Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When the supply of substrate to the brain is threatened, homeostatic mechanisms induce cerebral vasodilatation to compensate for the insufficiency. When a region of the brain is rendered completely ischemic, local infarction occurs. The size of the infarct depends partly on the availability of collateral circulation and the adequacy of the homeostatic mechanisms controlling blood flow in stillpatent vessels. Several approaches to acute-phase treatment of stroke derive from clinical and experimental studies of cerebral blood flow and metabolism. We must conclude that both surgical and nonsurgical therapeutic measures have been of limited value in the treatment of cerebral infarction and that the basic therapy for completed stroke remains good medical management of complications and attentive nursing care.
 ...
PMID:Atherosclerotic cerebral infarction: pathophysiologic aspects. 0 79

Cerebral hemispheric blood flow and metabolism were measured before and after therapy with intracarotid infusion of combined PBZ and PPL in 15 patients with recent cerebral infarction. HBF was unaltered despite decrease in cerebral perfusion pressure. Cerebral hemispheric oxygen comsumption and carbon dioxide production decreased while cerebral hemispheric lactate production increased. Biphasic cerebral uptake of tyrosine was observed during and immediately after PBZ and PPL infusion. CSF HVA increased, indicating altered DA turnover. CSF 5HIAA levels also increased, suggesting altered 5HT turnover after PBZ and PPL. Release of cyclic AMP from ischemic brain into cerebral venous blood seen in the steady state was abolished after therapy. Cerebral hemodynamic studies suggest a functional balance between monaminergic neurogenic influences in the control of cerebral circulation. Imbalance of such controlling factors in ischemic brain may lead to paradoxical vascular responses to induced hypertension and hypotension. PBZ and PPL enhance such responses perhaps by increasing central neurotransmitter turnover and release. Further shift toward cerebral anaerobic metabolism may occur in ischemic brain following the use of phenoxybenzamine and propranolol. Worsening of neurological deficit occurred in four cases. Combined therapy with PBZ and PPL does not appear beneficial in the therapy of patients with recent stroke.
Stroke
PMID:Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients. 0 7

In the gerbil cerebral infarction was produced by unilateral carotid ligation. 3.5 hours later, when the neurological deficit was fully developed, hemisphere dopamine (DA) showed little change from normal. It seems unlikely that changes in DA are the direct cause of the turning behavior shown by these animals. Slight changes in norepinephrine (NE) occurred on the operated side but 4 hydroxy-3-methoxy phenyl-ethyleneglycol sulphate (MOPEG-SO4) levels were not affected. Significant falls in 5-hydroxytryptamine (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) were found on the operated side but there was also a trend for both 5HT and 5-HIAA to fall on the unoperated side. These changes occurred in clincally affected and unaffected animals and their clinical significance is unproven.
Stroke
PMID:Effect of experimental ischemia on neurotransmitter amines in the gerbil brain. 3 64

Dopamine (DA), serotonin (5-HT), tryptophan (TRP), 5-hydroxyindole acetic acid (5-HIAA), and GABA were assayed spectrofluorometrically in various regions of 16 human post-mortem brains with acute and old cerebral infarction. In both recent and older strokes a total depletion of DA and 5-HT in the necrotic tissue was associated with mild reduction of these compounds in remote non-ischemic areas of the injured, and less of the contralateral cerebral hemispheres. 5-HIAA was significantly reduced in acute ischemic necrosis, while the perifocal edema zone showed considerable accumulation of both 5-HT and 5-HIAA. Marked elevation of the 5-HT precursor TRP and of GABA was present in both the necrotic center and perifocal edema of acute infarcts, which also showed a mild reduction of total proteins. The degradation zone surrounding old infarcts showed a mild decrease of both 5-HT and 5-HIAA with normal TRP levels, indicating normalization of the previously increased 5-HT metabolism and turnover after decrease of acute cerebral edema. These data which confirm previous studies in experimental cerebral ischemia and stroke indicate that disorders in the metabolism of brain monoamines and other putative neurotransmitters contribute to the development of postischemic brain damage and the complicating cerebral edema. They are also in keeping with the concept that unilateral focal ischemia produces bilateral effects on brain monoamines.
 ...
PMID:Changes of some putative neurotransmitters in human cerebral infarction. 3 76

Plasma fibrinogen chromatography is a method for quantification of high molecular weight fibrinogen complexes (HMWFC), native fibrinogen and other fibrinogen derivatives in plasma. Enchanced formation of fibrin, intravascular coagulation, thrombus formation, etc., are reflected by elevation of plasma HMWFC, and the method distinguishes between subjects with normal and pathological rates of fibrin formation. Serial standard blood coagulation assays, including plasma fibrinogen chromatography, and neurological studies were performed on 220 patients admitted to a stroke unit. Findings from patients with cerebral infarction were compared against those of three control groups: (1)normals, (2)a stroke control group and(3)a stroke risk factor group. Plasma HMWFC findings were significantly (p less than 0.001) higher in the stroke risk factor group than in the normals. Plasma HMWFC values were significantly higher (p less than 0.001) in the cerebral infarction patients than in any of the control groups, and plasma fibrinogen, plasminogen, alpha1-antitrypsin and alpha2-macroglobulin also were significiantly higher (p less than 0.001) in the patients. The greater the degree of initial neurological deficit, the greater were plasma HMWFC values (p less than 0.001), and high HMWFC values were associated with poor clinical outcome. Plasma HMWFC values were significantly higher (p less than 0.001) in patients with intracerebral hemorrhage, subarachnoid hemorrhage and cerebral embolism. These findings docunment the fact that a high proportion of stroke patients have coagulopathy, characterized by pathological enhancement of fibrin formation.
Stroke
PMID:Blood coagulation and plasma fibrinolytic enzyme system pathophysiology in stroke. 6 Aug 7

One hundred seventy-eight patients with transient ischemic attacks (TIAs) or small strokes with slight symptoms persisting for more than 24 hours (incomplete recovery = IR) (TIA-IR) from both the carotid and the vertebrobasilar systems were treated with anticoagulants. Ten patients stopped the treatment because of severe side effects. Only one patient had a lethal cerebral infarction when the thrombotest values were above the therapeutic level; no other infarction happened during the treatment period. Moreover, the frequency of TIA decreased during the treatment, compared with descriptions of the natural course of TIA. One hundred four patients were observed for a mean of 21 months after the anticoagulant treatment ended. During the observation period, six patients had cerebral infarctions. This was a sixfold increase compared with the stroke incidence during treatment, and was almost identical with the incidence of strokes seen during the natural course of TIA. All the cerebral infarctions were in patients who had their initial TIA/TIA-IR from the carotid territory (within the same carotid artery which earlier had given symptoms). The investigation shows that long-term anticoagulant treatment is useful, especially in patients with carotid TIA/TIA-IR, and that this treatment should continue as long as the patients can manage it. In patients with vertebrobasilar symptoms of malignant character, it seems feasible to terminate the treatment after about one year. The mechanism of the anticoagulant treatment is obscure, but it does not appear to influence the progress of the atherosclerotic process.
Stroke
PMID:Long-term anticoagulant therapy for TIAs and minor strokes with minimum residuum. 6 Aug 8

Ten patients with MS were studied with leukocyte migration in agarose technique to detect changes in reactivity to encephalitogenic protein in connexion with a relapse. Six showed significant reactivity within a few days after the relapse. It decreased or disappeared during the 2 weeks after the relapse, but sometimes reappeared and was found in tests performed 2-3 months later. Five patients with cerebral infarction were studied in a similar way--in three, marked reactivity was noted within a few days after the stroke; in these, reactivity decreased or disappeared in later tests. In the two other patients, reactivity appeared in the second and/or third test. The possibility of a reactivity as in epiphenomenon due to CNS tissue destruction is discussed, and the need for antigens with a more restricted specificity for such an analysis is stressed.
 ...
PMID:Effect of encephalitogenic protein on migration in agarose of leukocytes from patients with multiple sclerosis. A longitudinal study of patients with relapsing multiple sclerosis or with cerebral infarction. 6 98

Ten patients with MS were studied with leukocyte migration in agarose technique to detect changes in reactivity ot encephalitogenic protein in connexion with a relapse. Six showed significant reactivity within a few days after the relapse. It decreased or disappeared during the 2 weeks after the relapse, but sometimes reappeared and was found in tests performed 2-3 months later. Five patients with cerebral infarction were studied in a similar way--in three, marked reactivity was noted within a few days after the stroke; in these, reactivity decreased or disappeared in later tests. In the two other patients, reactivity appeared in the second and/or third test. The possbility of a reactivity as an epiphenomenon due to CNS tissue destruction is discussed, and the need for antigens with a more restricted specificity for such an analysis is stressed.
 ...
PMID:Effect of encephalitogenic protein on migration in agarose of leukoytes from patients with multiple sclerosis. A longitudinal study of patients with relapsing multiple sclerosis or with cerebral infarction. 6 94

Both naturally occurring disease processes and experimental models of human disease in the Mongolian gerbil were reviewed. The gerbil was highly susceptible to cerebral infarction following unilateral ligation of one common carotid artery and was useful in studies of the pathogenesis of stroke. Spontaneous epileptiform seizures mimicked those of human idiopathic epilepsy, and both seizure-sensitive and resistant strains have been bred. Perhaps because of its more efficient nephron, the gerbil accumulated four to six times as much renal lead as the rat, and the gerbil has been proposed as an experimental model of lead nephropathy. On standard diets, about 10% of the animals became obese, and some showed decreased glucose tolerance, elevated serum immunoreactive insulin and diabetic changes in the pancreas and other organs. Some breeders exhibited hyperactivity of the adrenal cortex associated with hyperglycemia, hyperlipidemia and degenerative vascular disease. Although dietary supplements of cholesterol were toxic and did not induce atherosclerosis, the gerbil was useful in other studies of cholesterol absorption and metabolism. Spontaneous, insidious periodontal disease became evident after about 6 months on standard diets, and dental caries were induced by cariogenic diets or by pathodontic streptococci. Spontaneous neoplasia occurred in 8.4--24% of gerbils, usually after 2 years of life. Adrenal cortical, ovarian and cutaneous tumors were the most consistently reported neoplasms.
 ...
PMID:The pathology of the Mongolian Gerbil (Meriones unguiculatus): a review. 9 95

Experimental regional cerebral ischemia was produced in the middle cerebral artery (MCA) territory in primates (M. mulatta) by macrosphere embolization. Determinations of percentage tissue dry weight and tissue sodium and potassium concentrations were obtained in samples from the ischemic and non-ischemic hemispheres at various time from 12 to 48 hours after the onset of cerebral ischemia. Samples from the cortex normally supplied by the occluded MCA showed maximal accumulation of edema fluid with fluxes in sodium and potassium in reciprocal directions at 12 hours and similar edematous changes in putamen at 24 hours after embolization By 48 hours after MCA occlusion and despite the presence of infarction, partial reversal was observed in the redistribution of water and electrolytes in these gray matter structures. In contrast to cerebral cortex and putamen, the adjacent subcortical white matter showed progressive increases in water content from 12 to 48 hours and definite increases in tissue sodium with decreases in potassium were not observed until 48 hours after MCA occlusion. This late severe white matter edema associated with cerebral infarction appears to be a major factor responsible for the hemispheric swelling observed at this state.
Stroke
PMID:Experimental regional cerebral ischemia in the middle cerebral artery territory in primates. Part 3: effects on brain water and electrolytes in the late phase of acute MCA stroke. 9 10


1 2 3 4 5 6 7 8 9 10 Next >>