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

Temporal ischemic changes in glycerol and energy metabolites were studied in the striatum, hippocampus and cortex of gerbils subjected to 15 min of bilateral carotid artery occlusion alone or with various periods of recirculation. The same tissue sample served for the determination of glycerol and energy reserve by a simple enzymatic fluoro- and spectrometric assay after perchloric acid extraction. Cerebral ischemia increased the levels of glycerol (8- to 10-fold) and depleted the energy stores. During the first hour of recirculation, the glycerol content decreased and thereafter (at 2 h), normalized in all structures. However, the glycerol content was still twice as high in the striatum and hippocampus as compared to their respective controls. At the same time, an incomplete restoration of energy reserves was observed in these structures. The findings indicate that glycerol is not a stable postischemic indicator of the ischemia-induced membrane damage.
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PMID:Regional and temporal glycerol changes induced by forebrain ischemia in gerbils. 130 May 8

Complex clinical-neurophysiological investigation of 200 patients with cerebral acute focal ischemia was carried out. It included polymodal monitoring of brain functional activity: monitoring of electroencephalography (EEG), compressed spectral array and toposelective mapping of somatosensory evoked potentials, acoustic short-latency evoked potentials, transcranial cortical electric stimulation, electromyo- and electroneuromyography. The development of acute focal cerebral ischemia was shown to be independent of its location, kind and prognosis, accompanied by functional reorganization of whole brain: its supersegmented specialized motor and sensory functional systems, nonspecific formations of segmental peripheral system. These changes in cerebral functional activity can be found already during first hours of ischemia and they remain generalized during 3-5 days.
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PMID:[Dynamics of the functional state of the brain in acute focal ischemia]. 130 2

With the animal model of cerebral ischemia and reperfusion, we conducted experiments on such model to study the effects of Ligustrazine(LZ) and Salvia Miltirrhizae(SM). The results obtained are as follows: (1) The ischemic brain showed hyperperfusion (congestion period) after 10 min reperfusion following 50 min of ischemia, and then entered a delayed hypoperfusion period after 60 minutes reperfusion and afterward the hypoperfusion was remained till the end of 120 min reperfusion. (2) Following 50 min of ischemic insult, ATP and glucose contents in brain tissue were almost depleted and much of lactate accumulated. Although rapid recovery of energy metabolism occurred within 60 min of reperfusion, a secondary deterioration emerged at 120 min of reperfusion. (3) Apparent brain edema occurred after cerebral ischemia and its further development was observed at the early stage of reperfusion owing to congestive response. Despite the degree of brain edema alleviated obviously after 60 min of reperfusion, the condition become worse at 120 min of reperfusion, which was accompanied by secondary metabolic deterioration. (4) Experimental results showed that LZ and SM could significantly elevate rCBF during the delayed hypoperfusion period, and limit the development of secondary deterioration in energy metabolism and brain edema after 120 min of reperfusion. (5) Notably, LZ and SM had no significant effect on MABP when these two Chinese drugs manifested their therapeutic actions in the animal model of cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in gerbil brain tissue following cerebral ischemia and postischemic reperfusion and studies of the effects of the Chinese drugs]. 130 98

Twenty-four-hour noninvasive ambulatory blood pressure (ABP) was performed in 131 consecutive elderly subjects (61 with isolated systolic hypertension, ISH; 19 with mixed/diastolic hypertension, MDH; 29 with borderline hypertension, BLH; 23 in the normotensive group, NT). It was found that in ISH blood pressure rised during awaking period and fell during sleeping period (P < 0.05); the circadian systolic blood pressure rhythm was similar to ones in MDH, BLH and NT. However, the circadian diastolic blood pressure rhythm was attenuated in ISH. We conclude that circadian blood pressure rhythm alters in ISH, which may be related to the ischemia in organs, especially cerebral ischemia.
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PMID:[Circadian blood pressure rhythm and its characterization in isolated systolic hypertension (ISH)]. 130 16

The present study reports on the acute effects of MK-801 on the histopathological outcome and blood flow changes during focal cerebral ischemia and reperfusion. In addition, acute changes in the EEG and blood pressure are also reported. In 16 halothane-anesthetized cats, the left middle cerebral artery (MCA) was occluded for 2 h followed by 4 h of reperfusion. Thirty minutes after the onset of ischemia, eight animals were treated with 1 mg/kg of MK-801, while eight animals received saline. Blood flow from the peripheral MCA territory was measured with H2 clearance. There was a comparable reduction in blood flow (down to 20% of control) in the ischemic gyri of the two groups followed by a partial recovery after recirculation. There was a similar decrease in the EEG amplitude over the ischemic central MCA territory in the treated and the untreated group. Treatment with MK-801 induced a burst suppression in the EEG and a transient drop (11.4 +/- 6.5 mm Hg) in the mean arterial pressure. The volume of early ischemic damage decreased by one-third in the MK-801-treated group compared to the untreated one, both in the total hemisphere (from 29 +/- 10 to 20 +/- 5%) and in the hemispheric cortex (range 36 +/- 8 to 24 +/- 13%). A major fraction of this improvement was localized to the middle and posterior parietal (mainly perifocal) regions of the MCA territory. These results show that in our model, MK-801 improves histopathological outcome despite the lack of apparent effect on the cortical blood flow, and an adverse effect on the systemic blood pressure. This is the first report that describes data on a reproducible model of reperfusion after temporary occlusion of the MCA in a cat, extending the findings of the Glasgow group, who observed similar neuroprotection in models of permanent MCA occlusion.
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PMID:Acute improvement in histological outcome by MK-801 following focal cerebral ischemia and reperfusion in the cat independent of blood flow changes. 131 41

Ins(1,4,5)P3 3-kinase and 5-phosphatase are important enzymes responsible for the metabolism of Ins(1,4,5)P3, a second messenger for mobilization of intracellular Ca2+ stores. Focal cerebral ischemia induced in Long Evans rats through occlusion of the right middle cerebral artery (MCA) and both common carotid arteries resulted in a time-dependent decrease in the 3-kinase activity but not the 5-phosphatase activity. Approximately 50% of the 3-kinase activity in the cerebral cortex of the right MCA territory disappeared after 60 min of ischemia, and the enzyme activity was not restored during reperfusion. Reperfusion for 24 hr after a 60 min ischemic insult almost abolished the 3-kinase activity but the 5-phosphatase activity remained unaltered. These results suggest that the Ins(1,4,5)P3 3-kinase is one of the target enzymes of cerebral ischemia. The changes in Ins(1,4,5)P3 metabolism may be associated with the changes in intracellular Ca2+ homeostasis that underlies the pathophysiology of neuronal cell death.
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PMID:Effects of focal cerebral ischemia on inositol 1,4,5-trisphosphate 3-kinase and 5-phosphatase activities in rat cortex. 131 36

Astrocytic activation plays a major role in homeostatic maintenance of the central nervous system in response to neuronal damage. To assess the reactivity of astrocytes in transient cerebral ischemia of the gerbil, we studied the levels of glial fibrillary acidic protein (GFAP) and its mRNA. GFAP mRNA increased by 4 h after carotid artery occlusion, reached peak levels by 72 h with a 12-fold increase over control and then started declining as early as 96 h postischemia. An examination of the specific regions of the brain revealed an increase in GFAP mRNA associated with the forebrain, midbrain, hippocampus and striatum. GFAP mRNA in the non-ischemic cerebellum however, remained expressed at constitutively low levels. Immunoblot analysis with anti-GFAP antibodies demonstrated a 2- to 3-fold increase in the protein after 24 and 48 h of reperfusion. Pretreatment with pentobarbital and 1-(5'-oxohexyl)-3-methyl-7-propyl xanthine (HWA 285), the drugs that have been shown to protect against ischemic damage, prevented the increase in GFAP mRNA in the cortex following ischemic injury. Forebrain ischemia also induced vimentin mRNA and protein quantities by 12 h of reperfusion in the cortex. The levels of c-fos and preproenkephalin mRNA increased rapidly within 1 h after ischemic injury, demonstrating a temporal difference in mRNA changes following ischemia. These results indicate that an increase in GFAP and vimentin, the two glial intermediate filament proteins in the area of the ischemic lesion may be associated with a glial response to injury.
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PMID:Transient ischemia stimulates glial fibrillary acid protein and vimentin gene expression in the gerbil neocortex, striatum and hippocampus. 131 93

The effects of cellular mediators that contribute to ischemia-induced neuronal degeneration on gamma-aminobutyric acid (GABAA)-receptor function were studied. In vitro, phospholipase A2 (PLA2) inhibited muscimol-induced 36Cl- uptake in cerebral cortical synaptoneurosomes. The major hydrolysis product of PLA2 activity, arachidonic acid, also inhibited GABA-mediated 36Cl- uptake. The unsaturated nature of arachidonic acid makes it (and its metabolites) highly susceptible to peroxidation by oxygen radicals. Incubation of synaptoneurosomes with the superoxide radical-generating system, xanthine and xanthine oxidase, decreased muscimol-induced 36Cl- uptake, suggesting that the peroxidation of arachidonic acid and/or its metabolites interferes with GABAA-receptor function. Another factor involved in ischemia-induced neuronal degeneration is an increase in intracellular Ca2+. Calcium also inhibited GABA-mediated 36Cl- flux, consistent with its ability to activate PLA2. In contrast, Mg2+, which blocks Ca2+ channels, enhanced muscimol-induced 36Cl- uptake, consistent with its neuroprotective effects. Each of these cellular processes is activated during cerebral ischemia and can lead to neuronal degeneration. We used a model of transient forebrain ischemia in gerbils to determine if GABAA-receptor regulation is altered in vivo at a time when CA1 hippocampal cells have degenerated. Four days after a 5 minute bilateral carotid artery occlusion, receptor autoradiography was performed to measure the binding of [35S]t-butylbicyclophosphorothionate (TBPS) to the GABA-gated chloride channel. Significant decreases in TBPS binding were observed only in the dendritic layers (stratum oriens and lacunosem moleculare) of the CA1 hippocampus. The results suggest that ischemia-induced cellular processes that contribute to cell death can decrease GABA-gated chloride channels on dendrites of CA1 pyramidal cells, and that GABAA receptors may also reside on neurons afferent to or intrinsic to the dendritic layers of CA1 hippocampus.
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PMID:Cellular regulation of the benzodiazepine/GABA receptor: arachidonic acid, calcium, and cerebral ischemia. 131 67

After 6-12 h of recovery from transient cerebral ischemia, the pyramidal cells of the hippocampal CA1 region take up excessive amounts of calcium upon electrical stimulation, which has been suggested to be important for the development of delayed neuronal death. The aim of this study was to further characterize this enhanced calcium uptake with respect to time-course of development, relationship to neuronal damage, and amplitude of evoked field potentials as well as the dependency on N-methyl-D-aspartate (NMDA) and non-NMDA receptors. Adult Wistar rats were used and calcium-sensitive microelectrodes were placed in the stratum radiatum of the CA1 hippocampus for recording of the extracellular calcium concentration ([Ca2+]ec) during 20 min of ischemia and for 6 h of reflow. High-frequency stimulation of the perforant pathway elicited burst firing in CA1 and a transient decrease in [Ca2+]ec which reflects neuronal uptake. Shifts in [Ca2+]ec could not be evoked 0-1 h after ischemia. However, from 1-2 h burst firing could be evoked and the accompanying shift in [Ca2+]ec increased thereafter in amplitude with prolonged reflow, exceeded preischemic levels after 4 h, and reached 250 +/- 116% (mean +/- SD) of control after 6 h of reflow (p less than 0.05). The extracellular reference potential shift during electrical stimulation and the amplitude of evoked field potentials were still subnormal after 6 h [85 +/- 25% and 83 +/- 25%, respectively (mean +/- SD)]. There was a significant correlation between the degree of stimulated calcium uptake at 6 h postischemia and the extent of CA1 damage evaluated 7 days after the ischemic insult (r = 0.849; p less than 0.001). The shifts in [Ca2+]ec were reduced by the NMDA antagonist MK-801 (0.5-2 mg/kg, i.v.) to approximately 50% of the initial level during both control and postischemic conditions (p less than 0.01). The non-NMDA antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo[F]quinoxaline (NBQX) (42 +/- 13 mg/kg, i.p.; mean +/- SD) decreased the amplitude of the evoked field potentials (to 30 +/- 28% of control, p less than 0.05) and completely abolished the evoked shifts in [Ca2+]ec. In conclusion, the uptake of calcium into CA1 pyramidal cells during electrical stimulation was enhanced already 4 h after ischemia in spite of the fact that other measures of excitability were subnormal. This calcium uptake correlated to the extent of CA1 pyramidal cell damage and was dependent on both NMDA and non-NMDA receptor activation.
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PMID:Enhanced calcium uptake by CA1 pyramidal cell dendrites in the postischemic phase despite subnormal evoked field potentials: excitatory amino acid receptor dependency and relationship to neuronal damage. 132 52

Regional blood flow and oxygen metabolism were determined by positron emission tomography, using the steady state technique with 15O, in the hypothalamus and in the whole brain of fifty two normal persons and patients suffering from cerebral ischemia and degenerative dementia. During normal ageing regional blood flow and oxygen consumption appeared to increase slightly in the hypothalamus and to decrease in the whole brain in 24 persons. In the young age group the hypothalamus was more protected against ischemia than in the elderly group. In the aged group with cerebral ischemia and degenerative dementia regional blood flow and oxygen consumption were decreased in the hypothalamus to the same extent as in the whole brain.
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PMID:Positron emission tomography study of the human hypothalamus during normal ageing and in ischemic and degenerative disorders. 132 8


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