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

Recent advances in high-resolution MR imaging and multinuclear spectroscopy have stimulated studies of the functional relationships between tissue hypoperfusion, cellular energy depletion, and brain edema associated with cerebral ischemia. The very slow (microns/sec) random translational motion of water protons in various brain tissues and intracranial fluid compartments can now be assessed with MR diffusion imaging. More slowly diffusing protons in ischemic tissues can be differentiated from normal parenchyma, CSF, and flowing blood, enabling the detection and localization of ischemic regions within minutes of the onset of stroke. Perfusion imaging "snapshots," obtained in as little as 25 msec with echoplanar MR methods, permit the evaluation of tissue washin/washout kinetics of contrast agents in the microvasculature, and thus the quantification of brain perfusion on a regional basis. Also, delineation of major intra- and extracranial arterial and venous structures with MR angiography, acquired with two- or three-dimensional Fourier transformation techniques, has enabled accurate noninvasive assessments of vascular occlusive disease. Finally, improvements in MR spectroscopic techniques have facilitated investigations of metabolic regulation and bioenergetics in experimental animal models of cerebral ischemia, as well as in stroke patients. Combined MR imaging and spectroscopy will likely play an important role in differentiating reversibly from irreversibly ischemic brain tissues and in the investigation of various neuroprotective pharmaceuticals.
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PMID:Recent advances in MR imaging/spectroscopy of cerebral ischemia. 202 55

Changes in the levels of histamine, monoamines, and their metabolites in the cerebral cortex and striatum after occlusion of the middle cerebral artery in rats were examined. The water content of the ipsilateral brain regions gradually increased after occlusion. In the ischemic side, 1 h after occlusion, the cortical norepinephrine and striatal 5-hydroxy-tryptamine levels significantly decreased, and striatal 3,4-dihydroxyphenylacetic acid and homovanillic acid levels markedly increased. In contrast, the levels of histamine and tele-methylhistamine in either brain region gradually increased and the changes became pronounced and statistically significant 6-12 h after induction of ischemia. The striatal histamine and tele-methylhistamine reached levels three- and twofold higher, respectively, than those of the contralateral side. In rats treated with alpha-fluoromethylhistidine 1 h before induction of ischemia, elevation of histamine and tele-methylhistamine was not observed. The elevated histamine level in the ipsilateral straitum at 9 h after occlusion was further significantly increased by the treatment with metoprine, an inhibitor of histamine-N-methyltransferase. These results suggest that the histaminergic activity in the brain is gradually enhanced by cerebral ischemia.
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PMID:Changes in the metabolism of histamine and monoamines after occlusion of the middle cerebral artery in rats. 205 Nov 72

We studied the effect of focal cerebral ischemia on the "state" of brain water using proton nuclear magnetic resonance imaging. Focal cerebral ischemia was induced in five halothane-anesthetized rats via tandem occlusion of the left common carotid artery and the left middle cerebral artery. The proton transverse relaxation time, the proton density, and the water diffusion coefficient were measured at various times from the same region of brain tissue from 1.5 to 168 hours after occlusion. Early measurements indicated significant changes in the transverse relaxation time (p = 0.004) and water diffusion coefficient (p = 0.002) of ischemic brain tissue compared with a homologous region from the contralateral hemisphere. However, the transverse relaxation time, proton density, and water diffusion coefficient in ischemic brain tissue showed different temporal evolutions over the study period. Diffusion coefficient weighting was superior to relaxation time and proton density weighting for the visualization of early cerebral ischemia. Our data suggest that nuclear magnetic resonance imaging is sensitive in detecting changes in proton-associated parameters during early cerebral ischemia and confirm significant changes (p less than or equal to 0.01) in the temporal evolution of transverse relaxation times, proton densities, and diffusion coefficients following middle cerebral artery occlusion.
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PMID:Temporal evolution of ischemic damage in rat brain measured by proton nuclear magnetic resonance imaging. 205 81

In order to clarify the role of platelets as a factor aggravating cerebral ischemia, an experimental model of ischemia was investigated using thrombocytopenic rats. In addition, the prostacyclin derivative (OP-41483) and the thromboxane A2 synthetase inhibitor (OKY-046), both of which inhibit platelet aggregation, were tested for possible beneficial effects on cerebral ischemia. Cerebral ischemia was produced in spontaneously hypertensive male rats using bilateral common carotid artery ligation (BLCL). Thrombocytopenia was produced with an antiplatelet antiserum which reduced the platelet count to less than 6 x 10(4)/microliters by 24 h. OP-41483 was administered four times hourly (500 ng/kg x 4, i.p.), beginning 1 h prior to BLCL. Similarly, OKY-046 was injected four times hourly (10 mg/kg x 4, i.p.). Brain metabolites such as ATP, lactate and pyruvate and water content were determined after 3 h of cerebral ischemia. Brain levels of ATP in the ischemic rats with thrombocytopenia were higher than those of the ischemic rats without thrombocytopenia. In addition, thrombocytopenia reduced the increase of lactate and water content in the ischemic brain. Animals treated with OP-41483 also maintained higher levels of ATP and lower levels of lactate and water compared to animals given a vehicle. OKY-046 significantly reduced brain water content, but had no effect on the ischemic alteration of brain metabolite levels. These results indicate that platelets play an important role in the progression of metabolic change during ischemia.
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PMID:Role of platelets as a factor aggravating cerebral ischemia. 207 48

Cerebral ischaemia was produced in 2 groups of gerbils by occlusion of the common carotid arteries for 30 minutes, resulting in cerebral oedema. In group 1 cerebral oedema was measured by specific gravity microgravimetry, and in group 2 brain metabolism and blood flow were measured by 31P and 1H NMR spectroscopy and hydrogen clearance respectively. In group 1 the brain water content did not return to control levels by 180 minutes of reperfusion. Energy metabolism, determined by 31P NMR spectroscopy returned to control by 12 minutes, intracellular pH (pHi) by 20 minutes, and lactate, determined by 1H NMR spectroscopy, by 50 minutes. There was a lag of about 10 minutes before lactate began to be cleared from the brain. We suggest that while pHi is low, Na+/H+ exchange will negate the Na+ extrusion driven by the Na+/K+ ATPase. When pHi approaches normal there will be a net extrusion of Na+, taking osmotic water with it, and presumably with passive washout of lactate. This may be the cause of the initial delay in lactate clearance.
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PMID:Restoration of energy metabolism and resolution of oedema following profound ischaemia. 208 88

When rapid cellular swelling occurs, water moves from the extracellular space (ECS) into the cells and the concentration of ECS markers which do not move into the cells increases. Cellular swelling during cerebral ischaemia has therefore been demonstrated in vivo as an increase in ECS markers which is measurable with intracerebral electrodes. We attempted to detect the cellular swelling by brain microdialysis employing a similar principle. Dialysis probes were placed in the hippocampus, and perfused for 20 min with 14C-sucrose as an ECS marker. The probes were subsequently perfused without 14C-sucrose and the dialysate concentration of 14C-sucrose was determined at 1-min intervals. The dialysate concentrations of 14C-sucrose suddenly became elevated 1-3 min after the onset of cerebral ischaemia, indicating the occurrence of cellular swelling. The present technique is useful because it enables the mechanism of cellular swelling to be analyzed by observing the effects of pharmacological agents administered through a dialysis probe. Preliminary data indicating the role of excitatory amino acids in producing cellular swelling during cerebral ischaemia are presented as an example.
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PMID:Cellular swelling during cerebral ischaemia demonstrated by microdialysis in vivo: preliminary data indicating the role of excitatory amino acids. 208 91

Arachidonic acid is liberated from damaged cell membranes during ischemia and is the source of vasoactive prostanoids. In this study, specific drugs that influence AA metabolism were investigated for their effects on brain edema and energy metabolites during ischemia. The agents tested were: methylprednisolone (phospholipase A2 inhibition), indomethacin (cyclooxygenase inhibitor), trapidil (TXA2 synthetase inhibitor), and OP-41483 (prostacyclin derivative). Cerebral ischemia was produced using bilateral common carotid artery occlusion in spontaneously hypertensive rats. Brain water content and concentrations of ATP, pyruvate, and lactate were determined 3 hr after occlusion. Compared with its vehicle, methylprednisolone significantly reduced water content and lactate concentration and maintained high levels of ATP. Indomethacin had no effect on brain water content nor metabolite levels. Trapidil decreased water content and lactate levels and increased levels of ATP and pyruvate. OP-41483 had no effect on water content and lactate, but maintained ATP and pyruvate at high levels. These results indicate that some of the AA metabolites may play an important role in the development of brain edema and in the impairment of energy metabolism.
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PMID:Role of arachidonic acid metabolism on ischemic brain edema and metabolism. 211 11

Perfluorochemicals were developed as a blood substitute and were reported to have an advantage in oxygen transport compared with blood. The present study was undertaken to investigate the therapeutic effects of a perfluorochemical, FDA, on brain edema and metabolites in acute cerebral ischemia. Cerebral ischemia was induced in SHR by BLCO followed by recirculation. The FDA administration resulted in (a) the significant inhibition of brain edema as shown by brain water content in the treated group, and (b) significant amelioration of metabolic impairments as shown by lesser degree of ATP and pyruvate decrease and lactate accumulation. The TpO2 was compared between FDA-infused and nontreated group during ischemia. The FDA-infused group had significantly higher TpO2 than nontreated group. These results indicate that the improvement of brain edema and metabolite levels were due to alleviation of ischemic hypoxia by FDA under the same ischemic insult.
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PMID:Effects of fluosol-DA on brain edema, energy metabolites, and tissue oxygen content in acute cerebral ischemia. 211 12

Transient global forebrain ischaemia was produced in Mongolian gerbils by occluding both common carotid arteries for 10 min followed by 48 h recirculation. Dexamethasone, 5 mg/kg i.p., was given 5 h before the occlusion and every 12 h thereafter. After occlusion an increase in water, sodium and calcium content was found in the parietal cortex and hippocampus, while the concentration of potassium decreased. Exudation of plasma albumin was not found in the brain. The activity of Na+, K(+)-ATPase decreased in the hippocampus. Morphological signs of cerebral oedema were also observed, both in the CA1 region of the hippocampus and in the cortex. Dexamethasone treatment prevented the accumulation of water, sodium and calcium in the ischaemic brain. It also attenuated the oedematous morphological changes of the blood-brain barrier. Thus dexamethasone treatment may also have therapeutic relevance in the acute, high-risk phase of patients suffering from repetitive, transitoric cerebral ischaemia.
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PMID:Dexamethasone treatment attenuates the development of ischaemic brain oedema in gerbils. 215 6

Brain edema is a frequent complication of cerebral ischemia; however, its mechanism of formation is not well understood. Sodium is known to accumulate in brain during the early stages of partial ischemia. Therefore, the present studies were undertaken to determine the relation among BBB sodium transport, integrity of the BBB, and development of brain edema during the first 24 hr after the onset of cerebral ischemia. Partial cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. After recovery from the anesthetic, animals were scored for the presence of symptoms, and those with scores greater than 10 of 25 (n = 87) were chosen for this study. Measurements of tissue water, sodium, and potassium contents, and brain uptake of 22Na and 3H-mannitol were made in each group at 1.5, 3, 6, 12, and 24 hr after carotid ligation. Accumulation of sodium and water in the ischemic compared with the nonischemic cerebral cortex was progressive. This edema formation was not of the vasogenic type because the permeability of the BBB to mannitol was unchanged. Blood-to-brain sodium transport was reduced by 30% to 40% at all time points in the ischemic cortex. Nevertheless, the remaining sodium transport activity appeared to play a role in the development of brain edema because Na accumulated in the tissue at a rate that was approximately the same as the rate of 22Na uptake from blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood-to-brain sodium transport in ischemic brain edema. 216 71


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