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)

The distribution of blood pressure levels in elderly patients is described and the evidence that higher levels are associated with morbidity at this age is reviewed. In the absence of definitive evidence about the results of treating hypertension in the elderly, the physiological factors that have to be taken into account are surveyed with particular reference to aggravating cerebral ischaemia.More potent hypotensive agents should be avoided in older patients and in practice the decision on whether to treat may depend more on the clinical context than on the level of the blood pressure itself.
J R Coll Gen Pract 1976 Oct
PMID:Blood pressure in the elderly. 79 64

1. Cerebral ischemia applied for 15 min and followed by a 30 min reperfusion did not change the glutathione (GSH) levels and beta-adrenoceptor density (Bmax) in brain cortex. 2. A significant increase in erythrocyte-lysate GSH concentration (vs control) and a significant decrease of Bmax values in erythrocyte membranes (vs control) was found at the same time. 3. Pretreatment with the alpha-adrenoceptor antagonist phentolamine (5 mg/kg i.p.) prevented the erythrocyte GSH increase but not the decrease of Bmax value. Pretreatment with the beta-antagonist propranolol (2 mg/kg i.p.) did not influence the increase in erythrocyte GSH but circumvented the decrease of Bmax.
Gen Pharmacol 1992 Jan
PMID:Glutathione mobilization during cerebral ischemia and reperfusion in the rat. 131 10

1. We studied the postischemic time-course of dopamine D1 receptors in selectively vulnerable areas in the gerbil using receptor autoradiography. 2. [3H]SCH 23390 was used to label dopamine D1 receptors and transient cerebral ischemia was induced for 10 min. 3. [3H]SCH 23390 binding showed no significant alteration in selectively vulnerable areas at an early stage (1-24 hr) of recirculation. Thereafter, [3H]SCH 23390 binding showed a significant reduction in most selectively vulnerable areas 48 hr or 7 days of recirculation. The ventromedial striatum and dentate gyrus which were resistant to ischemia also exhibited a significant reduction in [3H]SCH 23390 binding. 4. Especially, marked reduction was noted in the dorsolateral striatum. However, this reduction in the dorsolateral striatum was not seen early in the recirculation prior to morphological neuronal damage. 5. The result suggests that transient cerebral ischemia can cause a severe reduction in dopamine D1 receptors in most selectively vulnerable areas. Furthermore, they suggest that dopamine D1 transmission is not always responsible for the evolution of ischemic brain damage. 6. These findings are discussed in relation to the mechanism of ischemic brain damage.
Gen Pharmacol 1992 Nov
PMID:Autoradiographic analysis of dopamine D1 receptors in the gerbil brain following transient cerebral ischemia. 148 17

1. We investigated the alterations in binding sites of three major second messengers, phorbol 12,13-dibutyrate, inositol 1,4,5-trisphosphate and forskolin following transient cerebral ischemia in gerbils, and examined the effects of a novel vinca alkaloid derivative, vinconate against the alterations in the binding of the second messengers following ischemia. 2. Transient cerebral ischemia produced by bilateral occlusion of the common carotid arteries was induced for 10 min, and intraperitoneal administration of vinconate (100 mg/kg and 300 mg/kg) was given 10 min before ischemia. 3. Morphological study indicated that transient ischemia can produce severe neuronal damage in striatum, hippocampal CA1 sector and hippocampal CA3 sector. 4. Transient cerebral ischemia caused the postischemic alterations in the binding of three second messengers. 5. The postischemic alterations in the binding of second messengers were ameliorated by pretreatment with vinconate. This effect was especially observed in the striatum which was most vulnerable to ischemia. 6. These findings are discussed in relation to the mechanism of ischemic neuronal damage.
Gen Pharmacol 1992 Jan
PMID:Protective effect of a novel vinca alkaloid derivative, vinconate, against alterations in binding sites of second messengers after transient cerebral ischemia in gerbils. 159 19

The effect of transient cerebral ischemia and intraventricular injection of kainic acid on adenylate cyclase and protein kinase C as labeled by [3H]forskolin ([3H]FOR) and [3H]phorboldibutyrate ester ([3H]PDBU) in several rat brain microregions was investigated in a quantitative autoradiographic study. Four days after transient four vessel occlusion a 80% loss of [3H]FOR and a 35% loss of [3H]PDBU binding could be measured in the CA1 stratum radiatum of operated Wistar rats as compared to control rats. Four days after intraventricular injection of kainic acid only a marginal loss of [3H]FOR and a 30% increase of [3H]PDBU binding was seen in the CA1 stratum radiatum while in the CA3 stratum lucidum and radiatum respectively a 30% loss of [3H]FOR and no significant change in [3H]PDBU binding was observed. As transient cerebral ischemia and intraventricular kainic acid injection are depleting the hippocampal CA1 region of CA1 pyramidal cells and axons of CA3 pyramidal cells respectively in rat brain, these findings strongly suggest that both adenylate cyclase and protein kinase C are localized in CA1 pyramidal cells of rat hippocampus.
J Neural Transm Gen Sect 1991
PMID:Post- and presynaptic lesions in the CA1 region of hippocampus: effect on [3H]forskolin and [3H]phorboldibutyrate ester binding. 203 10

Aspirin has been tested for its benefit in preventing cardiovascular disease in randomized trials in three categories of patients. In secondary prevention among those with a history of myocardial infarction (MI), stroke or transient cerebral ischemia, or unstable angina pectoris, 25 randomized trials demonstrated significant reductions from aspirin of 25% for the occurrence of an "important vascular event" (nonfatal MI, nonfatal stroke, or vascular death), 32% for nonfatal MI, 27% for nonfatal stroke, and 15% for vascular mortality. Among those evolving an MI, the Second International Study of Infarct Survival (ISIS-2) showed a significant reduction of 23% in five-week vascular mortality among those started on a one-month regimen of daily aspirin within 24 hours of the onset of symptoms of suspected MI. Aspirin also significantly reduced reinfarction, nonfatal stroke, and important vascular events. Finally, in primary prevention, the US Physicians' Health Study (PHS) showed a significant 44% reduction in the occurrence of a first MI among apparently healthy male physicians; numbers of strokes and vascular deaths were insufficient to permit conclusions for these endpoints. Thus, aspirin is of clear benefit in reducing MI, stroke, and vascular death in secondary prevention and among those evolving an MI. It is also beneficial in the primary prevention of MI among men over 40, but data concerning its effects on stroke and vascular death remain inconclusive.
J Gen Intern Med
PMID:Prevention of cardiovascular disease: risks and benefits of aspirin. 223 Oct 66

The cerebral dialysis technique was employed to monitor extracellular concentrations of dopamine (DA), norepinephrine (NE), dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) in the dorsal hippocampus of gerbils before and after cerebral ischemia induced by carotid artery occlusion. Extracellular concentrations of DA and NE in the dorsal hippocampus increased from baseline levels of less than 35 fmol/collection interval to 180 and 200 fmol/collection, respectively, within 36 minutes following carotid artery ligation (n = 8 animals). Extracellular concentrations of the DA metabolites, DOPAC and HVA, did not change significantly following carotid artery ligation. These data demonstrate that ischemia in the dorsal hippocampus is associated with a mared release of DA and NE. This release may contribute to the selective vulnerability of the dorsal hippocampus to neuronal damage during ischemia.
J Neural Transm Gen Sect 1990
PMID:Ischemia in the dorsal hippocampus is associated with acute extracellular release of dopamine and norepinephrine. 233 46

1. Smooth muscle contraction is related to the intracellular free Ca2+ concentration. 2. Potential dependent Ca2+ channels (PDCs) are generally more sensitive to Ca2+-antagonists (CAts) than receptor-operated Ca2+ channels (ROCs). However, there exists a wide variation in the sensitivity of ROCs and CAts, which largely depends on the vessel studied. 3. Cerebral and coronary arteries seem to be very sensitive to CAts. 4. New dihydropyridines possess selectivity for the cerebrovascular bed. 5. The vasospasm subsequent to subarachnoid hemorrhage appears to be sensitive to CAts. 6. CAts prevent or reduce the neurologic alterations elicited by cerebral ischemia, and some of them induce beneficial effects in the prophylaxis of migraine.
Gen Pharmacol 1988
PMID:Vascular effects of calcium antagonists. Uses in some cerebrovascular disorders. 245 95

This project was concerned with the clinical knowledge reported by general practitioners in relation to the diagnosis and management of seven common clinical conditions: acute otitis media, jaundice, iron-deficiency anaemia, transient cerebral vascular insufficiency, infectious mononucleosis, pulmonary infarction, and carcinoma of the prostate. Postal questionnaires were sent to three groups of doctors: a constant group of experienced general practitioners who were or had been trainers, randomly selected groups of 200 general practitioners, and small groups of consultants who were specialists in each condition. The last two groups were changed for each of the chosen clinical conditions; the constant group remained the same throughout. The study was not concerned with the attitudes and skills of general practitioners or consultants, and no attempt has been made to analyse the process of clinical problem-solving. The differences between the constant group and random group of general practitioners were minor. Consultants received questionnaires identical to those sent to general practitioners and were asked to answer them as they would expect a competent general practitioner to do; their answers suggested a more direct approach to the problem concerned than those given by general practitioners. The information obtained has implications for education for general practice and educational audit programmes. Areas for further research are suggested.
J R Coll Gen Pract Occas Pap 1984 Oct
PMID:Clinical knowledge and education for general practice. 615 93

1. Cerebral ischemia of 5 min duration was induced in unanesthetized gerbils by bilateral occlusion of the carotid arteries. 2. The extent of cerebral damage was assessed by the elevation of motor activity in comparison with pre-ischemic levels and by a histological assessment of the extent of neuronal degeneration of the CA1 area of the hippocampus. 3. The GABA transport inhibitor CI-966 (10 mg/kg i.p.) was tested for cerebroprotective activity in a gerbil stroke model. CI-966 reduced the extent of stroke injury as assessed by locomotor activity and measurement of hippocampal CA1 pyramidal cell injury. 4. It is proposed that enhancement of extracellular GABA levels during ischemia accounts for the cerebroprotective actions of CI-966.
Gen Pharmacol 1995 Sep
PMID:CI-966, a GABA uptake inhibitor, antagonizes ischemia-induced neuronal degeneration in the gerbil. 755 51


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