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

A review of the sensitivity of genetically hypertensive rats to cerebral ischemia was presented together with original data describing the systematic comparison of the effects of focal ischemia (permanent and temporary with reperfusion) performed in hypertensive and normotensive rats (i.e., blood pressures verified in conscious instrumented rats). Microsurgical techniques were used to isolate and occlude the middle cerebral artery (MCAO) of spontaneously hypertensive (SHR), Sprague-Dawley (SD) and Wistar Kyoto (WKY) rats at the level of the inferior cerebral vein. Following permanent (24 h) MCAO, persistent and similar decreases in local microvascular perfusion (i.e., to 15.6 +/- 1.7% of pre-MCAO levels) were verified in the primary ischemic zone of the cortex for all strains using Laser-Doppler flowmetry. A contralateral hemiplegia that occurred following MCAO, evidenced by forelimb flexion and muscle weakness, was greater in SHR (neurological grade = 2.0 +/- 0.1) than SD (1.0 +/- 0.4) or WKY (0.7 +/- 0.4) rats (N = 7-9, p less than 0.05). SHR also exhibited sensory motor deficits following MCAO compared to sham-operation, with decreased normal placement response of the hindlimb (% normal = 20 vs. 83, N = 23-30, p decreased rota-rod (41 +/- 7 vs. 126 +/- 19 on rod, N = 10-15, p less than 0.05) and balance beam (25 +/- 5 vs. 116 +/- 29 s on beam, N = 5-7, p less than 0.05) performance. However, an index of general motor activity was not affected by permanent MCAO. Triphenyltetrazolium-stained forebrain tissue analyzed by planimetry revealed a significantly larger and more consistent cortical infarction in SHR (hemispheric infarction = 27.9 +/- 1.5%) compared to SD (15.4 +/- 4.1%) and WKY (4.0 +/- 2.4%) rats (N = 7-9, p less than 0.05), occupying predominantly the frontal and parietal areas. Also, a significant degree of ipsilateral hemispheric swelling (4.6 +/- 0.9%, N = 7-9, p less than 0.05) and increased brain water content (78.4 +/- 0.3% to 80.4 +/- 0.2%, N = 8-9, p less than 0.05) was identified in SHR that was not observed in SD or WKY rats. A novel model of temporary MCAO also was evaluated in the hypertensive and normotensive rat strains. Initially, the effect of increasing MCAO-time followed by 24 h reperfusion in SHR was studied. During temporary MCAO (20 to 300 min), persistent and stable decreases in local microvascular perfusion (i.e., to 15-20% of pre-MCAO levels) were verified in the primary ischemic zones of the cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Genetic hypertension and increased susceptibility to cerebral ischemia. 163 Jul 32

Severe head injury often causes an increase in intracranial pressure (ICP) and decreases in cerebral blood flow (CBF) and cerebral oxygen delivery (CO2del). To determine if this reduction in CBF and CO2del would produce cerebral ischemia and if this reduction would be abrogated by maintaining global cerebral perfusion pressure (CPP), we studied CPP, ICP, CBF, CO2del, cerebral oxygen extraction ratio (CO2ER), and cortical water content (CWC) in a porcine model of focal cryogenic brain injury. Fifteen mature swine were randomized to two groups. The experimental group (n = 7) had a brain lesion and was studied for 24 hours. The control group (n = 8) was instrumented only. Cryogenic injury significantly increased ICP and decreased CBF and CO2del compared with controls. There were no significant differences in CPP between the groups for the entire experiment, and the CPP was well above the ischemic threshold. The CO2ER significantly increased in the first three hours after brain injury. However, CO2ER in experimental animals tended to decrease 12 hours after brain injury and was not significantly different from that in controls. Cryogenic injury significantly increased the CWC in the lesioned hemisphere. These data indicate that focal brain injury results in persistent ischemia despite the normalization of CPP, suggesting that a significant increase in cerebral vascular resistance (CVR) occurs after brain injury. We conclude that in addition to maintenance of CPP, intervention to reduce CVR may be important in the management of brain injury.
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PMID:Focal brain injury results in severe cerebral ischemia despite maintenance of cerebral perfusion pressure. 163 10

Brain edema in focal or global cerebral ischemia is associated with formation and release of pathophysiologically active mediator compounds. Therapeutical methods which interfere with mediator compounds under these circumstances might improve specificity of treatment of ischemic brain edema and thereby effectivity. Ischemic brain edema has a vasogenic and cytotoxic component. Extravasation of edema fluid under these conditions can be attributed to ischemic damage of the elements of the blood-brain barrier, the cerebrovascular endothelium. The development of ischemic cell swelling involving nerve- and glial cell processes can not be viewed only as manifestation of cell damage resulting from e.g. energy failure but also as an attempt to maintain or reestablish homeostasis important for cell survival and nerve cell function. The acidosis-induced cell swelling is a case in point. Accumulation of H(+)-ions in the cell causes activation of ion exchange mechanisms to protect or normalize the intracellular pH, respectively. Consequently, Na(+)- and Cl-ions together with water accumulate in the cell as the final process underlying cell swelling. Further, the increased concentrations of glutamate and K(+)-ions found in ischemic brain tissue cause glial cell swelling secondary to an active accumulation of this material together with water in the intracellular compartment in an attempt to normalize the extracellular milieu. A therapeutical inhibition of those mechanisms underlying ischemic cell swelling would prevent reestablishment of the homeostasis and, thereby, enhance secondary tissue damage. A focal brain tissue necrosis, such as an ischemic infarct or traumatic contusion can be utilized to illustrate the pathophysiological significance of the formation and release of mediator compounds of secondary brain damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mediator substances of brain edema in cerebral ischemia]. 167 75

Focal cerebral ischemia was produced by occluding the left middle cerebral artery in 769 rats. Permeability of the blood-brain barrier to small or large molecules was evaluated qualitatively using Evans blue or sodium fluorescein and quantitatively using the transfer indexes of iodine-125-labeled bovine serum albumin or [14C]sucrose. Water content was determined using wet and dry weights and sodium and potassium contents using flame photometry. Cortical tissue in the middle cerebral artery territory was sampled less than or equal to 14 days after occlusion. A significant increase in the albumin transfer index was first found 12 hours after occlusion, and the index remained approximately the same until water content peaked 3 days after occlusion. In contrast, the sucrose transfer index increased gradually, significantly correlated with increases in the water and sodium contents. Tissue staining by sodium fluorescein was more extensive than that by Evans blue. As edema fluid decreased gradually 4-10 days after occlusion, the albumin and sucrose transfer indexes increased markedly. These findings indicate that disruption of the blood-brain barrier to small molecules is accompanied by accumulation of edema fluid during the later stages of ischemia. Opening of the barrier to serum protein is probably related to the resolution of edema.
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PMID:Brain edema and cerebrovascular permeability during cerebral ischemia in rats. 169 34

Bradykinin (BK) is known to be involved in the inflammatory process causing various tissue reactions such as peripheral vasodilation and increased vascular permeability. The aims of this study was to investigate the involvement of the kallikrein-kinin system (K-K system) in the generation and progression of cerebral edema following an ischemic incident. First, after infusion of BK into the internal carotid artery, the cerebral water content was measured and electron microscopic observations were made to investigate changes of permeability using the horseradish peroxidase (HRP) tracer method. Secondly, the plasma and tissue BK levels, cerebral water content and energy metabolites (ATP, lactate and pyruvate) were measured at scheduled intervals. This was achieved using the cerebral ischemia model induced in spontaneously hypertensive rats (SHR) in which the common carotid artery were occluded (BLCO) with clips in both sides. The plasma and tissue BK were measured by radioimmunoassay. Furthermore, aprotinin and soybean trypsin inhibitor (SBTI), which specifically inhibit the K-K system, were applied to the same model and the effects on cerebral edema and metabolism were tested. At three hours after infusion of BK, cerebral edema was observed on the infused hemisphere and an increase of pinocytosis in the vessels was observed in the electron microscopic study. The chronological observation of cerebral water content revealed that it started to increase after BLCO, reaching a peak level at 30 min after reperfusion, before decreasing slightly. The plasma BK levels also showed an increase at the end of BLCO and reached a peak level at 30 min after reperfusion, decreasing thereafter. The tissue BK levels elevated significantly at 30 min after reperfusion and returned to control levels at 60 min. The ATP levels decreased remarkably after BLCO, and then increased after 30 min of reperfusion. The lactate levels increased during ischemia and became higher at 30 min after reperfusion and then decreased. The pyruvate levels did not change during this time period. In the treated group, aprotinin showed significantly lower levels of cerebral water content compared to the control. This group also showed lower lactate accumulation and preservation of ATP levels than the control. SBTI also had significantly lower water content than the control, but there was no difference in the metabolites. These results showed that BK augments the progression of brain edema and that the BK level corresponded with progression of ischemic brain edema and the suppression of BK decreased edema formation. These novel findings indicate a close relationship between BK and ischemic brain edema.
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PMID:[Studies on the involvement of bradykinin in the formation of ischemic brain edema]. 169 63

Proton magnetic resonance spectroscopy (MRS) with the depth resolved surface coil spectroscopy technique and the 1331-2662 water suppression method was used to examine two cerebral ischemia patients and 10 normal volunteers. In all cases, N-acetyl-aspartate, creatine, phosphocreatine, and residual lipid were clearly observed. No lactic acid peak was observed in normal volunteers, but a large lactic acid peak appeared in the early stage of cerebral ischemia. This MRS abnormality was observed before abnormalities appeared in conventional imaging such as computed tomographic scanning and magnetic resonance imaging.
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PMID:Clinical application of proton magnetic resonance spectroscopy to cerebral ischemia. 172 Feb 15

Oxygen-derived free radicals have been implicated in the pathogenesis of vasogenic edema and infarction caused by ischemia and reperfusion injury. In earlier studies, exogenously supplied liposome-entrapped CuZn superoxide dismutase (CuZn-SOD) ameliorated ischemic brain edema and infarction in rats following focal cerebral ischemia. To ascertain directly the role of SOD in the protection against superoxide radical-induced injury, we measured infarct size and water content 24 hr following focal cerebral ischemia in nontransgenic mice and in transgenic mice bearing the human SOD1 gene. These transgenic mice have 3.1-fold higher cellular CuZn-SOD activity in the brain than do their nontransgenic littermates. We also measured antioxidant levels (reduced glutathione and reduced ascorbate) of contralateral cortex, infarct cortex, surrounding cortex, and striatum. Infarct size and brain edema were significantly decreased in transgenic mice compared with nontransgenic mice. Reduced glutathione and reduced ascorbate levels decreased in the ischemic hemisphere, but levels in surrounding cortex and striatum were significantly higher in transgenic mice than in nontransgenic mice. These results indicate that increased endogenous SOD activity in brain reduces the level of ischemic damage and support the concept that superoxide radicals play an important role in the pathogenesis of infarction and edema following focal cerebral ischemia.
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PMID:Attenuation of focal cerebral ischemic injury in transgenic mice overexpressing CuZn superoxide dismutase. 176 30

We examined the effects of a new hyperosmotic agent (NIK-242inj.) on brain edema, energy metabolites and regional cerebral blood flow (r-CBF) during acute cerebral ischemia. Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) using spontaneously hypertensive rats (SHR). The experimental animals were divided into 4 groups, A:20% NIK-242inj., B:20% mannitol, C:10% glycerol in 5% fructose, D:normal saline. All the animals were administered the agent or saline intravenously beginning at 1h after BLCL and continuing for 2h for a total dose of 6.8 ml/kg body weight. Brain water content and metabolites (ATP, lactate, pyruvate) were determined 3h after BLCL. Regional cerebral blood flow (r-CBF) in thalamus was also measured by the hydrogen clearance technique. The brain water content in the NIK-242inj. group was significantly lower than that of saline group. The concentration of brain ATP in the NIK-242inj. group remained higher than those of saline group. Accumulation of lactate in the NIK-242inj. group was less than in the mannitol and saline groups. The lactate/pyruvate ratio of the NIK-242 inj. group was significantly lower than that of the saline and mannitol groups. At 3h after BLCL, the reduction of r-CBF in the NIK-242inj. group was smaller than that of saline group. The present study suggests that NIK-242inj. as well as glycerol could ameliorate brain edema, disruption of brain energy metabolism and reduction of r-CBF in acutely induced cerebral ischemia.
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PMID:Effect of a new hyperosmotic agent, NIK-242 injection, on brain water content, metabolites and cerebral blood flow in cerebral ischemia in the spontaneously hypertensive rat. 176 86

The effects of cerebral ischemia in rat brain were monitored as a function of time using proton MR imaging. Spin-spin relaxation time (T2), proton density, and magnetization transfer contrast (MTC) were measured by MR imaging at various time intervals during a 1-week period following the induction of ischemic damage. Ischemic injury was characterized by a maximization of both T2 value and MTC appearance at 24 hr postischemic injury. These changes were accompanied by a gradual increase in MR observable water density over the first few days of ischemia. A reduction in the magnetization exchange rate between "free" and "bound" water protons as measured by MTC imaging is at least partially responsible for the elevation in T2 values observed during ischemia, and may accompany breakdown of cellular structure.
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PMID:Investigation of cerebral ischemia using magnetization transfer contrast (MTC) MR imaging. 176 13

Twelve rabbits were submitted to 20-min global cerebral ischemia. Half of them were treated continuously with prostacyclin (PGI2) for 3 min before and during ischemia, and for 15 min after it. Untreated animals were not given PGI2 medication. The cases treated with PGI2 were found to have recovered bioelectric activity of the brain in half the time that its return took in the untreated cases. In the group that received PGI2, the ischemic ultrastructural changes in the cytoplasm of neuroglial cells were abolished, however, PGI2 did numerous vesicular structures, nuclear inclusions and chromatin clumping and margination. The vesicular structures were enclosed in a single smooth membrane without contact with the nuclear envelope. It is suggested that the vesicular structures may form as the result of disturbances in the water-electrolyte exchange between the cytoplasm and karyoplasm of neuroglial cells. The inclusions consisted of filaments and/or membranes. The amassing in the karyoplasm of vesicular structures and intranuclear inclusions with chromatin clumping and margination probably leads later to the death of the neuroglial cells after total cerebral ischemia. Hence, the described data indicate that the curative effects of PGI2 are directed only to early changes in the neuroglial cells cytoplasm and reflect a transient facilitation of functional recovery and/or metabolism rather then permanent brain protection after complete cerebral ischemia.
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PMID:The effects of prostacyclin on early ultrastructural changes in the cytoplasm and nuclei of neuroglial cells following complete cerebral ischemia. 179 Dec 98

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