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

In newborn rabbits, the early cerebral metabolic changes caused by hypoxic-ischemic (H-I) insult was examined by using volume localized 1H-MRS (STEAM). Partial ischemia was caused by unilateral carotid artery ligation, and hypoxia was induced by 10% oxygen inspiration for 150 minutes. Lactate immediately increased after hypoxia induction and almost disappeared 120 to 150 minutes after removal of hypoxia in both H-I and hypoxia-only experiments. Lactate production correlated well with decrease of the blood oxygen saturation. More lactate was produced on ischemic side 50 minutes post-hypoxia induction in H-I study. Ischemia alone did not cause any significant lactate production. Lactate caused by hypoxia can be dynamically monitored by localized 1H-MRS. Existence of regional ischemia can induce greater anaerobic glycolysis and may affect the pattern of brain injury under hypoxia. 1H-MRS is a sensitive tool to detect the acute metabolic change caused by H-I insult.
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PMID:A model for detecting early metabolic changes in neonatal asphyxia by 1H-MRS. 872 9

The relaxation properties of water and metabolites were measured in rat brain following the occlusion of the middle cerebral artery (MCA) with localized 1H MRS. The PRESS sequence was employed to select volumes of 39 microL in the ischemic and the contralateral hemisphere. T1 and T2 relaxation times and peak intensities of water, choline containing compounds (Cho), creatine and phosphocreatine (Cre) and N-acetyl aspartate (NAA) in both hemispheres were determined at 3-6 h, 1 day and 3 or 4 days after occlusion. Lactate in the ischemic hemisphere was also quantified. The relaxation properties and peak intensities of NAA, Cre and Cho remained unchanged in the ischemic volume during the first 3-6 h of ischemia as compared to the contralateral volume. Water T2 was slightly increased in the ischemic volume. After 24 h the T1 and T2 of water and Cre and the T1 of Cho had increased significantly in the ischemic volume, while the peak intensities of Cho, Cre and NAA were reduced. It appears therefore that tissue changes which occur in the early phase of ischemia have no significant effects on the relaxation behaviour of the metabolites. However, ischemic brain damage affects the relaxation behaviour and concentration of the metabolites and water at later stages.
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PMID:T1 and T2 relaxation times of the major 1H-containing metabolites in rat brain after focal ischemia. 873 80

We are applying multi-nuclear high-field (500 MHz) MR spectroscopy of metabolising whole tissue preparations of the mammalian brain to studies on individual components of convulsions, which include prolonged depolarization, metabolic deprivation, and the effects of excitotoxins. The responses of glial cells and neurones can be partially distinguished by following labelling patterns of metabolic intermediates from 13C-labelled glucose or acetate (which enters only glial cells). This approach clearly confirmed our earlier indications that the metabolic response to depolarization (40 mM extracellular K+) occurs essentially in glial cells. Some evidence for metabolic shuttling between glia and neurones was obtained from the changes in C3/C4 ratios of glutamate and glutamine, and the C2/C3 of GABA. Mechanisms for metabolic support of neurones by glia may be of importance in neuronal protection under such metabolic stress as occurs in epilepsy. Changes in free intracellular divalent cations ([Ca2+]i and [Zn2+]i) were monitored using the 19F-MRS indicator, 5FBAPTA. Large increases in [Ca2+]i and decreases in PCr were produced by excitotoxins (glutamate and NMDA), depolarization or ischemia, but intracellular Zn2+ appeared only after exposure to the excitotoxins. The NMDA receptor blocker, MK801, removed all of the responses to NMDA, but only prevented the appearance of Zn2+ observed with glutamate. These results indicate that the damage caused to neurones by such insults as convulsions is not due simply to the presence of excessive excitotoxic glutamate.
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PMID:High-field MRS studies in brain slices. 875 Mar 39

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

The adenosine A3 receptor is expressed in brain, but the consequences of activation of this receptor on electrophysiological activity are unknown. We have characterized the actions of a selective adenosine A3 receptor agonist, 2-chloro-N6-(3-lodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA), and a selective A3 receptor antagonist, 3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1, 4-(+/-)-dihydropyridine-3,5-dicarboxylate (MRS 1191), in brain slices from rat hippocampus. In the CA1 region, activation of A3 receptors had no direct effects on synaptically evoked excitatory responses, long-term potentiation, or synaptic facilitation. However, activation of A3 receptors with Cl-IB-MECA antagonized the adenosine A1 receptor-mediated inhibition of excitatory neurotransmission. The effects of Cl-IB-MECA were blocked by pretreatment with MRS 1191, which by itself had no effect on A1 receptor-mediated responses. The presynaptic inhibitory effects of baclofen and carbachol, mediated via GABA(B) and muscarinic receptors, respectively, were unaffected by Cl-IB-MECA. The maximal response to adenosine was unchanged, suggesting that the primary effect of Cl-IB-MECA was to reduce the affinity of adenosine for the receptor rather than to uncouple it. Similar effects could be demonstrated after brief superfusion with high concentrations of adenosine itself. Under normal conditions, endogenous adenosine in brain is unlikely to affect the sensitivity of A1 receptors via this mechanism. However, when brain concentrations of adenosine are elevated (e.g., during hypoxia, ischemia, or seizures), activation of A3 receptors and subsequent heterologous desensitization of A1 receptors could occur, which might limit the cerebroprotective effects of adenosine under these conditions.
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PMID:Activation of hippocampal adenosine A3 receptors produces a desensitization of A1 receptor-mediated responses in rat hippocampus. 898 83

Metabolic disruption resulted from cerebral ischemia and post-ischemia reperfusion injury was studied using proton magnetic resonance spectroscopy (1H MRS). We also analyzed the effect of 3-methyl-1-phenyl-2-pyrazolin-5-one (MCI-186) which can scavenge free radicals induced in the brain tissue due to ischemic-reperfusion in this experiment. The ischemic model was produced using rat forebrain ischemic model (Pulsinelli's 4 vessels occlusion model). Post-ischemic reperfusion was also induced by the re-opening of the occluded common carotid arteries. The occluded time was 30 min and reperfusion time 0, 10, 30, 60 min. We obtained the specimens in the cortex under microwave fixation. Choline and acetate increased during ischemia and gradually decreased during reperfusion period. These two signals seen in 1H MRS are supposed to represent cell membrane components (products) and the increase of these signals after reperfusion seems to be related to the post ischemic reperfusion injury due to the explosive increase of free radicals. Lactate, which is induced by anaerobic glycolysis, increased during ischemia and promptly disappeared after reperfusion. The treatment of pre-ischemic administration of MCI-186 significantly suppressed increases of choline and acetate. As far as lactate is concerned, post-ischemic administration of this drug significantly reduced its increase at the point of reperfusion. Our results suggest that MCI-186 alternates changes induced by ischemic-reperfusion injury in membranous metabolism, probably due to its free radical scavenging action.
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PMID:[In vitro evaluation of metabolic change in forebrain ischemia model of rat using proton magnetic resonance spectroscopy]. 922 72

The possible cardioprotective roles of adenosine A1 and A3 receptors were investigated in a cardiac myocyte model of injury. The adenosine A3 receptor is a novel cardiac receptor capable of mediating potentially important cardioprotective functions. Prolonged hypoxia with glucose deprivation was used to simulate ischemia and to induce injury in cardiac ventricular myocytes cultured from chick embryos 14 days in ovo. When present during the prolonged hypoxia, the adenosine A3 agonists N6-(3-iodobenzyl)adenosine-5'-N-methyluronamide (IB-MECA) and 2-chloro-N6-(3-iodobenzyl)adenosine-5'-N-methyluronamide (CI-IB-MECA) caused a dose-dependent reduction in the extent of hypoxia-induced injury as manifested by a decrease in the amount of creatine kinase released and the percentage of myocytes killed. The adenosine A1 agonists 2-chloro-N6-cyclopentyladenosine (CCPA), N6-cyclohexyladenosine, and adenosine amine congener were also able to cause a decrease in the extent of myocyte injury. The A1 receptor-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine blocked the cardioprotective effect of the A1 but not of the A3 agonists. Conversely, the selective A3 antagonists MRS-1191 and MRS-1097 blocked the protection induced by CI-IB-MECA but had minimal effect on that caused by CCPA. Thus the cardioprotective effects of A1 and A3 agonists were mediated by their respective receptors. This study defines a novel cardioprotective function of the cardiac A3 receptor and provides conclusive evidence that activation of both A1 and A3 receptors during hypoxia can attenuate myocyte injury.
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PMID:A novel cardioprotective function of adenosine A1 and A3 receptors during prolonged simulated ischemia. 924 24

Using in vivo proton-magnetic resonance spectroscopy (1H-MRS), which allows the measurement of metabolites of adequate tissue concentration, the origin of lactate in peritumoral edema has been assessed by comparison with lactate levels in the central and marginal areas of the tumor in 18 patients with cerebral gliomas. In the majority of cases lactate content in the area of peritumoral edema was lower than that in the tumor margin or tumor center, which is consistent with the assumption that the tumor is the source of lactate, which then reaches the surrounding area of edema by diffusion. In 3 of the 18 cases the amount of lactate in the peritumoral edematous tissue was higher than in the tumor, indicating that the lactate is locally produced on account of ischemia due to regional elevation of tissue pressure in the edematous area.
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PMID:The origin of lactate in peritumoral edema as measured by proton-magnetic resonance spectroscopic imaging. 941 13

Biochemical changes that occur within hepatic tissue of the rat during ischemia and subsequent reperfusion were investigated using magnetic resonance spectroscopy of liver extracts. Hepatic ischemia was produced in the rat by a continuous clamping of the left branches of the hepatic artery and portal vein. In the reperfusion experiments, the vascular clamps were released after 30 or 120 min of ischemic periods. At the end of the periods of ischemia and/or reperfusion, the left and middle hepatic lobes were dissected and processed for subsequent 1H-MRS and 31P-MRS analyses. Phosphatidylcholine, sphingomyelin, phosphatidic acid and phosphatidylethanolamine contents all showed reduction of about 30% after 120 min of ischemia. In contrast, the content of lysophosphatidylcholine showed relatively small changes following ischemia. Ten minutes after initiation of reperfusion, further decline of the total phospholipid content resulting in as much 42% reduction was observed. Then it recovered to nearly the control level when ischemia was for 30 min, but to only 65% of the control level when ischemia was for 120 min. The cholesterol/-N-(CH3)3 ratio, generally regarded as a parameter for membrane fluidity, showed about a 40% increase when ischemia was for 120 min, a change toward decreased membrane fluidity. These results appear to reflect ischemia/reperfusion-induced changes of membrane phospholipid metabolism.
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PMID:Effects of ligation and reperfusion of hepatic afferent vessels on the composition of liver cell membrane in the rat: 1H- and 31P-magnetic resonance spectroscopic analysis. 944 28


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