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

We have previously developed a reproducible model of transient forebrain ischaemia in rats by bilateral carotid artery occlusion combined with temporary increase of ICP. With this model, reversibility of the energy metabolism and intracellular pH (pHi) was investigated by 31P-MRS during 120 min of recirculation in three groups of, respectively, 30, 60, and 120 min of ischaemia. With the induction of ischaemia, ATP and phosphocreatine (PCr) disappeared, and measurement of pHi showed severe acidosis in all rats. In the 30 min ischaemia group, both energy metabolism and pHi recovered almost completely. In the 60 min ischaemia group, ATP recovered to 74% of control values, but pHi showed full recovery. In the 120 min ischaemia group, ATP recovered to about 50% of control values, and recovery of pHi was variable. Showing logarithmical changes during recirculation in ATP and PCr, the rate of metabolic recovery was fast during 60 min of recirculation, but it decreased and reached plateau thereafter in all groups. Recovery of pHi was affected by ATP levels, and was precipitously accelerated as ATP levels exceeded 50% of pre-ischaemic values. These results suggest that prolongation of the duration of ischaemia limits the restoration of the energy state, and the quality of pHi recovery after cerebral ischaemia is affected by the degree of ATP recovery during 60 min of recirculation.
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PMID:Reversibility of energy metabolism and intracellular pH after cerebral ischaemia evaluated by 31P-MRS. 136 56

In vivo NMR techniques are currently well established in pharmaceutical research and will likely become increasingly important in the future, as they procure noninvasively morphological, physiological, and biochemical information. The status of magnetic resonance imaging (MRI) and spectroscopy (MRS) in drug development is discussed on the basis of the characterization and evaluation of a rat model of ischemic stroke and the development and profiling of drugs for cerebral ischemia in this model. It can be concluded that MRI is well suited for drug screening (quantitative determination of lesion size), while dynamic MRI and MRS techniques provide relevant information on the mechanism of drug actions. The possibility to follow changes, pathological and therapeutic, in the same individual is important from two points of view. First, variations due to interindividual differences may be eliminated, increasing the statistical power of the results. Second, dose and/or time dependence of a drug can be explored in the same individual. As a result, the number of animals required for a study will be reduced, which from both ethical and economic aspects is highly desirable.
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PMID:In vivo NMR in pharmaceutical research. 146 Oct 65

In summary, then, the major strength of MRI in evaluating cerebral ischemia is in the sensitivity that this methodology provides for detection of the disease process. However, it must be realized that edema is a nonspecific event related to various insults affecting the brain. There is still an uncertain capability of MRI in separating acute hemorrhagic from acute ischemic events. The superior sensitivity of MRI should help in investigations aimed at evaluating various forms of intervention in acute ischemia. Because some of these acute changes are at the biochemical rather than morphologic level, proton MRI alone probably will be insufficient to explore numerous variables. For this reason, the potential offered by MRS in cerebral ischemia research and in clinical settings is important. Vascular imaging is relatively complex. Several techniques show promising results but at the present time have poor resolution in comparison to ultrasound and angiography. For the immediate future, they will remain investigational.
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PMID:Magnetic resonance imaging of cerebral ischemia and infarction. 307 44

N-methyl-D-aspartate (NMDA) receptor antagonists have been demonstrated widely to be neuroprotective in cerebral ischemia, hypoxia, and traumatic brain injury. However, although noncompetitive NMDA antagonists have typically proven efficacious under all of these conditions, competitive antagonists have not been shown to be beneficial following moderate traumatic brain injury. The present study has used phosphorus magnetic resonance spectroscopy ([31P]MRS) to examine the effects of the competitive antagonist cis-4-(phosphonomethyl) piperidine-2-carboxylic acid (CGS-19755) and the noncompetitive antagonist dextromethorphan on biochemical outcome following fluid percussion-induced traumatic brain injury in rats. Five minutes prior to induction of moderate (2.8 +/- 0.2 atm) fluid percussion brain injury, animals received either CGS-19755 (10 mg/kg iv), dextromethorphan (10 mg/kg iv), or equal volume saline vehicle. [31P]MRS spectra were then acquired for 4 h post-trauma and intracellular pH, free magnesium concentration, cytosolic phosphorylation potential, and oxidative capacity determined. Both CGS-19755-treated animals and saline treated controls demonstrated significant and sustained declines in intracellular free magnesium concentration and bioenergetic status following trauma. In contrast, administration of dextromethorphan significantly attenuated free magnesium decline and improved bioenergetic state during the post-traumatic monitoring period. These results suggest that the neuroprotective actions of NMDA antagonists following traumatic brain injury are associated with attenuation of free magnesium decline and that such actions seem to be preferentially mediated by noncompetitive blockers.
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PMID:Efficacy of competitive vs noncompetitive blockade of the NMDA channel following traumatic brain injury. 763 18

Proton magnetic resonance spectroscopy (1H-MRS) is a non-invasive technique which has proved to be useful for monitoring various brain metabolites (N-acetyl-aspartate, choline, creatine-phosphocreatine, lactate). A total of 18 patients underwent a combined magnetic resonance imaging (MRI)/1H-MRS protocol in order to evaluate the distribution of the metabolites in the various stages of cerebral ischemia. Our results show a marked decrease of N-acetyl-aspartate and a large content of Lactate during the early phases, and a decrease in N-acetyl-aspartate, choline and creatine-phosphocreatine (Cr-PCr) during the chronic phase.
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PMID:Proton magnetic resonance spectroscopy in patients with ischemic stroke. 787 59

Focal cerebral ischemia causes rapid intensity changes in diffusion-weighted images (DWI) and elevated lactate as detected by localized proton spectroscopy (1H-MRS). To investigate whether such changes can also be evoked by perischemic depolarizations, we combined DWI and 1H-MRS measurements with DC potential recordings. About 40 min after occlusion of the middle cerebral artery in a rat, a negative DC deflection was observed indicating transient cell depolarization. Coincidentally with the depolarization a transient increase of the DWI signal intensity and a partially reversible increase of lactate occurred in the periphery of the ischemic territory. These results show that peri-ischemic depolarization, known to contribute to the evolution of cerebral infarction, evokes disturbances that can be detected by DWI and 1H-MRS.
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PMID:Transient cell depolarization after permanent middle cerebral artery occlusion: an observation by diffusion-weighted MRI and localized 1H-MRS. 805 8

Focal cerebral ischaemia was produced in 11 rats by permanent occlusion of the right middle cerebral artery (MCA) using a suture model modified to enable manipulation with the animals in situ in an NMR spectrometer. The development of the ischaemic insults and the resultant infarcts were observed for up to 6 h by localized 1H MRS and diffusion-weighted MRI while performing continuous monitoring of electroencephalogram and extracellular DC potential. The ischaemic areas were depicted as regions of hyperintensity in the diffusion-weighted images. Signals due to lactate became visible in the 1H spectra after MCA occlusion indicating the onset of anaerobic glycolysis. A depletion of N-acetylaspartate was seen in all animals post-occlusion. Transient or stepwise increases of lactate were observed to occur coincidentally with the events of spontaneous transient peri-infarct depolarization detected by the electrophysiological measurements. Expansion of the ischaemic area delineated in the diffusion-weighted images also accompanied peri-infarct depolarizations. These observations are consistent with transient peri-infarct depolarization playing a role in the growth of infarcts.
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PMID:Evolution of acute focal cerebral ischaemia in rats observed by localized 1H MRS, diffusion-weighted MRI, and electrophysiological monitoring. 866 6

Sequential 31P and 1H MRS was used to measure cerebral phosphate metabolites, intracellular pH, and lactate in normoglycemic and hypoglycemic rats during 30 min of complete cerebral ischemia and 5.5 h of reperfusion. These results were correlated with brain levels of free fatty acids (FFAs), excitatory amino acids, cations, and water content at death. The lactate/N-acetyl aspartate ratio was not significantly different between groups before or during occlusion. During reperfusion, the ratio was higher in normoglycemic rats from 3 to 85 min (p < or = 0.05), and recovery time was faster in hypoglycemic rats (29 vs 45 min; p = 0.04), suggesting reduced lactate production and faster recovery of aerobic metabolism. During occlusion, significant but comparable decrease of intracellular pH occurred in each group. Intracellular pH was higher in hypoglycemic rats at 140 min and 260 min of reperfusion. Water content, Na and K+ concentrations, and FFA and excitatory amino acid levels were not significantly different between groups, but hypoglycemic rats had less depletion of levels of Mg2+ (p = 0.011). These results show that hypoglycemia has a limited but potentially beneficial effect on postischemic lactic acidosis.
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PMID:Hypoglycemia prevents increase in lactic acidosis during reperfusion after temporary cerebral ischemia in rats. 877 Oct 92

To obtain a better understanding of the mechanisms underlying early changes in the brain water apparent diffusion coefficient (ADC) observed in cerebral ischemia, dynamic changes in the ADC of water and in the energy status were measured at postnatal day 8 or 9 in neonatal rat brains after cardiac arrest using 1H MRS/MRI and 31P MRS, respectively. The time courses of the MR parameters were compared with changes in the extracellular space (ECS) volume fraction (alpha) and tortuosity (lambda), determined from concentration-time profiles of tetramethylammonium applied by iontophoresis. The data show a decrease of the ADC of tissue water after induction of global ischemia of which the time course strongly correlates with the time course of the decrease in the ECS volume fraction and the increase in ECS tortuosity. This indicates that cell swelling is an important cause for the ADC decrease of water.
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PMID:Dynamic changes in water ADC, energy metabolism, extracellular space volume, and tortuosity in neonatal rat brain during global ischemia. 879 20

The purpose of the study was to determine whether diffusion-weighted magnetic resonance imaging (DWI) could identify focal lesions that develop in ischemia-sensitive cerebral tissues during reperfusion following global brain ischemia. Localized 1H-Magnetic Resonance Spectroscopy (1H-MRS) measurements were also obtained to determine whether abnormal spectroscopic markers were associated with focal lesions and to define time correlations between DWI and metabolic changes. Brain diffusion-weighted magnetic resonance imaging measurements were made in a cat model of repetitive global cerebral ischemia and reperfusion. Five animals were exposed to three episodes of 10 min vascular occlusions at hourly intervals. Three animals were evaluated as controls. DWI, T2WI, and 1H-MRS data were acquired for up to 12 h. Transient focal DWI hyperintensity was detected in the hippocampus, basal ganglia, and cortical watershed areas. These focal abnormalities usually appeared during the final reperfusion and eventually spread to encompass all of the gray matter. Spectroscopic measurements demonstrated the expected elevation of the lactate signal intensity during vessel occlusion, which returned to normal during early reperfusion. A subsequent rise in the lactate signal occurred approximately 3-4 h after the beginning of the third reperfusion. This late lactate elevation occurred after focal hyperintensities were identified by DWI. No significant signal changes were seen in spectroscopic metabolites other than lactate. The study illustrates that DWI and 1H-MRS are sensitive to focal cerebral lesions that occur during reperfusion following global cerebral ischemia.
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PMID:Imaging focal reperfusion injury following global ischemia with diffusion-weighted magnetic resonance imaging and 1H-magnetic resonance spectroscopy. 889 60


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