Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Whether proton magnetic resonance spectroscopy (1H-MRS) can be used in the diagnosis of tumorous and nontumorous lesions of the brain was studied. The results of studies were analyzed in 80 patients, including 54 patients with brain tumors (astrocytomas and meningiomas), 20 with nontumorous lesions of the brain, and 6 apparently healthy individuals (controls). The nontumorous lesions of the brain involved cerebral circulatory disorders as ischemia (n = 14) and postradiation changes (n = 6). The studies were performed on a 1.5-T Signa-Horizont magnetic resonance tomograph by using the PROBE/SV programme package. The peak ratios of the following metabolites: N-acetylaspartate (NAA), choline (Cho), creatine, lactate (Lac), lipids (Lip) were examined in the spectra obtained. The spectra of astrocytomas showed a reduced peak of NAA, an elevated peak Cho; there was an increase in the peak of Lac along with higher tumor malignancy stage. The spectra of meningiomas presented a high peak of Cho along with a noticeable reduction in the peaks of other metabolites, the peak of NAA was not visualized. In ischemic lesion of the brain, the peak of Lac appeared within the first hours when the peaks of other metabolites were unchanged. A rise in the peak of Lac and a reduction in that of other metabolites were detectable with time. In radiation-induced lesions, the spectrum displayed a high peak of Lac and the peak of Lip appeared with virtually complete reduction in the peaks of other metabolites. 1H-MRS should be considered as an axillary technique used in combination with routine MRI in the diagnosis of various lesions of the brain, which can estimate chemical compositions, time-course of metabolic changes in the study tissue.
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PMID:[Proton magnetic resonance spectroscopy in diagnostics of tumorous and nontumorous lesions in brain]. 1122 36

Adenosine (ADO) is a well-known regulator of a variety of physiological functions in the heart. In stress conditions, like hypoxia or ischemia, the concentration of adenosine in the extracellular fluid rises dramatically, mainly through the breakdown of ATP. The degradation of adenosine in the ischemic myocytes induced damage in these cells, but it may simultaneously exert protective effects in the heart by activation of the adenosine receptors. The contribution of ADO to stimulation of protective effects was reported in human and animal hearts, but not in rat hearts. The aim of this study was to evaluate the role of adenosine A1 and A3 receptors (A1R and A3R), in protection of isolated cardiac myocytes of newborn rats from ischemic injury. The hypoxic conditions were simulated by exposure of cultured rat cardiomyocytes (4-5 days in vitro), to an atmosphere of a N2 (95%) and CO2 (5%) mixture, in glucose-free medium for 90 min. The cardiotoxic and cardioprotective effects of ADO ligands were measured by the release of lactate dehydrogenase (LDH) into the medium. Morphological investigation includes immunohistochemistry, image analysis of living and fixed cells and electron microscopy were executed. Pretreatment with the adenosine deaminase considerably increased the hypoxic damage in the cardiomyocytes indicating the importance of extracellular adenosine. Blocking adenosine receptors with selective A1 and A3 receptor antagonists abolished the protective effects of adenosine. A1R and A3R activation during the hypoxic insult delays onset of irreversible cell injury and collapse of mitochondrial membrane potential as assessed using DASPMI fluorochrom. Cardioprotection induced by the A1R agonist, CCPA, was abolished by an A1R antagonist, DPCPX, and was not affected by an A3R antagonist, MRS 1523. Cardioprotection caused by the A3R agonist, Cl-IB-MECA, was antagonized completely by MRS 1523 and only partially by DPCPX. Activation of both A1R and A3R together was more efficient in protection against hypoxia than by each one alone. Our study indicates that activation of either A1 or A3 adenosine receptors in the rat can attenuate myocyte injury during hypoxia. Highly selective A1R and A3R agonists may have potential as cardioprotective agents against ischemia or heart surgery.
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PMID:Cardioprotective effects of adenosine A1 and A3 receptor activation during hypoxia in isolated rat cardiac myocytes. 1126 59

MR offers unique tools for measuring molecular diffusion. This review focuses on the use of diffusion-weighted MR spectroscopy (DW-MRS) to non-invasively quantitate the translational displacement of endogenous metabolites in intact mammalian tissues. Most of the metabolites that are observed by in vivo MRS are predominantly located in the intracellular compartment. DW-MRS is of fundamental interest because it enables one to probe the in situ status of the intracellular space from the diffusion characteristics of the metabolites, while at the same time providing information on the intrinsic diffusion properties of the metabolites themselves. Alternative techniques require the introduction of exogenous probe molecules, which involves invasive procedures, and are also unable to measure molecular diffusion in and throughout intact tissues. The length scale of the process(es) probed by MR is in the micrometer range which is of the same order as the dimensions of many intracellular entities. DW-MRS has been used to estimate the dimensions of the cellular elements that restrict intracellular metabolite diffusion in muscle and nerve tissue. In addition, it has been shown that DW-MRS can provide novel information on the cellular response to pathophysiological changes in relation to a range of disorders, including ischemia and excitotoxicity of the brain and cancer.
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PMID:Diffusion NMR spectroscopy. 1132 May 36

Carotid endarterectomy (CEA) is known to be effective in reducing recurrent ischemic attacks, sometimes accompanied with the functional improvement, for patients with internal carotid artery (ICA) flow lesions by increase in perfusion and/or removal of embolic sources. However, the exact mechanism of how the CEA affects the cerebral metabolism in relations to the perfusion increase in noninfarcted hypoperfused peripheral areas to the center of the lesion (e.g., ischemic penumbra or border zone) is not yet clearly known. The existence of the ischemic penumbra and its long-term viability has also been argued. We designed a prospective study to investigate the metabolic changes in the ischemic penumbra for patients with ICA flow lesions and cerebral infarct (or ischemia) before and after CEA using localized in vivo proton magnetic resonance spectroscopy ((1)H-MRS). The results of (1)H-MRS showed significantly decreased choline (Cho)/creatine (Cr) and increased N-acetylaspartate (NAA)/Cho ratios in the periphery of the lesion for the patients after CEA as compared to those who underwent only medical treatments. The more significant changes in the cerebral metabolite levels were observed in the patients who showed the improved cerebral perfusion by single photon emission computed tomography after CEA than in those who did not. In conclusion, our data suggest the existence of the ischemic penumbra, which were viable for a longer period than previously thought; CEA seems to improve the cerebral metabolism that may result from the improved perfusion at the ischemic penumbra.
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PMID:Metabolic changes in the ischemic penumbra after carotid endarterectomy in stroke patients by localized in vivo proton magnetic resonance spectroscopy (1H-MRS). 1142 Jan 59

Focal brain lesions can be associated with proton magnetic resonance spectra (1H-MRS)-detectable mobile lipids, reflecting severe tissue degradation and necrosis. However, advanced fitting procedures, such as the LCModel, fail to adequately fit spectra in the presence of lipid resonances. To overcome this, different approaches to generate lipid model spectra were compared using a phantom, real in vivo data, and simulated data. Twenty-six in vivo short-echo time (TE) 1H-MRS from 21 malignant gliomas, four infections, and one ischemia were analyzed to evaluate the performance of the modified LCModel fit. Adding simulated aliphatic resonances at 1.3 and 0.9 ppm improved the overall fitting quality remarkably and allowed good separation of lactate and alanine. Also, a better differentiation of glioblastomas and anaplastic gliomas was achieved. In conclusion, we propose a simple way to efficiently include lipid resonances in the LCModel, allowing a better fit of in vivo short-TE 1H-MRS, and demonstrate the diagnostic potential of quantitative assessment of mobile lipids in brain tumors.
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PMID:Improved analysis of 1H-MR spectra in the presence of mobile lipids. 1155 Feb 57

The aim of this study was to compare the ischemic and postischemic energetic changes of rat skeletal muscle in response to hypothermia or room temperature, monitored noninvasively and continuously by in vivo (31)P-magnetic resonance spectroscopy ((31)P-MRS). A model of pedicled rat rectus femoris muscle was developed and analyzed by in vivo (31)P-MRS at a magnetic field strength of 2.35 T. Measurements were performed at three time points: before ischemia, after 4 hours of ischemia, and after 1 hour of reperfusion. Three groups were studied: (1) sham-operated rats (n = 6); (2) rats subjected to room temperature (24-26 degrees C, n = 6); and (3) rats subjected to hypothermia (9-12 degrees C, n = 6). Blood perfusion was measured by laser Doppler flowmetry (LDF). In the hypothermic group, phosphocreatine (PCr) recovered to 75% and adenosine triphosphate (ATP) to 86%; in the room temperature group, the recovery was 53% and 51%, respectively (P < 0.05). Skeletal muscle subjected to hypothermia (9-12 degrees C) was found to recover to a higher postischemic energetic level compared with skeletal muscle subjected to room temperature. Hypothermia appears to be a simple and effective method with which to reduce the damage related to ischemia and reperfusion.
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PMID:Effect of hypothermia on the ischemic and reperfused rat skeletal muscle, monitored by in vivo (31)P-magnetic resonance spectroscopy. 1175 63

The phosphocreatine (PCr) overshoot is a well-documented phenomenon and is readily observable by 31P MRS. In addition, a second 31P MRS observation during ischemia with reperfusion is a diminution in ATP levels. Combining these two as the 'PCr Overshoot' the PCr/ATP ratio may provide an index of viability. However little information is available regarding the duration of this 'overshoot'. For this approach to be useful clinically, the duration of this phenomenon must be ascertained. An open chest canine model of 12 min of ischemia followed by reperfusion (6h) was used. A 2 cm surface coil was sutured to the myocardium and spectra were acquired at 4.7 T. Gated spectra were acquired in <2.5 min with an interpulse delay of 5 s. Integrals of the PCr and ATP (beta) resonances were analyzed using a line-fitting routine. Overall, the PCr signal increased from 22.0+/-0.8 to 25.5+/-0.9 and ATP decreased from 11.7+/-0.4 to 10.0+/-0.4 (arbitrary units). The PCr remained elevated for the entire 6h period and the percentage increase was 15.9%. The ATP remained depleted for the entire 6h period and the percentage decrease was 17.0%. Thus, the clinically relevant and readily observable PCr/ATP is a product of both an increase in PCr and a decrease in ATP for a calculated net increase in PCr/ATP of 39.6%. The PCr/ATP ratio of the ischemia group for baseline, ischemia, 6h reflow, were: 2.33+/-0.18, 1.04+/-0.29 and 3.22+/-0.21. We demonstrate that the 'PCr overshoot' is readily observable and can be monitored noninvasively and nondestructively for 6h. Therefore, the 'PCr overshoot' may be a viable marker of reversible injury in this model and may prove to be applicable for detecting myocardial viability in patients.
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PMID:PCr overshoot': a study of the duration in canine myocardium. 1184 May 53

A transient (lasting for 15 min) bilateral carotid artery occlusion model was created by using male Mongolian gerbils ( n=20, weight 50-60 g). The animals were divided into a group with mild hypothermia (34 degrees C, n=10) and a normothermic group (37 degrees C, n=10). High-energy phosphate metabolism (ATP, PCr, Pi) and intracellular pH were sequentially measured using (31)P-MRS during ischemia and after reperfusion for 1 week. The same animals were also subjected to a histopathological evaluation. During ischemia, there were no statistically significant differences between the two groups in the quantities of the metabolites. However, after reperfusion the rate of metabolic recovery by the mildly hypothermic (MH) group was significantly higher (by 10-20%) than the normothermic (NT) group. The intracellular pH decreased about 0.4 in both groups after ischemia; and after reperfusion the intracellular pH of the MH group returned to baseline levels faster than in the NT group. One week after ischemia, energy metabolism gradually decreased about 10-20% in both groups. In the histopathological evaluation, pyramidal cell damage in the hippocampus was 33% on average in the MH group and 79% in the NT group. The neuronal damage to the cerebral cortex was 26% in the MH group and 61% in the NT group. Astrocyte reactivity in the hippocampus and cerebral cortex was 2.9% and 1.1% in the MH group and 9.7% and 5.2% in the NT group. The results of this experiment indicate that the protective effect of mild hypothermia is due to the high recovery rate of ATP and PCr and the prevention of a secondary decline in high phosphate energy.
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PMID:Effect of mild hypothermia on energy state recovery following transient forebrain ischemia in the gerbil. 1207 Jul 48

It is of great clinical interest to improve postischemic tissue recovery during microsurgical transfers. The effect of singlet oxygen energy (SOE) as photon illumination at 634 nm on rat skeletal muscle during ischemia and postischemic reperfusion was investigated noninvasively and continuously by in vivo (31)P-magnetic resonance spectroscopy ((31)P-MRS). A model of pedicled rat rectus femoris muscle was used, where phosphorous metabolites were followed before onset of ischemia (control), after 4 h of ischemia, and after 1 h of reperfusion. Two groups were studied: one control group (n = 10), and one SOE-treated group (n = 10). Blood perfusion was measured by laser Doppler flowmetry (LDF) during the study. After 4 h of ischemia, ATP levels were 72% and 51% of normal control values in the illuminated group and the control group, respectively (P < 0.05). After 1 h of postischemic reperfusion, phosphocreatine (PCr) recovered to 79% and adenosine triphosphate (ATP) to 71% in the illuminated group, whereas in the control group, the recovery was 57% and 51%, respectively (P < 0.05). It is concluded that singlet oxygen energy has a beneficial effect on the energy state of skeletal muscle during ischemia and postischemic reperfusion.
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PMID:Improved energetic recovery of skeletal muscle in response to ischemia and reperfusion injury followed by in vivo 31P-magnetic resonance spectroscopy. 1211 81

Ischemia-reperfusion induces both necrotic and apoptotic cell death. The ability of adenosine to attenuate reperfusion-induced injury (RI) and the role played by adenosine receptors are unclear. We therefore studied the role of the A(3) receptor (A(3)R) in ameliorating RI using the specific A(3)R agonist 1-[2-chloro-6-[[(3-iodophenyl)methyl]amino]-9H-purin-9-yl]-1-deoxi-N-methyl-b-D-ribofuranuronamide (2-Cl-IB-MECA). Isolated rat hearts and cardiomyocytes were subjected to ischemia or simulated ischemia, followed by reperfusion/reoxygenation. The end points were percent infarction/risk zone and annexin-V (apoptosis) and/or propidium iodide positivity (necrosis), respectively. In isolated hearts, 2-Cl-IB-MECA significantly limited infarct size (44.2 +/- 2.7% in control vs. 21.9 +/- 2.4% at 1 nM and 35.8 +/- 3.3% at 0.1 nM, P < 0.05). In isolated myocytes, apoptosis and necrosis were significantly reduced compared with controls (5.7 +/- 2.6% vs. 17.1 +/- 1.3% and 13.7 +/- 2.0% vs. 23.1 +/- 1.5%, respectively, P < 0.0001). In both models, the beneficial effects were abrogated using the A(3)R antagonist MRS-1191. The involvement of A(2a) receptor activation was also examined. This is the first study to demonstrate that A(3)R activation at reperfusion limits myocardial injury in the isolated rat heart and improves survival in isolated myocytes, possibly by antiapoptotic and antinecrotic mechanisms.
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PMID:Adenosine A(3) receptor activation protects the myocardium from reperfusion/reoxygenation injury. 1223 80


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