentioning

confidence: 99%

Oxidative Stress in the Molecular Mechanism of Pathogenesis at Different Diseased States of Organism in Clinics and Experiment

Karageuzyan

2005

CDTIA

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“…Membrane phos pholipids are strongly implicated in synaptic transmission (27,28) and phospholipid metabolism dysfunction could impair synaptic transmission (29,30). In addition, it has been reported that fatty acids inhibit oxidative phosphorylation of in vitro mito chondrial preparations (31 ), and arachidonic acid has been shown to be capable of inducing brain edema in vitro (32) and in vivo (33).…”

Section: Discussionmentioning

confidence: 99%

Effects of idebenone (CV-2619) on the concentrations of acetylcholine and choline in various brain regions of rats with cerebral ischemia.

1984

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Abstract-The concentrations of acetylcholine (Ach) and choline in various brain regions of rats with and without cerebral ischemia and the effects of 6-(10-hydroxy decyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone, CV-2619) on the levels of these parameters were investigated.Cerebral ischemia was induced by a 200-sec occlusion of both common carotid arteries in animals in which both vertebral arteries had been permanently cauterized.The concentrations of Ach and choline in the brain were determined by means of pyrolysis gas chromato graphy.In normal rats, CV-2619 (10, 30 and 100 mg/kg, i.p.) did not alter the concentrations of Ach and choline in the brain regions examined. In the ischemic rats, a significant decrease in Ach and a marked increase in choline were observed in the cerebral cortex, hippocampus, striatum, and diencephalon. A slight increase in the concentration of choline was also observed in the cerebellum and brain stem. Pretreatment with CV-261 9 (10 mg/kg, i.p.) inhibited the decrease in Ach and the increase in choline in the forebrain regions.Moreover, the same dose of CV-261 9 inhibited the increment of lactate content and tended to inhibit the decrement of ATP content in the cerebral cortex. These results indicate that CV-261 9 inhibits alterations of the concentrations of Ach and choline in the brain of the ischemic rats; this inhibition may be due to the ameliorating effect of CV-261 9 on the dis turbance of cerebral energy metabolism under ischemic conditions.

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“…The alternative is accumulation of "ideogenic" osmoles, e.g., lactate. 29 We cannot exclude this possibility but wish to note that lactate content normalizes in hypo-and hyperglycemic animals long before edema 31 As the initial sampling interval was 1.5 hours any potentially significant earlier changes were not observed. The resolution of edema was then followed by an interval with normal water content and electrolyte values in all regions evaluated.…”

Section: Normogfycemiamentioning

confidence: 99%

Ischemia in normo- and hyperglycemic rats: effects on brain water and electrolytes.

Warner¹,

Smith²,

Siesjö³

1987

Stroke

100

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Previous investigations have shown that preischemic hyperglycemia worsens cerebral outcome. This study sought to delineate the temporal relations between postischemlc brain edema and the development of spontaneous epileptic activity. Fasted rats were subjected to 10 minutes of forebrain ischemia. One-half of the animals were made hyperglycemic by glucose infusion prior to ischemia. At serial recirculation intervals regional specific gravity and cortical electrolytes were measured. Normoglycemic animals showed a biphasic increase in brain water content that was fully resolved by 96 hours and had no convulsive activities. Hyperglycemic brains, although displaying a slower resolution from an initial transient decrease in specific gravity, also developed an interval with normal water content that persisted at 18 hours postischemia. At 24 hours, an increase in water content recurred and was soon followed by the onset of seizure activity. Cortical electrolyte changes were unremarkable until seizures occurred. Significant increases in total Na + , Cl", and Ca 2+ and a decrease in K + were then seen. We conclude that while the normoglycemic brain is capable of resolving postischemic edema in this model, the hyperglycemic brain develops a delayed secondary increase in water content followed by the onset of seizure activity accompanied by a deterioration of ionic homeostasis. The pathophysiology of this ischemic edema has been intensely explored in animal experiments. 2 " 7 Such studies demonstrate that the early swelling, noticeable within the first 30 minutes of vascular occlusion, is due to cellular ("cytotoxic") edema; later, a vasogenic mechanism with extravasation of proteins contributes to fluid accumulation. 18It is less clear to what extent edema contributes to the brain damage incurred as a result of transient ischemia. Long periods of global or regional ischemia (30-60 minutes) are followed by accumulation of water, with electrolyte changes characteristic of cellular edema.*" 12 Under favorable conditions, though, the edema is transient. Controversy revolves around the question of whether a vasogenic component contributes to yield a secondary increase in tissue water content. Thus, while one group has reported that ischemia as brief as 5 minutes will cause vasogenic edema after a delay of many hours, 8 " another group has published results demonstrating that transient ischemia of 30 minutes duration does not cause vasogenic edema unless the ischemia gives rise to infarction. 10The question of whether edema contributes to the final damage resulting from transient ischemia received increased attention when it was shown that preischemic hyperglycemia aggravates damage, and that macro-and microscopic swelling was a conspicuous feature in this aggravation.13 " 16 The question also Received April 3, 1986; accepted November 21, 1986. arose whether the exaggerated extra-and intracellular acidosis in hyperglycemic animals caused edema. 17 In this study, we exploited the fact that while most fasted animals exposed to...

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Brain Edema

Cited by 8 publications

References 132 publications

Oxidative Stress in the Molecular Mechanism of Pathogenesis at Different Diseased States of Organism in Clinics and Experiment

Oxidative Stress in the Molecular Mechanism of Pathogenesis at Different Diseased States of Organism in Clinics and Experiment

Effects of idebenone (CV-2619) on the concentrations of acetylcholine and choline in various brain regions of rats with cerebral ischemia.

Ischemia in normo- and hyperglycemic rats: effects on brain water and electrolytes.

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