Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 26,294 consecutive patients monitored in a comprehensive drug surveillance program, 1067 (4 per cent) received methyldopa for treatment of hypertension. Adverse reactions attributed to methyldopa were reported in 149 patients (14 per cent), the most frequent being hypotension. Life-threatening adverse effects were reported in nine patients (6 per cent of reactors)--the major problems being hypotension associated in several patients with signs of cardiac or cerebral ischemia. Hypotension attributed to methyldopa was more frequent in younger patients, in those with uremia, in lighter subjects, and in those receiving a high daily dose. Marked interaction between these factors was demonstrated and eightfold differences in the frequency of hypotension were observed in different sub-groups of methyldopa recipients. Adverse effects other than hypotension were reported infrequently and did not correlate well with the previously mentioned factors. The findings suggest that methyldopa therapy should be commenced cautiously in younger patients, in the non-obese, and in those with impairment of renal function as manifest by elevated blood urea nitrogen levels.
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PMID:Adverse reactions to methyldopa with particular reference to hypotension. 26 90

In five patients with chronic renal failure, rapid correction by dialysis of hypertension and/or high blood urea levels provoked acute neurological disorders, followed by slowly reversible neuropsychiatric disturbances. Focal EEG alterations were noted in three patients with normal carotid angiograms. Our cases differed from those usually described as suffering from the dialysis disequilibrium syndrome because of their duration, the severity of mental disturbances, and the asymmetrical pattern of EEG abnormalities. We propose that the symptoms observed could be due to cerebral ischemia. This possibility emphasizes the importance of limiting the duration and efficiency of the first dialyses in patients with severe hypertension and high nitrogen retention, especially if high performance dialyzers are used.
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PMID:Unusual aspects of the dialysis disequilibrium syndrome. 95 37

OPC-14117 is a potent drug which has both brain function activating effect and protective effect against cerebral ischemia. Occurrences of these effects might be expected due to superoxide dismutase-like activity of OPC-14117. The present study has been conducted to evaluate the active oxygen scavenging activity of OPC-14117 and to explain the mechanisms of its pharmacological activities. The reaction of OPC-14117 and superoxide anion, generated in potassium superoxide, was examined by electron spin resonance technique at both liquid nitrogen (77 K) and room (22 degrees C) temperatures. OPC-14117 showed a higher superoxide scavenging activity than that of alpha-tocopherol in an aprotic solvent system. The active moiety of OPC-14117 to provide the scavenging effect was found due to the phenolic hydroxyl group of its indan skeleton.
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PMID:Evaluation of superoxide scavenging activity of OPC-14117 by electron spin resonance technique. 166 73

The influence of etomidate on post-ischaemic cerebral metabolism was examined in 1-year-old male Wistar rats. Ten rats were randomly allocated to each of three groups. Group 1 animals received etomidate for 60 min without undergoing cerebral ischaemia. In Group 2, there was a 60-min recovery period following 15 min of complete cerebral ischaemia. Etomidate was administered to Group 3 animals after 15 min of ischaemia. At the end of the study period, the brains were frozen in situ using liquid nitrogen. The cortex was then biochemically analysed. Considering glycolysis as well as the citric-acid cycle, the pattern of metabolite changes with etomidate application was almost identical to the pattern of spontaneous recovery. The content of energy-rich phosphates was reduced when Groups 2 and 3 were compared with the non-ischaemia group, indicating previous depletion of energy reserves of brain tissue. However, the energy charge as a parameter of energy balance had already been returned to normal values. We conclude that post-ischaemic application of etomidate has no favourable effect on recovery after complete cerebral ischaemia in the rat.
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PMID:The influence of etomidate upon cerebral metabolites after complete brain ischaemia in the rat. 187 20

This experiment was designed to determine if nitrous oxide alters neurologic and pathologic outcome from temporary focal cerebral ischemia in spontaneously hypertensive rats deeply anesthetized with a barbiturate. Two groups of rats were given intravenous methohexital such that a stable EEG pattern of burst suppression was achieved. In one group of rats (n = 11), the lungs were mechanically ventilated with 70% N2O/30% O2, and in the other group (n = 10), ventilation was done with 70% nitrogen/30% O2. The middle cerebral artery was then occluded for 2 h, during which time mean arterial pressure, blood gases, hematocrit, plasma glucose, and head temperature were held constant between groups. The total doses of methohexital administered were similar in both groups as were the plasma methohexital concentrations immediately prior to onset of ischemia. After reperfusion of the middle cerebral artery, the animals were allowed to awaken. Neurologic evaluations were performed prior to ischemia and at 24 and 96 h postischemia. Cerebral infarct volume was measured at 96 h postischemia using triphenyl tetrazolium chloride staining and computer imaging techniques. There were no neurologic differences between the N2O and nitrogen groups at any experimental interval although both groups exhibited deficits at both 24 and 96 h postischemia relative to preischemic values. The two groups also had nearly identical cerebral infarct volumes (N2O = 231 +/- 97 mm3; nitrogen = 226 +/- 75 mm3; mean +/- SD).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitrous oxide does not alter infarct volume in rats undergoing reversible middle cerebral artery occlusion. 222 37

Xanthine oxidase (XO) has been implicated as a source of free radicals mediating ischemia-reperfusion injury. Conversion of the non-free radical generating xanthine dehydrogenase (XD) to the free radical producing XO during ischemia has been demonstrated in several tissues. We examined the irreversible conversion of XD to XO in the dog brain after ischemia and after ischemia and reperfusion. Under pentobarbital sodium anesthesia and by use of a cerebrospinal fluid compression model of global cerebral ischemia, dogs were subjected to 30 min of ischemia (n = 8) or 30 min of ischemia and 60 min of reperfusion (n = 8). A cerebral perfusion pressure of 60 mmHg was maintained during reperfusion. Eight control dogs were not subjected to ischemia. After the dogs were killed their brains were rapidly removed and frozen in liquid nitrogen. XO and XD + XO activities were measured with a radioassay utilizing 8-[14C]hypoxanthine and separating substrate and products by thin-layer chromatography. Total XD + XO activity was significantly (P less than 0.05) decreased after ischemia and reperfusion (35.6 +/- 8.0 vs. 60.8 +/- 20.8 nmol.min-1.g protein-1 in controls, means +/- SD) but not after ischemia alone (48.2 +/- 20.4). XO/(XD + XO) was approximately 20% in all three groups. Irreversible XD to XO conversion is not an important mechanism leading to early tissue injury in global cerebral ischemia.
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PMID:No conversion of xanthine dehydrogenase to oxidase in canine cerebral ischemia. 226 Jun 92

Arachidonic acid metabolites are postulated to play a role in the pathogenesis of cerebral ischemia. In order to test the development of lipoxygenase metabolites of arachidonic acid in cerebral ischemia, we measured free arachidonic acid and slow reacting substance of anaphylaxis (SRS-A) and leukotriene C4 in the brain tissue. Moreover, we studied the influence of inhibitor of SRS-A release on postischemic cerebral edema. Severe forebrain ischemia in rats was induced by the modification of the method described by Pulsinelli and Brierley. Both vertebral arteries were electrocauterized through the alar foramen and then bilateral common carotid arteries were clamped by aneurysmal clips and mean arterial pressure was reduced to 80-90 mmHg. EEG activity was isoelectric throughout the period of carotid clamping. After forebrain ischemia had been maintained for 30 minutes, recirculation was started by removal of the arterial clamps and by increasing blood pressure to the preischemic level. Following the desired ischemic or postischemic periods, the brains were frozen in situ with liquid nitrogen. The brains were then chiselled out during irrigation with liquid nitrogen and stored at -80 degrees C until analysis. The brain extracts were analysed by high performance liquid chromatography for free arachidonic acid, by bioassay using the ileum of guinea pig for SRS-A and by radioimmunoassay for leukotriene C4. Brain water content was calculated with dry weight method. Inhibitor of SRS-A release, tranilast, was given intraperitoneally, 100 mg/kg 30 minutes before induction of ischemia and 50 mg/kg immediately before recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain tissue leukotrienes in cerebral ischemia and the effect of inhibitor of SRS-A release on postischemic cerebral edema]. 246 14

Two simple cerebral ischemic models of mice were used for studying brain energy metabolism and the effects of drugs. Model one is partial occlusion of the left carotid artery and total occlusion of the right one including the vagus. The behavior of the animals appeared splaying of the contralateral extremities, circling around counterclockwise and in a comatose motionless state. Following the designated ischemic time, the animals were put into liquid N2. Model two is decapitation induced ischemia of mouse brain. The whole animal (control) and the severed head were rapidly frozen in liquid nitrogen 0, 10, 30, 60 s after decapitation. Brain samples were powdered at liquid N2 temperature, extracted and determined for ATP, phosphocreatine (Pcr) and lactic acid (LA). The data from model one indicate that after an ischemic period of 10 min, brain LA level increased significantly compared with values from the sham operated group, while no significant alteration was observed in brain ATP, and Pcr level. At 180 min of ischemia, levels of ATP and Pcr were considerably reduced while LA level increased significantly. The degree of symptoms induced by brain ischemia showed good correlation with brain energy metabolism. In model 2 brain LA level was found to be increased, while ATP and Pcr levels decreased after whole brain ischemia. However, brain ATP and Pcr levels were increased and LA level was decreased significantly in the normal and ischemic animal after administration of phenobarbital (225 mg/kg ip). LA level decreased significantly in the unischemic mice treated with Rb1 (100 mg/kg ip). It is indicated that both models of cerebral ischemia were simple and sensitive methods for studying brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain energy metabolism of cerebral ischemic mice and the effects of some drugs]. 280 Nov 43

To evaluate the scavenging effect of mannitol, vitamin E and betamethasone in cerebral ischemia, spin trapping technique was applied to the detection of the free radicals generated in ischemic brain homogenate. Thirty Wistar rats were used for this study. In the control group, the brain homogenate prepared immediately after decapitation was preserved at 37 degrees C under N2 gas. Before the preservation and at 30 min, 60 min and 120 min from the start of the preservation, two reaction mixtures containing of spin trapping reagent phenyl-t-butyl nitrone (PBN), NADPH, Fe-EDTA and brain homogenate was prepared from each brain sample--one to be incubated for 20 min at 37 degrees C in air and one to be incubated in nitrogen gas under similar condition. Then the free radical adducts of PBN were measured by electron spin resonance (ESR). In pre-treated group, mannitol, vitamin E and betamethasone were administered intravenously 30 min prior to the decapitation and spin adducts of PBN were detected by same procedures as in control group. The ESR spectra, which hyperfine coupling constants were AN = 16.0-16.6 G and AH beta = 3.0-3.8 G, were obtained from the reaction mixtures in each group. Analyses of their relative intensity in control group revealed that the formation of free radical adducts of PBN was increased dependent on the preservation period under aerobic incubation, and increased gradually for 60 min of preservation time followed by a decrease under anaerobic incubation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Protective effect of radical scavengers on cerebral infarction--experimental study utilizing the spin trapping method of ESR]. 299 96

Spin trapping technique has been applied to the detection of free radicals generated in NADPH stimulated lipid peroxidation process in ischemic brain homogenate. Using male Wistar rats, complete cerebral ischemia for 30 min, 60 min or 120 min was produced by decapitation followed by preservation of the heads at 37 degrees C. Global cerebral ischemia of 30 min or 60 min duration was induced by occlusions of three vessels (bilateral common carotid and basilar artery) in the ventilated rats. In some animals, bilateral carotid occlusions were released for 30 min following 30 min of ischemia to study postischemic event. Two reaction mixtures containing of brain homogenate, NADPH, Fe-EDTA and spin trapping reagent, phenyl-t-buthylnitrone (PBN), were prepared from each brain sample--one to be incubated in air and the other to be incubated in nitrogen gas. After the incubation for 20 min at 37 degrees C, free radical adducts of PBN were measured by electron spin resonance (ESR). In preliminary experiments, no ESR signals were obtained from the reaction mixtures without the addition of NADPH and Fe-EDTA. And the dependence of ESR signal intensity upon the NADPH concentration was observed. The six-line signals (triplet of doublets), which hyperfine splitting constants were AN = 16.2-16.5 G and A beta H = 3.6-3.8 G, were obtained from both ischemic models. These signals were dependent upon the presence of oxygen in the reaction systems, as evidenced by the fact that the signal intensity obtained from aerobic incubation was consistently stronger than that obtained from anaerobic incubation in each brain sample.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Detection of free radicals generated in NADPH-dependent lipid peroxidation in ischemic brain homogenates--use of the spin trapping technic]. 300 94


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