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

An experimental test was performed to determine whether superoxide dismutase, an oxygen-free radical scavenger, reduces neurological dysfunction after transient global cerebral ischaemia. Three groups of 13 rats each were used. Group 1 served as normal controls. Groups 2 and 3 were subjected to transient global cerebral ischaemia. Before ischaemia, the right carotid bifurcation was isolated and the right external carotid artery was retrogradely cannulated, with the catheter tip positioned near the origin of the internal carotid artery. Once global cerebral ischaemia was complete, either isotonic saline (group 2) or superoxide dismutase solution (group 3) was injected through the above-mentioned catheter, before, during and after reperfusion. Consequently, the injected solutions were distributed through the circle of Willis to all of the ischaemic brain tissue. Somatosensory evoked potentials were registered in the three groups of animals and were used as a measure of neuronal function. In control animals (group 1) mean P1 latency was 8.1 msec and while the mean P1 latency was 11.9 msec in the isotonic saline treated animals (group 2), it was reduced to 8.8 msec in rats treated with the superoxide dismutase solution (group 3). P1 latency was significantly higher in group 2 than in groups 1 and 3 (P less than 0.001). As evaluated by somatosensory evoked potentials, we have concluded that the intra-arterial injection of superoxide dismutase to the ischaemic tissue improves neuronal function in rats subjected to transient global cerebral ischaemia.
Neurol Res 1991 Sep
PMID:Prevention of cerebral ischaemic reperfusion injury by intra-arterial administration of superoxide dismutase in the rat. 168 23

Excessive activity or release of excitatory amino acids has been implicated in the neuronal injury that follows transient cerebral ischemia. To investigate the metabolism of the endogenous excitotoxin, quinolinic acid, and its potential for mediating cell loss following ischemia, the concentrations of quinolinic acid, L-tryptophan, 5-hydroxytryptamine, and 5-hydroxyindoleacetic acid were quantified in gerbil brain regions at different times after 5 or 15 min of ischemia induced by bilateral carotid artery occlusion. Significant elevation of brain tryptophan levels, accompanied by increased 5-hydroxyindoleacetic acid concentrations, occurred during the first several hours of recirculation, but regional brain quinolinic acid concentrations were found either to decrease or remain unchanged during the first 24 h after the ischemic insult. However, significant increases in quinolinic acid concentrations occurred in striatum and hippocampus at 2 days of recirculation after 5 min of ischemia. After a further 4 and 7 days, strikingly large increases in quinolinic acid concentrations were observed in all regions examined, with the highest levels observed in the hippocampus and striatum, regions that also show the most severe ischemic injury. These delayed increases in brain quinolinic acid concentrations are suggested to reflect the presence of activated macrophages, reactive astrocytes, and/or microglia in vulnerable regions during and subsequent to ischemic injury. While the results do not support a role for increased quinolinic acid concentrations in early excitotoxic neuronal damage, the role of the delayed increases in brain quinolinic acid in the progression of postischemic injury and its relevance to postischemic brain function remain to be established.
J Cereb Blood Flow Metab 1990 Sep
PMID:Delayed increases in regional brain quinolinic acid follow transient ischemia in the gerbil. 169 82

We tested the efficacy of preischemic and postischemic systemic treatment with 30,000 units polyethylene glycol-conjugated superoxide dismutase in a reperfusion model of focal cerebral ischemia. Forty-one anesthetized cats underwent 2 hours' occlusion of the left middle cerebral artery and both common carotid arteries followed by 4 hours of reperfusion. Cats were blindly assigned to one of three groups: treatment with vehicle (10% polyethylene glycol in saline, n = 17), pretreatment with drug 3 hours before ischemia (n = 12), and posttreatment with drug at the time of reperfusion (n = 12). Size of the ischemic injury was calculated from 2,3,5-triphenyltetrazolium chloride staining. Injury in the caudate nucleus was significantly reduced with pretreatment (28 +/- 6% of ipsilateral caudate volume, mean +/- SEM) compared with the vehicle (56 +/- 8%). Posttreatment did not significantly ameliorate caudate injury (46 +/- 10%). Between the first and second hours of ischemia ipsilateral caudate blood flow determined using microspheres increased significantly from 11 +/- 4 to 16 +/- 5 ml/min/100 g with pretreatment, but blood flow remained constant throughout ischemia with vehicle (8 +/- 2 ml/min/100 g) and posttreatment (10 +/- 3 ml/min/100 g). The size of cortical injury (vehicle, 17 +/- 5%; pretreatment, 11 +/- 3%; posttreatment, 17 +/- 5% of hemispheric volume) did not differ significantly among groups. Somatosensory evoked potential recovery did not differ among groups. We conclude that pretreatment with conjugated superoxide dismutase can ameliorate the extent of injury in an end-artery region, such as the caudate nucleus, in a reperfusion model of focal ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1991 Sep
PMID:Conjugated superoxide dismutase reduces extent of caudate injury after transient focal ischemia in cats. 171 62

Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia. MAP2 immunoreactivity decreased significantly by 1 h in the subiculum-CA1 and CA2 areas which correspond to reactive change, while no decrease was observed in CA1 until day 4. Before the initiation of delayed neuronal death, MAP2 immunoreactivity was not changed in CA1. On the other hand clathrin immunoreactivity increased in the pyramidal cell layer of CA1 by 3 h after ischemia and remained high for 2 days. Clathrin immunoreactivity in the pyramidal cell layer of CA1 diminished after delayed neuronal death. The transient change of clathrin was noted especially in CA1 in the period prior to delayed neuronal death. These results imply an abnormal change in clathrin turnover after ischemia, which may participate in the pathogenesis of delayed neuronal death.
Brain Res 1991 Sep 27
PMID:An immunohistochemical study of MAP2 and clathrin in gerbil hippocampus after cerebral ischemia. 172 31

In subarachnoid hemorrhage (SAH) late cerebral ischemia may develop without significant visible narrowing of arteries at angiography, but in severe ischemic conditions "vasospasm" invariably seems to be present. The majority of patients with aneurysm rupture develop some degree of vasospasm, whereas relatively few suffer from ultimate brain infarction. The prophylactic use of the calcium antagonist Nimodipine is linked to a beneficial anti-ischemic effect in SAH, although narrowing of large bore arteries still seems to develop despite administration of this drug. Attenuation of vascular spasm, mainly in the arterioles has been implicated as the major mechanism of action, although a neuronprotective effect of Nimodipine has been suggested as well. The present paper presents fragmentary evidence that Nimodipine does elicit a vasoactive response in the cerebral vasculature early during the development of late cerebral vasospasm, and that this response seems closely linked to reversal of attendant ischemic symptoms.
Neurochirurgia (Stuttg) 1991 Sep
PMID:Nimodipine evoked dilation of cerebral arteries early during the development of late vasospasm in subarachnoid hemorrhage. 174 23

Previous studies have demonstrated that the xanthine compound, propentofylline, has beneficial effects in models of cerebral ischemia and can enhance some and exhibit other effects of adenosine. We investigated the in vitro effects of propentofylline and its hydroxy metabolite, A72,0287, on the binding of [3H]cyclohexyladenosine ([3H]CHA), [3H]2-[p-(2-carbonyl-ethyl)-phenylethyl-amino]-5'-N- ethylcarboxamido adenosine ([3H]CGS 21680) and [3H]nitrobenzylthioinosine ([3H]NBMPR) to adenosine A1 and A2 receptors and NBMPR-sensitive nucleoside transporters, respectively, in 10-microns coronal rat brain sections. Both xanthines had micromolar affinity for each of these sites with approximately 10-fold lower affinity for A2 receptors than for A1 receptors and [3H]NBMPR binding sites. Saturation analysis of [3H]CHA or [3H]CGS 21680 binding in the presence of increasing concentrations of propentofylline produced significant increases in KD values without affecting Bmax values; thus propentofylline is a competitive inhibitor at A1 and A2 receptors. The effects on A2 receptors apparently require higher concentrations (Ki approximately 200 microM) than the effects on A1 receptors (Ki approximately 20 microM). Propentofylline was also found to be a competitive inhibitor of [3H]NBMPR binding. Therefore we conclude that propentofylline interacts with adenosine-responsive systems to increase interstitial adenosine concentrations and to selectively inhibit A1 receptors.
Eur J Pharmacol 1991 Sep 24
PMID:Effects of propentofylline on adenosine A1 and A2 receptors and nitrobenzylthioinosine-sensitive nucleoside transporters: quantitative autoradiographic analysis. 174 57

The lipid peroxidation inhibitors U74006F (21-[4-(2,6-di-1-pyrrolidinyl-4-pyrimidinyl)-1-piperazinyl]-16 alpha-methylpregna-1,4,9]-(11)-triene-3, 20-dione) and U74512E (21-[4-(3-ethylamino-2-pyridinyl)-1-piperazinyl]-16 alpha-methylpregna- 1,4,9]-(11)-triene-3,20-dione) were tested for cerebroprotective properties in the rat. Focal cerebral ischemia was induced by irreversible occlusion of the middle cerebral artery (MCA-O). The 21-aminosteroids U74006F (1 mg/kg or 10 mg/kg, i.p.) and U75412E (1 mg/kg or 30 mg/kg, i.p.) were injected 30 min prior and 2, 6, and 24 h after MCA-O. The higher doses of U74006F or U75412E caused reductions in cortical infarct size ranging from 28 to 34%. The data suggest the 21-aminosteroids to be mildly effective after irreversible occlusion of the MCA but possibly to be more beneficial as part of a combined drug therapy in conjunction with Ca2+ or NMDA antagonists.
Brain Res 1991 Sep 27
PMID:The effects of two 21-aminosteroids on overt infarct size 48 hours after middle cerebral artery occlusion in the rat. 176 Jul 23

Intracellular pH was determined by neutral red color histophotometry in cerebral tissue from rats subjected to 10 minutes of cardiac arrest and from rats that had recovered for 1 and 6 hours following 8-10 minutes of total cerebral ischemia (TIA). Tissue concentrations of ATP, lactate and glucose were measured corresponding to the pH determinations. As expected, tissue ATP was depleted while tissue lactate was markedly elevated after 10 minutes of ischemia without reflow in the cerebral cortex, striatum and hippocampus. However, both metabolites were near control following 1 and 6 hours of recovery in all three regions. Tissue glucose was not significantly different from control following 1 and 6 hours of reperfusion. During ischemia, the intracellular pH dropped to 6.5-6.7 in all three regions (p less than 0.05). But, since the initial pH of the hippocampus was 7.79 while that of the cerebral cortex and striatum was approximately 7.02, the net drop in pHi the hippocampus was greater than in the other two regions. Following 1 hour of reperfusion, a trend towards tissue alkalosis was observed in the cerebral cortex and striatum.
Metab Brain Dis 1991 Sep
PMID:Regional changes in intracellular pH determined by neutral red histophotometry and high energy metabolites during cardiac arrest and following resuscitation in the rat. 177 24

The effect of nitrendipine, an antihypertensive calcium antagonist, on the impairment of cerebral blood flow and EEG observed after 10-min complete cerebral ischemia in anesthetized rabbits was compared with those of nicardipine. The ischemia was produced by neck tourniquet in combination with hypotension (50-60 mmHg). Blood flow was measured by hydrogen-clearance method. Transient reactive hyperemia was observed immediately after the cessation of ischemic procedure, and was followed by a decrease in blood flow in the range of 58-73% of corresponding basal values in the total brain, cortex and thalamus. The postischemic decrease in blood flow was suppressed when nitrendipine (0.3-1 mg/kg) or nicardipine (3-10 mg/kg) was given intraduodenally before ischemia. The postischemic decrease in total intensity and frequency index in EEG recovered rapidly when nitrendipine was pretreated, whereas the recovery of EEG parameters was not obtained by the nicardipine pretreatment. These results suggest that the effect of nitrendipine and nicardipine on the postischemic cerebral blood flow may be due to the inhibition of calcium-induced contraction in cerebral vessels, whereas the discrepancy between the effects of these agents on EEG may not be due solely to the improvement in cerebral circulation. Furthermore, the improvement in postischemic cerebral energy metabolism was confirmed by nitrendipine pretreatment (0.3 mg/kg).
Tohoku J Exp Med 1991 Sep
PMID:Nitrendipine facilitates recovery of cerebral blood flow, EEG and metabolites following cerebral ischemia in anesthetized rabbits. 179 73

We investigated 100 consecutive cerebral ischemia patients for hemorheological alterations. We measured whole and adjusted blood viscosity at 75 and 1,500 sec-1, plasma viscosity, red blood cell aggregation by the zeta sedimentation ratio, and red blood cell deformability using the centrifugal deformability technique. Patients were studied within 72 hours of the acute ischemic event, and 66 were available for follow-up evaluation approximately 2 months later. Two age- and sex-matched control groups were evaluated: 20 nonvascular neurological inpatients (patient controls) and 45 normal volunteers (normal controls). Compared with normal controls, we found significant acute increases in whole blood viscosity (1,500 sec-1), plasma viscosity, fibrinogen concentration, and zeta sedimentation ratio; the latter two variables were also increased at follow-up. Fibrinogen concentration was significantly associated with zeta sedimentation ratio and plasma viscosity and was increased for patient controls. There was a trend toward normalization of acute abnormalities over the 2-month follow-up period, and patients with more severe strokes tended to have more extensive hemorheological abnormalities. Among patients with severe stroke, fibrinogen concentration was significantly associated with the platelet activation peptide beta-thromboglobulin acutely (r = 0.63, p less than 0.005). We conclude that hemorheological abnormalities in cerebral ischemia are largely nonspecific findings, with the likely exception of patients with severe stroke.
Stroke 1991 Sep
PMID:Hemorheological factors in cerebral ischemia. 183 61


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