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)

The authors report 31 cases of "vascular epilepsy" among 280 cerebral strokes confirmed by cranial computerized tomography. A high incidence of ischemia (28 cases : 90%) is noted. Epileptic seizures are initial (14 cases) or sequellar (17 cases) manifestations of cerebral stroke. Partial seizures are the most frequent (58%), particularly "Jacksonian" motor fits, which, when initial, often lead to status epilepticus. Frequency and bad prognosis of initial status epilepticus are pointed out.
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PMID:[Vascular epilepsy: clinical, electroencephalographic, and computerized tomographic aspects (author's transl)]. 626 3

The Hypoxic-Ischemic Encephalopathy (HIE) is a severe illness of the unborn, respectively of the newborn. About 90 percent of the causes occur in utero, about 10 percent after birth. The risk for HIE arises from anatomical and pathophysiological particularities: little overlapping between the great cerebral arteries, poor periventricular vascularisation, and a loss of the autoregulation of cerebral blood flow during asphyxia. Most important is the early detection of intrauterine asphyxia. After birth the general measures include: thermoneutral temperature, oxygenation, normal pCO2, regular blood pressure monitoring, glucose infusion, therapy of convulsions and of an inherent brain edema. After birth the five most common clinical settings in which HIE occurs, are: postpartum asphyxia, PFC, septic shock, pneumothorax and apneas. Therapeutic measures (e.g. volume therapy) have to be prompt but subtle, to prevent ischemia, avoiding overtherapy with its risk of intracranial hemorrhage.
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PMID:[Hypoxic-ischemic encephalopathy. Clinical considerations]. 643 98

Free arachidonic acid is released rapidly in the brain at the onset of ischemia and during convulsions. The transient nature of this phenomenon indicates the existence of an active reacylation system for this fatty acid, likely an arachidonoyl-CoA synthetase-arachidonoyl transferase. The first of these enzymatic activities in brain microsomes was studied and it was found that [1-14C]arachidonic acid is rapidly activated and shows an absolute requirement for ATP and CoA. MgCl2 enhances this activity 10-fold. The optimum pH is 8.5, and the apparent Km values for the radiolabeled substrate, ATP, CoA, and MgCl2 are 36, 154, 8, and 182 microM, respectively. The apparent Vmax is 32.4 nmol/min/mg protein for arachidonic acid. The presence of Triton X-100 (0.1%) in the assay medium caused a significant reduction in apparent Km (9.4 microM) and Vmax (25.7 nmol/min/mg protein) values. The enzymatic activity is thermolabile with a T1/2 of less than 1 min at 45 degrees C and a maximal activity at 40 degrees C. The breaking point or transition temperature is 25 degrees C in an Arrhenius plot. The activation energies were 95 kJ/mol from 0 to 25 degrees C and 30 kJ/mol from 25 to 40 degrees C. Fatty acid competition studies showed inhibition by unlabeled docosahexaenoic and arachidonic acids with a Ki of 31 and 37 microM, respectively, in the absence and 18 and 7.7 microM in the presence of Triton X-100. Palmitic acid and oleic acid slightly inhibited the reaction whereas linoleic acid inhibited it to a moderate extent. It is concluded that this very active enzyme can activate arachidonic acid as well as docosahexaenoic acid in brain microsomes. In addition, this reaction may be involved in regulating the pool size of these free fatty acids in brain by rapid removal through activation, thus limiting eicosanoid formation. Moreover, the rapid formation of polyenoic acyl-coenzyme A may participate in the retention of essential fatty acids in the central nervous system.
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PMID:Kinetic properties of arachidonoyl-coenzyme A synthetase in rat brain microsomes. 663 46

This study examined the temporal profile of ischemic neuronal damage following transient bilateral forebrain ischemia in the rat model of four-vessel occlusion. Wistar rats were subjected to transient but severe forebrain ischemia by permanently occluding the vertebral arteries and 24 hours later temporarily occluding the common carotid arteries for 10, 20, or 30 minutes. Carotid artery blood flow was restored and the rats were killed by perfusion-fixation after 3, 6, 24, and 72 hours. Rats with postischemic convulsions were discarded. Ischemic neuronal damage was graded in accordance with conventional neuropathological criteria. Ten minutes of four-vessel occlusion produced scattered ischemic cell change in the cerebral hemispheres of most rats. The time to onset of visible neuronal damage varied among brain regions and in some regions progressively worsened with time. After 30 minutes of ischemia, small to medium-sized striatal neurons were damaged early while the initiation of visible damage to hippocampal neurons in the h1 zone was delayed for 3 to 6 hours. The number of damaged neurons in neocortex (layer 3, layers 5 and 6, or both) and hippocampus (h1, h3-5, paramedian zone) increased significantly (p less than 0.01) between 24 and 72 hours. The unique delay in onset of ischemic cell change and the protracted increase in its incidence between 24 and 72 hours could reflect either delayed appearance of ischemic change in previously killed neurons or a delayed insult that continued to jeopardize compromised but otherwise viable neurons during the postischemic period.
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PMID:Temporal profile of neuronal damage in a model of transient forebrain ischemia. 710 25

Syncope with and without convulsion was studied in unselected blood donors in a community blood center. Convulsive syncope occurred in 0.03% of all blood donors and was more commonly observed when nursing personnel were alerted to its possible occurrence. It was more common in men. Although tonic extensor spasm was the most common convwithout convulsion was studied in unselected blood donors in a community blood center. Convulsive syncope occurred in 0.03% of all blood donors and was more commonly observed when nursing personnel were alerted to its possible occurrence. It was more common in men. Although tonic extensor spasm was the most common convwithout convulsion was studied in unselected blood donors in a community blood center. Convulsive syncope occurred in 0.03% of all blood donors and was more commonly observed when nursing personnel were alerted to its possible occurrence. It was more common in men. Although tonic extensor spasm was the most common convulsive movement, other complex convulsive phenomena occurred, some simulating epileptic seizure. No statistical difference in changes of pulse or blood pressure was found between subjects with convulsive versus nonconvulsive syncope. Similarly, no difference was found between subjects with tonic spasm and those with other convulsive phenomena, nor between those with "early" and those with "delayed" reactions. Marked individual variation may exist in the susceptibility of the central nervous system to ischemia. Some individuals appear to be predisposed to development of seizures in situations of global cerebral ischemia such as occur in hypotension and bradycardia.
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PMID:Convulsive syncope in blood donors. 710 29

The authors report on 8 cases of full term neonates presenting, between the 8th and 72nd hours of life, with several often subintrant partial seizures, always in the same area for a given child. Pregnancy, delivery and the first hours of life had been normal. The first CT scan (performed a few hours to 3 days after the first fits) showed a triangular hypodensity with internal vertex, still observed at the second examination, with reduced dimensions and fuzziness of the edges. The features and localization, always in an elective arterial area, suggested an arterial infarction. The date of occurrence, the probably embolic nature and the etiology of such an arterial ischemia are discussed. The clinical, electric and CT-scan homogeneity of the picture is emphasized, as it makes diagnosis easy. Prognosis is relatively favorable among neonatal seizures states, except for possible intellectual and epileptic sequellae.
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PMID:[Ischemic cerebral softening in newborn infants. Possible etiology of neonatal convulsive states]. 716 62

Rhabdomyolysis caused 28 out of 903 (3.1%) of cases of severe acute renal failure (ARF) treated at Leeds General Infirmary over a 14-year period (1980-1993). The commonest cause of rhabdomyolysis was muscle compression, usually due to drug- or alcohol-induced coma. Other causes included fits, infection, acute limb ischemia, trauma, and heat stroke. Prognosis was relatively good, with a 78.6% survival rate and recovery of renal function to normal in all survivors who were followed up. The creatinine/urea ratio was higher in ARF due to rhabdomyolysis than in an unselected group of patients with other causes of ARF but not when the comparison was with sex- and age-matched controls with ARF. This suggests that this previously described feature of rhabdomyolysis simply reflects the increased muscle mass of a younger group of patients, rather than a specific effect of muscle damage. Clinical features of muscle damage were often absent and so the possibility of rhabdomyolysis should be considered in appropriate settings if the diagnosis is to be made early enough to administer treatment that may prevent ARF and the consequences of the compartment syndrome.
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PMID:The clinical and biochemical features of acute renal failure due to rhabdomyolysis. 756 17

At physiological and pharmacological doses, adenosine protects tissues against a varieties of injuries: ischemia-reperfusion, convulsions, inflammation.... We tested the hypothesis that the antiinflammatory properties of adenosine occur via a down-regulation of TNF. Agonists of adenosine receptors (ARA) and agents potentiating endogenous adenosine (APA) were evaluated for their effects on TNF production by endotoxin-stimulated human monocytes. Additionally, one of the most potent agonists, R-phenylisopropyladenosine (R-PIA), was tested on two experimental models of acute phase response, endotoxin shock and carrageenan-induced plantar oedema. Several ARA and APA inhibited monocyte TNF production in a concentration-dependent manner. R-PIA and other ARA were active at micromolar concentrations. The property is pharmacologically relevant since rats receiving a lethal dose of endotoxins were protected by R-PIA and endotoxin-induced serum TNF levels were abolished by a pretreatment with R-PIA. Inhibitory effects on serum TNF production were obtained with similar doses of dexamethasone sodium phosphate and one hundred-fold higher doses of pentoxifylline. R-PIA was also found active on carrageenan-induced oedema. The anti-oedematous properties of R-PIA were associated with a marked reduction of locally-produced TNF and were also observed after the administration of dexamethasone, pentoxifylline and a neutralizing anti-TNF antibody. Our results indicate that adenosine is a potent inhibitor of TNF production induced by different stimuli. This property could lead to therapeutic applications in inflammatory diseases and other in which TNF is known to play a pathogenic or aggravating role. Comparison between ARA and APA in terms of tolerance and efficacy merits further attention.
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PMID:[Activity of adenosine in relation to tumor necrosis factor (TNF). Therapeutic outlook]. 778 49

A comprehensive series of time-related behavioral, physiological and cerebral metabolic studies was conducted using conscious Sprague-Dawley rats to discern the anti-endothelin (ET) properties of the specific ETA receptor antagonist, FR139317. Endothelin-1 (9 pmol given by injection into one lateral ventricle, i.c.v.) produced convulsions, acute arterial hypertension, arterial hyperglycemia, and hyperventilation. Brain structures close to the i.c.v. site of injection, such as the caudate nucleus, lateral septal nucleus, corpus callosum and hippocampal CA3 medial lamellae, as well as 14 other individual structures, displayed moderate-to-intense levels of metabolic activation after endothelin. Data were assessed quantitatively by means of the autoradiographic [14C]deoxyglucose technique combined with image analysis. Neural circuits in the efferent projection paths of the stimulated forebrain structures, such as the midbrain oculomotor complex, amygdaloid nuclei, substantia nigra pars reticulata and caudal subicular subregions of the hippocampal formation, were stimulated focally by endothelin. Specific medullary nuclei and cerebellar cortical subregions displayed high rates of glucose metabolism following endothelin injection at the time of maximum behavioral and physiological stimulation. I.c.v. treatment with > or = 14 nmol FR139317 before endothelin significantly inhibited the effects produced by the peptide. At the highest dose of FR139317 (28 nmol), there was only mild behavioral stimulation following endothelin injection, and hypermetabolic responses in the brain were abolished except in two specific areas of the cerebellar cortex (approx 40% increases in metabolic activity in the copula pyramis and paramedian lobule). The results indicate that the cerebral stimulatory effects of i.c.v. endothelin are mediated by the A type of endothelin receptor. By itself, i.c.v. FR139317 had no effects on the parameters assessed. Further evaluation of FR139317 is warranted as a possible therapeutic agent for neuropathologies suspected of deriving from central neural or vascular stimulation by endothelin, such as aneurysmal vasospasm, ischemia, excitotoxicity, and peptide-mediated epilepsies.
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PMID:FR139317, a specific ETA-receptor antagonist, inhibits cerebral activation by intraventricular endothelin-1 in conscious rats. 786 51

To examine the possible role of endothelin and vasospasm in eclamptic seizures, we studied and analyzed the electroencephalograms (EEG) of endothelin-1 (ET-1)-treated pregnant, nonpregnant and sham control (dextrose-treated) rabbits. After multiple intravenous bolus injections of ET-1 (500 pmol/kg) or 5% dextrose in the rabbits, we recorded EEG directly from the brain cortex and analyzed by Fast Fourier Transform (FFT). Water content was measured in the brain of all groups (n = 7). Repeated seizures occurred in all of the pregnant and 2 of the nonpregnant rabbits by variable doses of ET-1. FFT analysis showed remarkable changes in frequency and power arrays characterized by mild to severe form of dysrhythmia, high-voltage spikes, high-voltage fast and slow waves after ET-1 injections. Water content was increased in brain mass in ET-1-treated rabbits (p = 0.001) suggesting an ET-1-induced edema. Histologically we confirmed that ET-1 caused ischemic changes in brain tissues. However, ET-1 induced more pronounced changes in behavior, EEG, brain edema or ischemia in pregnant than in nonpregnant groups. The injections of exogenous ET-1 into the brain substances were strongly suggested by immunohistochemical study with polyclonal antiendothelin antibody in brain tissue sections. Therefore, we assume that endothelin along with other vasoactive substances causes acute cerebral vasospasm and ischemia inducing EEG changes leading to ultimate clinical convulsions in eclampsia.
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PMID:Eclampsia-like seizures and electroencephalographic changes in pregnant rabbits with endothelin-1 injections. 789 Feb 45


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