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

Effects of S-adenosyl-L-methionine (SAMe).2 sulphate.tosylate upon the ischemia-induced brain edema and survival rate in Mongolian gerbils and spontaneously hypertensive rats were investigated, since SAMe is known to be important as a physiologically active substance in numerous metabolic processes including those that are inhibited in ischemia. SAMe suppressed increases in water and Na+ content in the ischemic brain which was produced by ligation of the common carotid artery for a short term (20-30 min) in Mongolian gerbils. This ameliorating effect of SAMe was observed dose-dependently at higher doses than 100 mg/kg administered repeatedly every 0.5 or 1 hr, starting within 2 hr, at least, after the reperfusion. Similar effects were also obtained in spontaneously hypertensive rats whose common carotid artery on both sides were ligated permanently. SAMe also increased survival rate in Mongolian gerbils with ischemic brain. Although the SAMe solution employed in the present experiments was hypertonic and contained mannitol as a filler, the beneficial effects were due to neither the hypertonicity of the solution nor mannitol, but due to SAMe itself.
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PMID:Effects of S-adenosyl-L-methionine upon ischemia-induced brain edema in Mongolian gerbils and spontaneously hypertensive rats. 313 70

Ornithine decarboxylase, rate-limiting in polyamine formation, has been found to be necessary for the development of vasogenic edema after cryogenic cerebral injury and is postulated to be of importance in late ischemic brain edema formation. Ornithine decarboxylase activity and accompanying edema was studied after transient cerebral ischemia in Mongolian gerbils. Bilateral carotid artery occlusion was utilized to produce dense forebrain ischemia. After 4 h of reperfusion a significant elevation in ornithine decarboxylase activity was present (72.5 +/- 24.7 vs 8.5 +/- 2 pmoles/mg protein/h, p less than 0.05). Immunohistochemical localization of ornithine decarboxylase indicated its presence in cortical neurons of ischemic gerbils. This was typically located in the perinuclear cytoplasm and extended into proximal dendrites. Nonischemic animals did not contain ornithine decarboxylase immunoreactivity. These studies show the presence and location of ornithine decarboxylase in cerebral tissue subjected to transient ischemia. The increase in this marker of polyamine activity paralleled previous studies in this model of cerebral edema formation and reperfusion deficit in blood flow and evoked potential, suggesting that ornithine decarboxylase is a marker for and may be associated with those late metabolic events leading to progressive functional deterioration after incomplete cerebral ischemia.
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PMID:Ornithine decarboxylase activity and immunohistochemical location in postischemic brain. 319 49

The brain lesions in stroke-prone spontaneously hypertensive rats (SHRSP) are characterized by multifocal microvascular and spongy-cystic parenchymal alterations particularly in the gray matter. An essential feature of the lesions is the presence of edema with massive extravasation of plasma constituents as evidenced by specific gravity measurements, Evans blue technique and immunohistochemistry. The nerve cell injury occurring in the brain lesions in SHRSP is further characterized by light and electron microscopy in the present study. Two types of neuronal changes were seen within the blood-brain barrier (BBB) leakage sites. A small number of neurons with dark condensed nucleus and cytoplasm were found most often at the periphery of recent lesions. The majority of injured neurons were pale and showed intracellular edema confined to the dendrites and perikarya sparing axons and synapses. Their nuclei were well preserved with finely dispersed chromatin. The swollen and watery cell processes of neurons and astrocytes gave a spongy appearance to the neuropil. The intracellular edema seemed to result in cytolysis. The results suggest that primary anoxia-ischemia is not the major pathogenetic mechanism behind the nerve cell injury in severely hypertensive SHRSP, rather it is the massive BBB leakage and consequent brain edema that causes cytolytic destruction of neurons. Secondary focal ischemia as a consequence of occlusion in microvessels may, however, contribute to the nerve cell destruction.
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PMID:Nerve cell injury in the brain of stroke-prone spontaneously hypertensive rats. 321 25

The resistance of the brain to ischemia depends not only on the duration and severity of flow reduction but also on a number of pre- and post-ischemic metabolic and hemodynamic factors which are able to improve or impair the post-ischemic recovery process. Among pre-ischemic protective factors, the suppression of metabolic rate by drugs or hypothermia, the increase of brain tissue energy reserves and the inhibition of membrane permeability of cations are of particular importance. In contrast, increase of metabolic rate and increase of tissue acidosis induced by hyperglycemia or residual blood flow, reduce the ischemic tolerance of the brain. As long as cell membranes do not depolarize during ischemia, restitution of blood flow results in spontaneous recovery. After depolarization of membranes, however, numerous post-ischemic complications evolve, such as the no-reflow phenomenon, post-ischemic hypoperfusion, post-ischemic brain edema, disturbances of the coupling between metabolic activity and blood flow, etc. These complications require therapeutic intervention in order to prevent irreversible injury. By optimizing this therapy in a model of 1 hour complete normothermic brain ischemia in cat and monkeys, post-ischemic recovery of energy metabolism, protein synthesis, spontaneous and evoked electrocortical activity and even integrative neurological performance were observed. The resistance of the brain to ischemia, in consequence, is much higher than previously assumed and can be substantially improved by adequate post-ischemic treatment.
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PMID:[Experimental principles of tolerance of the brain to ischemia]. 332 66

Three transient episodes of 5 min ischemia spaced at 1-h intervals were produced in Mongolian gerbils by bilateral carotid artery occlusion with an implanted vascular occlusion device. The interval of 1 h was chosen to allow for the development of post-ischemic hypoperfusion between the ischemic episodes. Three minutes and 1 h after each ischemic episode, and 6 and 24 h after the third occlusion, Evan's blue (EB) was injected intravenously to trace circulating blood, and the number of perfused capillaries was determined in various brain regions by fluorescence microscopy. Brain edema was evaluated by measuring specific gravity in tissue samples taken from adjacent areas. Repetitive ischemia caused progressively increasing brain edema and a progressive reduction of the number of perfused capillaries. Immediately after each ischemic episode, transient recruitment of capillaries occurred, thus excluding no-reflow as a main pathogenetic factor of microcirculatory disturbances. The pattern of microcirculation 6 and 24 h after the last occlusion revealed a redistribution of circulating blood, characterized by a reduction in the number of EB-filled capillaries associated with a noticeable dilatation of the larger vascular channels. Our studies suggest a close interrelationship between post-ischemic microcirculatory hypoperfusion and the development of brain edema, the degree and extent of which progresses with the repetition of ischemic episodes when they are carried out during the periods of hypoperfusion.
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PMID:Microvascular disturbances and edema formation after repetitive ischemia of gerbil brain. 334 85

Edema formation following severe permanent or temporary cerebral ischemia in gerbils with an artificially reduced platelet count was investigated. Acute focal cerebral ischemia was produced by extracranial carotid ligation, and the local cerebral blood flow was estimated using the hydrogen clearance method. Brain tissue water and sodium and potassium contents were taken as indexes of brain edema. The platelet count was reduced in some gerbils by intravenous injection of neuraminidase. After 60 minutes of ischemia, a marked increase in tissue water and sodium contents accompanied by a decrease in potassium content was observed in untreated gerbils. However, gerbils with a reduced platelet count revealed similar but significantly smaller changes in all the measured parameters. Restoration of blood flow after 60 minutes of ischemia resulted in further accumulation of water and sodium and in depletion of potassium in both groups. These changes were significantly smaller in the gerbils with a reduced platelet count. It is concluded that platelets, activated by cerebral ischemia, may be involved in the development of ischemic brain edema in gerbils.
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PMID:Are blood platelets involved in the pathogenesis of ischemic brain edema in gerbils? 336 76

Using two different models of non ischemic and transient cerebral ischemia in SHR, the effect of hyperosmolar solution with intravenous 10% glycerol on serum lipid peroxides, plasma prostaglandins (TXA2, PGI2), brain water content and brain metabolites were studied. Glycerol did not influence the levels of lipid peroxides, plasma prostaglandins and brain water content in the non ischemic rats. In the transient ischemia group, on the other hand, serum lipid peroxides were significantly reduced in the glycerol administrated group. On the study of plasma prostaglandins, there was no difference of TXA2 levels between two groups, but PGI2 levels were significantly increased in the glycerol administrated group. Brain water content was significantly decreased. And on the study of brain metabolites, ATP concentrations remained higher and lactate concentrations were lower in the glycerol administrated group compared with those in the control group. But there was no difference with pyruvate concentrations between two groups, furthermore L/P ratio improved in the glycerol administrated group. Besides the effect on reduction of brain edema as for hyperosmolar solution, glycerol may indicate improvement of ischemic impediments on brain by the action of antioxidation and reinforcement of PGI2.
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PMID:[Effect of glycerol administration on experimental cerebral ischemia--Part 1. Studies on lipid peroxides, prostaglandins, brain edema and brain metabolites]. 337 Jan 71

Regional changes in adenine nucleotides in the rat brain were studied after 1 h of ischemia produced by the embolization method. The animals were divided into three groups according to neurological symptoms: sham-operation group, group A (hemiparesis only), and group B (hemiparesis with unconsciousness). Marked ATP depletion was detected in the hippocampus on the embolized side and extended to the other regions on the same side in group B. The results suggest that this damage in regional energy metabolism arises from regional reduction in blood flow and/or tissue vulnerability. ATP levels in the hypothalamus, hippocampus, and striatum on the opposite side of embolization decreased markedly in group B, and may be caused by extension of brain edema or diaschisis.
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PMID:Regional changes in the cellular level of adenine nucleotides in ischemic rat brain subjected to single embolization. 337 98

Differences in disturbed water and ion homeostasis in the periphery and the center of focal cerebral ischemia were investigated. Focal cerebral ischemia was induced by occlusion of the right common carotid artery in gerbils. Water and electrolyte content were determined using punched-out samples. In 2 h of ischemia, water content of the cerebral cortex was 79.0 +/- 0.3, 82.0 +/- 0.4, and 80.7 +/- 0.4% (means +/- SE) for the nonischemic region, the periphery, and the center of the ischemic region, respectively (significantly different). Na+ content was increased and K+ content was decreased most prominently in the periphery of the ischemic region. K+ depletion and exogenous Ca2+ accumulation in the peripheral region were visualized by K+ staining and 45Ca autoradiography, respectively. Thus, water and electrolyte changes in the periphery of ischemia were different from those in the center. Brain edema was developed initially in the marginal region of the focal cerebral ischemia.
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PMID:Greater disturbance of water and ion homeostasis in the periphery of experimental focal cerebral ischemia. 355 5

Previous investigations have shown that preischemic hyperglycemia worsens cerebral outcome. This study sought to delineate the temporal relations between postischemic 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 Ca2+ 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.
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PMID:Ischemia in normo- and hyperglycemic rats: effects on brain water and electrolytes. 356 5


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