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

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

The relationship of the osmotic pressure gradient between blood and brain, and the development of ischemic brain edema was studied. Focal cerebral ischemia was produced by left middle cerebral artery occlusion in rats. Brain osmolality was determined with a vapor pressure osmometer, brain water content by wet-dry weight, and tissue sodium and potassium contents by flame photometry. Permeability of the BBB was tested by Evans blue. Measurements were made from the ischemic cortex within 14 days of occlusion. Brain osmolality increased from 311 +/- 2 to 329 +/- 2 mOsm/kg by 6 h after occlusion. Serum osmolality did not change significantly. The osmotic gradient between blood and brain peaked at approximately 26 mOsm/kg. Brain osmolality then decreased to 310 +/- 2 mOsm/kg by 12 h after occlusion and remained at about that same level. Water content increased progressively within 1 day of occlusion, then gradually decreased by 14 days. Brain tissue sodium plus potassium content did not increase within 6 h of occlusion, and Evans blue extravasation was not seen within that time. These findings indicate that an osmotic pressure gradient contributes to the formation of edema only during the early stage of cerebral ischemia. Furthermore, the increase in brain osmolality is not related to tissue electrolyte change or BBB disruption to protein.
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PMID:Ischemic brain edema and the osmotic gradient between blood and brain. 339 16

U74006F is a member of a new family of steroid drugs called 21-aminosteroids, which are potent inhibitors of lipid peroxidation with little or no glucocorticoid or mineralocorticoid activity. We investigated the effects of U74006F on the early ionic edema produced by middle cerebral artery occlusion in rats. Intravenous doses of 3 mg/kg U74006F were given 10 minutes and 3 hours after occlusion. Tissue concentrations of Na+, K+, and water at and around the infarct site were measured by atomic absorption spectroscopy and by wet-dry weight measurements 24 hours after occlusion. Compared with vehicle treatment, U74006F treatment reduced brain water entry, Na+ accumulation, K+ loss, and net ion shift by 25-50% in most brain areas sampled in the frontal and parietal cortex. However, reductions of ionic edema were most prominent and reached significance (p less than 0.005, unpaired two-tailed t test) mostly in the frontoparietal and parietal cortex areas adjacent to the infarct site. Our findings suggest that a steroid drug without glucocorticoid or mineralocorticoid activity can reduce edema in cerebral ischemia but that the effects are largely limited to tissues in which collateral blood flow may be present.
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PMID:21-Aminosteroid reduces ion shifts and edema in the rat middle cerebral artery occlusion model of regional ischemia. 340 99

Two consequences of cerebral ischemia are cell acidification and cytotoxic edema. To test the possibility that Na+/H+ exchange mediates acid-induced edema, we measured cytoplasmic pH (pHi) and cell volume changes in C6 glioma cells that were artificially acid-loaded using weak electrolytes. pHi was monitored fluorimetrically with 2',7'-bis-(2-carboxyethyl)-5,6-carboxyfluorescein. Upon acidification with sodium propionate, pHi dropped to 6.74 +/- 0.05 (n = 25), and then recovered to levels near the physiological value of 7.23 +/- 0.02 (n = 13). Cell volume, measured by electronic sizing, increased concomitantly by approximately 50% in sodium propionate solution. Both pHi recovery and cell swelling were Na+-dependent, amiloride-sensitive, and inhibited at pHo less than 6.0. These results demonstrate that in vitro: (1) intracellular acidification can lead to cell swelling, and (2) pHi recovery and the concomitant cell swelling are likely mediated by Na+/H+ exchange. These mechanisms may be related to postischemic cytotoxic glial edema.
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PMID:Cell swelling following recovery from acidification in C6 glioma cells: an in vitro model of postischemic brain edema. 342 48

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

Following major intracranial surgery in a 35-year-old man, sodium pentothal was intravenously infused to minimize cerebral ischaemia. Intense vasospasm with threatened gangrene arose in the arm used for the infusion. Since the cranial condition precluded use of more usual methods, lidocaine was given intra-arterially, with careful cardiovascular monitoring, to counteract the vasospasm. The treatment was rapidly successful.
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PMID:Drug-induced arterial spasm relieved by lidocaine. Case report. 356 23

Brain metabolism and intracellular pH were studied during and after episodes of ischaemia and hypoxia-ischaemia in lambs anaesthetised with sodium pentobarbitone. 31P and 1H magnetic resonance spectroscopy methods were used to monitor brain pHi and brain concentrations of Pi, phosphocreatine (PCr), beta--nucleoside triphosphate (beta NTP), and lactate. Simultaneous measurements were made of cerebral blood flow and cerebral oxygen and glucose consumption. Cerebral ischaemia sufficient to reduce oxygen delivery to 75% of control values was associated with a fall in brain pHi and increase in brain Pi. Progressively severe hypoxia-ischaemia was associated with a progressive fall in brain pHi, PCr, and beta NTP and increase in brain Pi. In two animals the increase in brain lactate during hypoxia-ischaemia measured by 1H nuclear magnetic resonance (NMR) could be quantitatively accounted for by the increased net uptake of glucose by the brain in relation to oxygen, but was insufficient to account for the concomitant acidosis according to previous estimates of brain buffering capacity. In four animals brain pHi, PCr, Pi, and beta NTP had returned to normal 1 h after the hypoxic-ischaemic episode. In one animal brain pHi had reverted to normal at a time when 1H NMR indicated persistent elevation of brain lactate.
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PMID:Brain metabolism and intracellular pH during ischaemia and hypoxia: an in vivo 31P and 1H nuclear magnetic resonance study in the lamb. 358 43

Volume regulation of C6 glial cells was studied in anoxia in vitro to improve the understanding of ischemic cell swelling in the brain. Contrary to in vivo conditions, anoxia or anoxia plus iodoacetate for additional inhibition of anaerobic energy metabolism did not induce glial swelling. However, intracellular K+ was markedly decreased while intracellular Na+ increased. Induction of energy failure by anoxia plus iodoacetate was found to prevent the regulatory volume decrease on hyposmotic exposure of the cells, which is regularly observed in normoxic control conditions. Hyposmotic exposure in anoxia plus iodoacetate led only to an initial tendency of cell volume normalization followed by secondary cell swelling. This was associated with a net increase of intracellular Na+ that may explain the failure of volume regulation under these circumstances. Maintenance of a normal glial cell size during complete energy deprivation by anoxia plus iodoacetate in isotonic medium strongly indicates that energy failure per se does not suffice to induce cell swelling. Cell swelling in cerebral ischemia in vivo thus is likely to require additional mechanisms, most likely an increase of membrane permeability to Na+, which may be caused by release and accumulation of excitotoxins such as glutamate or by an extracellular release of K+. Such a mechanism would hardly influence the extracellular homeostasis in vitro due to the large medium-to-cell volume ratio. The findings demonstrate, nonetheless, the significance of a competent energy metabolism to support cell volume regulation. This is concluded from the failure of regulatory volume decrease of hypotonically suspended glial cells in anoxia plus iodoacetate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Control of glial cell volume in anoxia. In vitro studies on ischemic cell swelling. 359 Feb 56

High levels of brain lactate may contribute to cellular death and dysfunction in acute cerebral ischemia. Although sodium dichloroacetate (DCA) has been shown to lower brain lactate in incomplete cerebral ischemia, functional outcome has not been assessed with DCA. We examined the effects of DCA treatment on functional neurologic outcome using a previously developed model for "spinal stroke" in the rabbit. Thirty male New Zealand white rabbits weighing 1.3-2.8 kg were studied. After anesthesia with 15-40 mg/kg pentobarbital IV, a laparotomy was performed and the aorta exposed. A metal clamp was placed on the aorta just distal to the left renal artery for 20 minutes and then removed. The abdominal wound was closed in two layers. Animals then received either 2cc normal saline (n = 15) or 300 mg/kg DCA in 2cc normal saline (n = 15) over 10 minutes. The animals were returned to their cages when awake and were examined at 24 hours, 48 hours, and 72 hours for neurologic assessment. The exams were performed by a blinded examiner who was unaware of the treatment given. A three point ambulatory score (0 = can't walk, 1 = walk but not hop, 2 = hopping) and a two point activity score (0 = inactive, 1 = active) were used. At 24 hours, 67% of the DCA-treated animals were actively moving about compared to only 27% of the controls (P = 0.03; Fisher Exact Test). Ten of fifteen control animals were unable to walk, while only five of fifteen DCA-treated animals were unable to walk (P = 0.07). Sixty percent of the DCA animals were able to hop compared to 27% of controls (P = 0.06). These results suggest that DCA can reduce morbidity from spinal cord ischemia in the rabbit.
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PMID:Effects of dichloroacetate in spinal stroke in the rabbit. 361 62

Ischemia causes disturbances of the ionic equilibrium, i.e., Na+ and water influx and K+ efflux. When the ischemic tissue keeps contact with cerebral blood flow, brain tissue equilibrates with systemic circulation and consequently shifts of electrolytes and water are induced. Therefore, brain edema should initiate in the peripheral area of focal cerebral ischemia. To test this hypothesis, we performed the following experiments. Focal ischemia was induced by occlusion of the right common carotid artery in gerbils and by embolization with microspheres in rats. Water and electrolyte content was determined using punched out samples and regional K+ and Ca2+ distribution was visualized by histochemical K+ staining and 45Ca-autoradiography, respectively. Cerebral blood flow and glucose metabolism were evaluated by 14C-iodoantipyrine or 18F-fluoroantipyrine and 14C-deoxyglucose autoradiographies, respectively. Two hours of ischemia in gerbils with definite hemiparesis caused K+ depletion in the ischemic area, often most pronounced in the periphery of the lesion. Water content of cerebral cortex was 79.0 +/- 0.9, 82.0 +/- 1.0, 80.7 +/- 0.9 (%; mean +/- SD) for nonischemic, periphery and center of ischemia, respectively (significantly different with each other). Na+ content was increased and K+ content was decreased most prominently in the periphery of ischemia. Exogenous Ca2+ was also accumulated in the periphery. In the embolized stroke in rats, K+ depletion and Ca2+ accumulation obviously rimmed the ischemic focus. Furthermore the infarcted area was only part of the disturbed area of acute-phase glucose metabolism. Thus water and ionic disturbances were different between in the periphery and in the center of focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain edema initially develops in the periphery of focal cerebral ischemia]. 373 Jan 97


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