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)

Effects of ergot alkaloids, nicergoline (NIC), on survival rate, brain water content, local cerebral blood flow (LCBF: 14C-iodoantipyrine) and glucose utilization (LCGU: 14C-2-deoxyglucose) were examined after bilateral carotid artery occlusion (BCAO) in spontaneously hypertensive rats. Two series of study were performed; the permanent BCAO and 3-hr-BCAO study. After permanent BCAO, the survival rate at 24 hrs of 32% (8 mg/kg, i.p.) or 38% (16mg/kg) in NIC group was higher than that in non-treated group (12%). At the end of 3-hr-BCAO, the increase in water content (dry-wet) in di-mesencephalon was less in NIC (100 micrograms/kg/min, i.v.) group than that in non-treated group. The decrease in LCBF in caudate-putamen (CP), parietal cortex (PC), thalamus (TH), hypothalamus (HT), and substantia nigra (SN) were less in NIC group than those in non-treated group. At the 2-hr-reperfusion after 3-hr-BCAO, the decrease in LCBF in TH and HT were less in NIC group than those in non-treated group. The LCGU in sensory motor cortex, CP, PC, HT, inferior colliculus and pons-reticular were higher in NIC group than those in non-treated group. From these results, it is concluded that nicergoline may have ameliorative effects on survival rate related to the prevention of decreased cerebral blood flow and metabolism following brain ischemia.
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PMID:[Nicergoline, an ergot alkaloid, improves ischemic brain damage by ameliorating the decreased cerebral blood flow and metabolism in spontaneously hypertensive rats]. 129 29

A marked neuronal cell loss has been determined in the hippocampal CA1-subfield of the rat 7 days after 10 min of ischemia. The purpose of the present study was to evaluate the consequences of ischemia-induced hippocampal neuronal damage on local cerebral glucose utilization (LCGU) and blood flow (LCBF). Forebrain ischemia of 10 min duration was induced in male Wistar rats. Seven days after ischemia LCGU was measured with the [14C]-2-deoxy-D-glucose method, and LCBF was determined with the [14C]-iodoantipyrine technique in sham-operated and in ischemic rats. Furthermore, postischemic LCGU and LCBF were determined in vinpocetine-treated ischemic rats. Vinpocetin (14-ethoxycarbonyl-(3 alpha, 16 alpha-ethyl)-14,15-eburnamine) has already proved to protect hippocampal neurons against ischemic damage. In comparison with sham-operated rats, LCGU increased and LCBF decreased significantly in the CA1-subfield 7 days after ischemia. Both effects were abolished by preischemic vinpocetine treatment supporting the presumption that this drug is protective against ischemic damage.
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PMID:Effects of vinpocetine on local cerebral blood flow and glucose utilization seven days after forebrain ischemia in the rat. 227 9

Regional cerebral blood flow and vasomotor reactivity were measured in 33 patients with surgically remediable hemispheric ischemia by the 133Xe inhalation method prior to superficial temporal to middle cerebral artery (STA-MCA) by-pass. Thirteen patients also underwent LCBF and L lambda measurements by the stable xenon CT method for comparison. Twenty-four had proximal occlusion of one or both internal carotid arteries, 9 had intracranial occlusive disease (4 internal carotid, 5 middle cerebral). Measurements were repeated at intervals up to 30 months following surgery and compared to measurements in a similar group (N = 13) treated medically. In the surgically treated group 22 patients had recurrent TIAs, of whom 12 also had minor residual neurological deficits from recent small cerebral infarctions with potential for recovery (RINDs) while the remaining 11 had RINDs without TIAs. After surgery 28 improved with cessation of TIAs and/or neurological recovery, 3 remained unchanged, 2 cases worsened. Compared to age-matched normal hemispheric F1 (gray matter) values, pre-operative F1 values in the STA-MCA group were reduced in both ischemic and opposite hemispheres. Ischemic regions showed imparied vasomotor reactivity to 5% CO2 or 100% O2 inhalation. After surgery, mean hemispheric F1 values increased + 12.8% on the by-pass side and + 10.5% on the contralateral side. Mean F1 increases reached a maximum 3 months after by-pass, most evident in ipsilateral frontal regions (+ 24.2%). Vasomotor reactivity did not significantly improve. Medically treated cases did not show similar F1 increases. Thirteen with carotid occlusive disease (8 with TIAs, 5 with small recent infarcts) underwent CT LCBF and L lambda measurements before and after STA-MCA by-pass. Cases with recent infarcts showed reduced LCBF and L lambda values which increased significantly after STA-MCA by-pass, however the total group operated upon showed only trends for CBF increases, probably due to large standard deviations encountered in serial measurements.
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PMID:Redistribution of cerebral blood flow following STA-MCA by-pass in patients with hemispheric ischemia. 714 91

Inositol 1,4,5-trisphosphate (IP3) has recently been known to play vital roles as one of the second messengers to control intracellular metabolism of calcium ion. Therefore, alterations of IP3 receptor binding and local cerebral blood flow (1CBF) were evaluated at 6 hours after occlusion of the right common carotid artery in the gerbil brain. The autoradiographic method developed in our laboratory enabled us to measure both parameters in the same brain. Animals attaining more than 5 in their ischemic scores, which were assessed at 1 hour after the occlusion, were utilized. LCBF was measured by the 14C-iodoantipyrine method at the end of the experiment. After frozen brains were cut into serial slices on a cryostat, the IP3 receptor binding was evaluated in vitro by using 3H-inositol 1,4,5-trisphosphate as the ligand. LCBF fell below 10 ml/100 g/min in most of the cerebral regions on the occluded side. In contrast a significant reduction in IP3 binding was noted only in the hippocampus CA1 on the occluded side. The IP3 binding tended to decrease when the values of 1CBF were reduced below 20 ml/100 g/min in this region. These findings suggest that the selective alteration of IP3 receptor binding in the hippocampus CA1 may be closely associated with the selective vulnerability of this region to ischemia.
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PMID:[Alteration of inositol 1,4,5-trisphosphate receptor binding after 6-hour hemispheric ischemia in the gerbil brain]. 825 24

Using autoradiographic image-averaging strategies, we studied the relationship between local glucose utilization (LCMRglc) and blood flow (LCBF) in a highly reproducible model of transient (2-hour) middle cerebral artery occlusion (MCAO) produced in Sprague-Dawley rats by insertion of an intraluminal suture coated with poly-L-lysine. Neurobehavioral examination at 60 minutes after occlusion substantiated a high-grade deficit in all animals. In two subgroups, LCBF was measured with 14C-iodoantipyrine at either 1.5 hours of MCAO, or at 1 hour of recirculation after suture removal. In two other matched subgroups, LCMRglc was measured with 14C-2-deoxyglucose at 1.5 to 2.25 hours of MCAO, and at 0.75 to 1.5 hours of recirculation after 2 hours of MCAO. Average image data sets were generated for LCBF, LCMRglc, and the LCMRglc/LCBF ratio for each study time. Middle cerebral artery occlusion for 2 hours induced graded LCBF decrements affecting ipsilateral cortical and basal ganglionic regions. After 1 hour of recirculation, LCBF in previously ischemic neocortical regions increased by 40% to 200% above ischemic levels, but remained depressed, on average, at about 40% of control. By contrast, frank hyperemia was noted in the previously ischemic caudoputamen. Mean cortical LCBF values during MCAO correlated highly with their respective LCBF values after 1 hour of recirculation (R = 0.93), suggesting that post-ischemic LCBF recovery is related to the depth of ischemia. Despite focal ischemia, LCMRglc during approximately 2 hours of MCAO was preserved, on average, at near-normal levels; but following approximately 1 h of recirculation, LCMRglc became markedly depressed (on average, 55% of control in previously densely ischemic cortical regions). Regression analysis indicated that this depressed glucose utilization was determined largely by the intensity of antecedent ischemia. By pixel analysis, the ischemic core (defined as LCBF 0% to 20% of control) comprised 33% of the ischemic hemisphere, and the penumbra (LCBF 20% to 40%) accounted for 26%. The penumbra was concentrated at the coronal poles of the ischemic lesion and formed a thin shell around the central ischemic core. During 2 hours of MCAO, the LCMRglc/LCBF ratio within the ischemic penumbra was increased four-fold above normal (average, 179 umol/100 mL). In marked contrast, after approximately 1 h recirculation, this uncoupling had almost completely subsided. The companion study (Zhao et al., 1997) further analyzes these findings in relation to patterns of infarctive histopathology.
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PMID:Transient middle cerebral artery occlusion by intraluminal suture: I. Three-dimensional autoradiographic image-analysis of local cerebral glucose metabolism-blood flow interrelationships during ischemia and early recirculation. 939 26

The effects of hypothermia on production of nitric oxide (NO) in ischemic brain were investigated by using in vivo microdialysis. Male Wistar rats were randomly divided into three groups; saline-treated normothermic group (37 degreesC, n=6), 30 mg/kg N-nitro-l-arginine methyl ester(l-NAME)-treated normothermic group (n=6), and saline-treated hypothermic group (30 degreesC, n=6). Transient forebrain ischemia was produced by bilateral common carotid artery occlusion combined with hypotension (MABP=50 mmHg). Saline-treated normothermic animals resulted in a reduction of LCBF to 9% of baseline. Saline-treated hypothermic rats revealed the similar changes of LCBF. In contrast, l-NAME administration reduced the basal CBF to 85% of saline-treated group and to 8% after ischemia. NO products were decreased during ischemia and transiently increased after reperfusion in saline-treated groups. However, the increase of NO products after reperfusion was less significant in the hypothermia. l-NAME-treated group showed a constant reduction of NO production during ischemia and after reperfusion.
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PMID:Consecutive in vivo measurement of nitric oxide in transient forebrain ischemic rat under normothermia and hypothermia. 976 79