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

Bilateral Clamping of both Carotid Arteries (BCCA) in normotensive rats is known to cause a transient reduction in cerebral blood flow. Using in vivo trans-striatal microdialysis and HPLC/ECD we measured the release of dopamine and DA-metabolites under these oligemic conditions. BCCA caused a substantial stimulation of striatal DA-release (40-fold) and a decrease of the outflow of DA-metabolites. The elevated DA-release returned to baseline levels before the onset of reperfusion. Upon reperfusion, DA-metabolites rose above their initial baseline values. Trans-striatal administration of glutamate-diethylester (GDEE, 10 mM) attenuated the oligemia-induced DA-release. A sudden reduction of blood flow appears to disrupt the compartmentation of dopamine in striatal dopaminergic nerve endings in a similar but more moderate manner as compared to ischemia.
 ...
PMID:Effect of transient reduction of cerebral blood flow in normotensive rats on striatal dopamine-release. 769 Feb 31

Cerebrolysin (FPF1070) is an extract from pig brain obtained after enzymic digestion, containing free amino acids (85%) and low-molecular weight amino acid sequences (15%). We studied FPF 1070 to determine its ability to protect against delayed neuronal death in the gerbil when administered before and after ischemia. Transient forebrain ischemia was produced by occluding both common carotid arteries. Morphological changes in the CA1 sector of the hippocampus were evaluated 4 days after 5 min. occlusion. The formation of hydroxyl radicals in the postischemic (15 min. occlusion) reperfused (2 min.) brain was measured with HPLC using salicylate (SA). SA reacts with hydroxyl radicals and yields 2,3- and 2,5-dihydroxybenzoic acid (2,3- and 2,5-DHBA), which can be detected by HPLC-ECD. Gerbils treated with FPF 1070 revealed significant protection of CA1 neurons when it was applied 2 hrs before the occlusion. In contrast, no clear beneficial effects were observed when FPF 1070 was administered immediately after the recirculation. Concentrations of 2,3- and 2,5-DHBA after reperfusion increased significantly compared to the basal levels both in the hippocampus and cerebral cortex. The 2,5-DHBA contents in the postischemic reperfused brain was significantly reduced when FPF 1070 was administered 2 hr. before the occlusion. The administration of dimethylsulfoxide (DMSO), a hydroxyl radical scavenger, prevented ischemia-reperfusion-induced delayed neuronal death, and significantly reduced the 2,5-DHBA content after reperfusion. The results indicated that hydroxyl radicals are produced in the postischemic-reperfused brain and that hydroxyl radical scavenging action of FPF 1070 played an important role in preventing delayed neuronal death.
 ...
PMID:[Protective effect of FPF 1070 (cerebrolysin) on delayed neuronal death in the gerbil--detection of hydroxyl radicals with salicylic acid]. 833 17

Three patients with subacute ischemic cerebral infarction examined by SPECT with 99mTc-ECD and PET within the same day showed signs of luxury perfusion in the subacute phase, which is between 9 to 20 days after the onset. A 99mTc-HMPAO SPECT study was also performed within 2 days of the ECD-SPECT study. ECD-SPECT images of three patients displayed a focal decreased uptake in the infarcted lesions, while in infarcted foci, there was almost equivalent or increased CBF compared to normal and unaffected areas, decreased CMRO2, and high HMPAO uptake. The ECD-SPECT results were similar to those of CMRO2 rather than CBF, though the HMPAO-SPECT image was similar to that of CBF. In one patient, HMPAO images revealed hyperfixation of the tracer. In the chronic phase and in the acute phase before 5 days after the onset, there were no discrepancies among the ECD-SPECT, CBF, HMPAO-SPECT, and CMRO2 images. These observations indicated that 99mTc-ECD is a good indicator of damaged brain tissues in subacute ischemic infarction. They also suggested that 99mTc-ECD is a potential agent with which to evaluate cerebral tissue viability in some pathological states of cerebrovascular disease. The characteristics may be suitable for confirming the effects of thrombolytic therapy in acute ischemia, because these conditions often show signs of luxury perfusion when the therapy is successful.
 ...
PMID:Discrepant 99mTc-ECD images of CBF in patients with subacute cerebral infarction: a comparison of CBF, CMRO2 and 99mTc-HMPAO imaging. 853 92

We have examined the neuroprotective efficacy of the selective dopamine (DA) D2/D3 receptor agonist pramipexole in two models of nigrostriatal (NS) degeneration. The first involves the delayed (28-day) postischemic retrograde NS degeneration that takes place in gerbils following a 10-min episode of bilateral carotid arterial occlusion-induced forebrain ischemia. In vehicle (40% hydroxypropyl cyclodextrin)-treated male gerbils, there was a 40-45% loss of NS cell bodies in the pars compacta and pars reticulata (TH immunohistochemistry and Cresyl violet histochemistry) by 28 days after ischemia/reperfusion. Daily postischemic oral dosing (1 mg/kg p.o., b.i.d., beginning at 1 h after insult) decreased the 28-day postischemic loss of NS DA neurons by 36% (P < 0.01 vs. vehicle-treated). The effect was specific for dopamine neurons since no significant salvage of hippocampal CA1 neurons was observed. In a second model, pramipexole's effects were examined on methamphetamine-induced (10 mg/kg, i.p. X 4, each 2 h apart) NS degeneration in male Swiss-Webster mice. In vehicle-treated mice, there was a 40% loss of NS neurons by day 5. In contrast, pramipexole dosing (1 mg/kg, p.o., 1 h after the last methamphetamine dose, plus daily) attenuated the NS degeneration from 40% to only 8% (P < 0.00001 vs. vehicle). We postulated that pramipexole acts in both of these models to reduce the elevated DA turnover and the associated elevation in hydroxyl radical production secondary to increased MAO activity that could be responsible for oxidative damage to the NS neurons. Indeed, in the gerbil ischemia model, we documented by HPLC-ECD a 135% postreperfusion increase in DA turnover (DOPAC + HVA/DA) at 5 min after reperfusion. Pramipexole at the 1 mg/kg, p.o., dose level was able to significantly reduce the increased DA turnover, but by only 16%. Thus, it is conceivable that other mechanisms may also contribute to pramipexole's dopaminergic neuroprotection. Based on a preliminary examination of pramipexole's oxidation potential, it appears that the compound may possess significant intrinsic antioxidant properties that might contribute to its neuroprotective effects.
 ...
PMID:Neuroprotective effects of the dopamine D2/D3 agonist pramipexole against postischemic or methamphetamine-induced degeneration of nigrostriatal neurons. 911 24

The aim of this study was to define the accuracy of 99mTc-ethyl cysteinate dimer-single photon emission computed tomography (99mTc-ECD-SPECT) in distinguishing transient ischemic attack from completed ischemic stroke at early stages after the onset of symptoms. In a prospective study we examined 82 patients within 6 hours after the onset of symptoms (neurologic deficit caused by middle cerebral artery ischemia) using both 99mTc-ECD-SPECT and computed tomography (CT). The follow-up was based on Scandinavian Stroke Scale (SSS) 24 hours and 5-7 days, as well as on CT 7 days, after the event. SPECT evaluation was performed both visually and using semiquantitative region-of-interest (ROI) analysis. According to visual SPECT analysis, on admission 59 of 82 patients had activity deficits in the symptomatic hemisphere. After 7 days, all these patients had neurologic symptoms (SSS 28 +/- 12 points), caused by a cerebral infarction as evidenced with CT. Twenty-three of 82 patients displayed no early activity deficit despite clinical symptoms. None of these patients had neurologic symptoms after 7 days (indicating transient ischemic attack or prolonged reversible ischemic neurologic deficit). In the semiquantitative SPECT analysis, all patients had abnormal count densities in the respective ROI (activity < 90% compared with the contralateral side). All patients with transient ischemia (n = 23) had count rate densities more than 70% of the respective contralateral ROI, whereas all patients with subsequent infarction (n = 59) had values < 70%. Use of 99mTc-ECD-SPECT allows transient ischemia to be distinguished from ischemic infarction using relative regional activity thresholds within the first 6 hours after onset of symptoms.
 ...
PMID:Differentiation between transient ischemic attack and ischemic stroke within the first six hours after onset of symptoms by using 99mTc-ECD-SPECT. 970 54

DOPA itself is a neuromodulator in striata. In rat striata, DOPA by itself released neuronal glutamate in slices and caused cell death via glutamate release in cultured fetal neurons, suggesting involvement of DOPA in an upstream process of mechanisms for in vivo neuronal cell death. We attempted to clarify whether or not this idea is truly the case in conscious Wistar rats. Four vessels were occluded for 10 min during microdialysis of striata. DOPA, dopamine and glutamate in perfusates collected every 10 min were measured by HPLC-ECD and spectrophotometer. Delayed neuronal cell death in striata and hippocampus was evaluated 96 hr after ischemia. DOPA was indeed evoked with dopamine and glutamate during and after ischemia, and peak increases by respective 6-, 210- and 8-fold of a basal level were seen at the fraction immediately after ischemia. Delayed neuronal cell death was slight to moderate in striata and severe in hippocampus. Intrastriatal perfusion of NSD-1015, a central DOPA decarboxylase inhibitor, at 30 microM 10 min before ischemia, markedly increased DOPA and glutamate release by ischemia with slight inhibition of dopamine release and exaggerated delayed neuronal cell death in striata. Meanwhile, intrastriatal perfusion of DOPA cyclohexyl ester (DOPA CHE) at 10-100 nM, a novel stable potent competitive DOPA antagonist, antagonized dose-dependently increases in glutamate release by ischemia without modification of dopamine release. DOPA CHE at 100 nM protected striatal neurons from delayed cell death. Hippocampal neuronal cell death was neither affected by NSD-1015 nor by DOPA CHE. Endogenously released DOPA itself seems to act on its recognition site and to be a causal factor for increase in glutamate release and resultant delayed neuronal cell death by transient ischemia in rats.
 ...
PMID:[Is endogenously released DOPA itself an upstream factor for increase in glutamate release and delayed neuronal cell death induced by transient ischemia in rats?]. 1019 Jan 42

Two patients with a cerebral embolism were evaluated by using both 99mTc-ethyl cysteinate dimer (ECD, or Bicisate) and 99mTc-hexamethylpropyleneamine oxime (HMPAO) single-photon emission computed tomography (SPECT). In one patient, 99mTc-ECD SPECT images revealed hypoactivity in a reflow hyperemic area where an infarct was seen later on CT scans. In another patient, a reperfused area showed hyperactivity on 99mTc-ECD SPECT without any abnormality on follow-up CT. 99mTc-ECD represents a potential agent with which to evaluate cerebral tissue viability in early reperfusion after ischemia.
 ...
PMID:99mTc-bicisate and 99mTc-HMPAO SPECT imaging in early spontaneous reperfusion of cerebral embolism. 1031 73

Cerebral infarct due to embolic stroke without recanalization was examined by cerebral blood flow (CBF) SPECT in the early acute stage, and the possibility of predicting the size it will reach in the later stages was evaluated. Twenty patients (67 +/- 13 years) were examined by CBF SPECT with 99mTc-ECD 4.5 +/- 3.1 hours after the onset of cardiogenic cerebral embolism. The ratio of the anteroposterior length of the cerebral hemisphere to that of the severe ischemic region, which was defined as an area of clear-cut severe reduction in CBF as observed by SPECT, was calculated. One week after the onset, the cerebral infarct was measured in the same manner by CT, and the relationship between the two measurements was evaluated. The CBF in the region of severe ischemia and the surrounding region was determined by the Patlak plot method, and the affected/non-affected (A/NA) ratio was calculated. In severe ischemic regions the CBF ranged from 1.7 ml/100 g/min to 20 ml/100 g/min (mean, 11 +/- 5 ml/100 g/min), whereas the A/NA ratio ranged from 4% to 45% (mean, 26 +/- 11%). On the other hand, the CBF in the surrounding regions ranged from 20 ml/100 g/min to 52 ml/100 g/min (mean, 34 +/- 8 ml/100 g/min) whereas the A/NA ratio ranged from 52% to 104% (mean, 77 +/- 11%). The coefficient of correlation between the infarct size predicted by SPECT and that measured by CT was r = 0.986, and the correlation equation was Y = 1.047X - 2.969. CBF SPECT performed in the early acute stage can be used to predict the size of cerebral infarct.
 ...
PMID:Prediction of cerebral infarct sizes by cerebral blood flow SPECT performed in the early acute stage. 1051 Aug 74

We have previously obtained evidence that DOPA is probably involved in an upstream process of mechanisms for in vivo neuronal cell death in striatum. We attempted to clarify whether or not this is also the case in hippocampal region of conscious Wistar rats. Four vessels were occluded for 5 min during microdialysis of hippocampus. DOPA, dopamine and glutamate (Glu) in perfusates collected every 10 min were measured by HPLC-ECD and spectrophotometer. Delayed neuronal cell death in hippocampus was evaluated 96 hr after ischemia. Five-min transient brain ischemia induced Glu release, with the peak being 2.5-fold of a basal release at the fraction immediately after ischemia. The release of DOPA and dopamine was not consistently detectable, but an increase was sometimes observed during and after ischemia. Delayed neuronal cell death was slight to moderate with 5-min ischemia. Intrastriatal perfusion of DOPA cyclohexyl ester (DOPA CHE) at 100 nM, a novel stable potent competitive DOPA antagonist, almost completely inhibited the ischemia-induced glutamate release, and protected hippocampal neurons from delayed cell death. Endogenously released DOPA itself seems to act on its recognition site and to behave as a causal and/or deteriorating factor on glutamate release and resultant delayed neuronal cell death by transient ischemia in rats.
 ...
PMID:[A DOPA antagonist, DOPA cyclohexyl ester inhibits transient brain ischemia-induced release of glutamate and delayed neuronal cell death in striatal and hippocampal region of in vivo rats]. 1062 77

The aim of this study was to investigate the prognostic utility of post-treatment technetium-99m ethyl cysteinate dimer (99mTc-ECD) single-photon emission tomography (SPET) for predicting ischemic tissue outcome in cases involving embolic middle cerebral artery occlusion treated with local intra-arterial thrombolysis. We examined twenty-five patients with a moderately ischemic area determined using pretreatment technetium-99m hexamethylpropylene amine oxime (99mTc-HMPAO) SPET, and with complete recanalization within 6 h. Post-treatment 99mTc-ECD SPET studies, consisting of scanning for 0.5-6.5 min (early scan) and 15-21 min (delayed scan) after tracer injection, were performed immediately after thrombolysis. The extent of the affected area outlined on pretreatment 99mTc-HMPAO SPET was used for the post-treatment early and delayed 99mTc-ECD SPET images, and the AR/CE ratio (ratio of affected regional activity to cerebellar activity) was calculated. The washout index of 99mTc-ECD in the affected area was also calculated by dividing the difference between the AR/CE ratio in the early and delayed images by the AR/CE ratio in the early image. Twelve patients without infarction or with small subcortical/basal ganglial infarction, ten with medium or large cortical infarction, and three with hemorrhage were identified by follow-up computed tomography. Although the AR/CE ratio in post-treatment early 99mTc-ECD SPET images was significantly higher in the hemorrhagic group than in the cortical infarction group, this value did not differentiate the reversible ischemia group from either the cortical infarction or the hemorrhagic group. The AR/CE ratio in post-treatment delayed 99mTc-ECD SPET images statistically differentiated the reversible ischemia group from both the cortical infarction and the hemorrhagic group. However, the difference between the cortical infarction and hemorrhagic groups was not statistically significant. The washout index of 99mTc-ECD statistically differentiated all three groups. This study demonstrated that a combination of early and delayed 99mTc-ECD SPET imaging performed immediately after thrombolysis predicts ischemic tissue outcome.
 ...
PMID:Combination of early and delayed SPET imaging using technetium-99m ethyl cysteinate dimer immediately after local intra-arterial thrombolysis. 1135 1


1 2 3 Next >>