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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proton nuclear magnetic resonance spectroscopy is a unique method to monitor noninvasively the concentrations of cerebral metabolites. N-Acetyl-L-aspartate, the concentration of which is assumed to be stable during hypoxia, has been used to form ratios with lactate. To determine the stability of the signal from N-acetyl-L-aspartate, we used a model of graded hypoxia in rats to monitor the percentage changes from baseline of the peak heights for lactate, lipids, and N-acetyl-L-aspartate. Anesthetized adult rats were exposed sequentially to 15% and 10% O2 while proton nuclear magnetic resonance spectra were collected with a surface coil in a 7-T 89-mm-bore spectrometer. Brain lactate concentration was either increased by feeding or infusion of glucose (n = 9) or lowered by fasting (n = 7). After death the brains were removed and frozen, and the water- and lipid-soluble compounds were extracted to identify the origin of the signals. We analyzed the data both as the percentage change from baseline for heights of the lactate (1.33 ppm), lipids (1.5 ppm), and N-acetyl-L-aspartate (2.02 ppm) peaks and as the ratios of heights of the 1.33 and 2.02 and the 1.5 and 2.02 ppm peaks. Both hypoxic episodes caused a 45% decrease from baseline in the 2.02 ppm peak. During the second hypoxic episode, the 1.33:2.02 ppm peak height ratio increased significantly in hyperglycemic rats (p less than 0.05) but was unchanged in hypoglycemic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1991 Jan
PMID:Effect of hypoxia on cerebral metabolites measured by proton nuclear magnetic resonance spectroscopy in rats. 184 48

We studied the relation of reactive hyperglycemia, stress hormone response, and outcome in 23 consecutive elderly patients (median age 80 [range 75-92] years) following an acute first stroke. The median delay from the onset of the stroke to the first blood sample (day 0) was 9 (range 4-22) hours. Subsequent blood samples were taken, after fasting, for the determination of blood glucose, cortisol, catecholamine, insulin, C-peptide, glucagon, and lactate concentrations on days 1, 2, 3, 7, 14, 30, and 90. For all 23 patients, a significant relation was found between the blood glucose concentration and survival (p = 0.03) and the blood glucose concentration decreased with time (p less than 0.001). There was also a significant relation between blood glucose concentration and outcome (p = 0.02). For the 15 patients with complete data, the major determinants of the blood glucose concentration were the cortisol, insulin, and glucagon concentrations (all p less than 0.001), which accounted for 42% of the variance. When all the indexes were analyzed together by logistic regression, only the cortisol concentration was related to outcome (p = 0.02). Hyperglycemia following a stroke probably reflects the intensity of the stress hormone response. We have confirmed that hyperglycemia is a predictor of outcome in persons with stroke.
Stroke 1991 Jul
PMID:Stress hormone and blood glucose response following acute stroke in the elderly. 159 19

We examined the 21-aminosteroid U74006F, a potent inhibitor of lipid peroxidation, for potential neuroprotective effects in a canine model of complete cerebral ischemia. Two 1.5-mg/kg boluses were administered to six dogs, the first bolus 15 minutes prior to a 12-minute episode of complete cerebral ischemia and the second bolus after 11 minutes of ischemia, 1 minute prior to reperfusion. Using this dosage regimen, plasma U74006F levels of greater than 0.3 microgram/ml were maintained for up to an hour postischemia. An additional six animals received equal volumes of the citrate vehicle solution. At 24 and 48 hours postischemia, the dogs were neurologically evaluated by an observer blinded as to treatment selection. All six U74006F-treated animals had a normal neurologic outcome at 48 hours postischemia, while the citrate vehicle-treated animals all suffered moderate to severe neurologic deficits. The difference in outcome was significant at both 24 and 48 hours (p less than 0.005). Although U74006F is a 21-aminosteroid, it is not reported to possess glucocorticoid activity. This is supported by the present finding that no changes in plasma glucose concentration were observed following administration of the drug. The systemic vitamin E levels of citrate vehicle-treated animals decreased significantly (from 4.10 +/- 0.46 micrograms/ml to 2.95 +/- 0.38 micrograms/ml, p less than 0.05), whereas the vitamin E levels in U74006F-treated animals did not decrease significantly. These results suggest that U74006F may be of benefit in improving neurologic outcome when administered prior to an episode of complete cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1991 Jul
PMID:Pretreatment with U74006F improves neurologic outcome following complete cerebral ischemia in dogs. 185 10

Positron emission tomography (PET) measurements of regional cerebral blood flow, blood volume, oxygen extraction, oxygen consumption and glucose consumption permit a detailed investigation of the pathophysiology of cerebral ischemia. The magnitude of the reduction of oxygen consumption appears generally as most important for tissue viability. In general, cerebral blood flow is severely reduced at the onset of an acute ischemic stroke. Subsequently, a very variable increase of cerebral blood flow may be found, often as "luxury perfusion" of irreversibly damaged tissue or relative hyperperfusion which is most frequently seen in the periphery of an ischemic infarct. Measurements of cerebral blood flow without measurement of oxygen metabolism are therefore of limited value. Glucose metabolism is less reduced than oxygen metabolism in most cases, indicating substantial anaerobic glycolysis. In few cases very high fluorodeoxyglucose uptake can be seen as an indicator of massive lactate production, which may cause additional toxic tissue damage. In cases of chronic or transient ischemias two stages of cerebral vascular decompensation can be distinguished by measurements of local blood volume, blood flow and oxygen consumption: the first stage is characterized by vasodilatation of peripheral vessels, resulting an increased ratio of cerebral blood volume to cerebral blood flow; the second stage is characterized by decreased blood flow and increased oxygen extraction. Ischemic brain lesions frequently cause alterations of blood flow and metabolism also in remote brain areas, apparently due to neuronal functional inactivation of incomplete ischemic damage. Global metabolic alterations correspond to the general clinical impairment of patients, whereas asymmetric focal deactivations correspond frequently to neuropsychological deficits. Studies of metabolic activation by functional stimulation appear promising as a tool to assess therapeutic strategies for rehabilitation.
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PMID:[Positron emission tomography for the determination of pathophysiology of cerebral ischemia]. 185 99

The present study compares simple hypothermic storage and hypothermic perfusion in a swine model of heart transplantation using metabolic and functional assessments. In both groups the hearts were initially protected with iso-osmolar potassium Tyers' cardioplegia. The donor hearts of group A were placed in simple hypothermic storage for 5 h. The donor hearts of group B were placed onto a perfusion apparatus for 5 h with perfusion pressure maintained at 28 cm of H2O and a myocardial temperature of 8-10 degrees C. The perfustate consisted of Tyers' solution with the addition of 2 mg/L of mannitol, 12.5 mg/L of glucose, 5 units/L of insulin, and 95% oxygen. The ischemic interval within both groups was 6 h, including orthotoipic transplantation. Investigation was conducted at three time periods: prepreservation (T1) in the donor, and postpreservation (T2) and immediately after loading (T3) in the recipient. Following volume loading for the hypothermic perfusion group there was significant improvement of myocardial function (cardiac index, p less than .05; stroke index, p less than .05) with no significant change in systemic vascular resistance, systemic blood pressure, and heart rate. There was also significant improvement in myocardial performance (p less than .05) for the hypothermic perfusion group following volume loading. Results of fatty acid turnover using 15-p-iodo (123I)-phenylpentodecanoic acid indicate significantly greater increase in metabolic rate for the perfusion group than for the hypothermic storage group. (p less than .05). This indicates improved metabolic status of the heart treated with the hypothermic perfusion technique. We conclude that a combination of functional and metabolic assessments is a good method for deduction of ischemic-reperfusion injury. We also conclude that hypothermic perfusion is superior to hypothermic storage for in vitro preservation of hearts for heart transplantation.
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PMID:Comparison of functional and metabolic assessments in preservation techniques for heart transplantation. 186 92

The central nervous system (CNS) is clinically involved in approximately 40% of all systemic lupus erythematosis (SLE) patients. Minor psychiatric symptoms and abnormalities on neuropsychological testing are being detected with increasing frequency. This review summarizes current thinking concerning the diagnosis and pathogenesis of CNS lupus. The main symptoms of CNS lupus can be diffuse (generalized seizures, psychosis) or focal (stroke, peripheral neuropathies). Neuropsychiatric symptoms often occur in the first year of SLE, but are rarely the presenting symptoms of the disease. In studies on the pathology of CNS lupus, vasculopathy, infarcts and haemorrhages are often observed, whereas vasculitis is rare. Endocardial lesions and mural thrombi have also been reported in 33-50% of CNS lupus patients. In diagnostic imaging of the CNS, magnetic resonance imaging (MRI) scans often provide evidence for edema or small infarcts, both in focal and diffuse CNS lupus, whereas computerized tomography (CT) scans only show gross abnormalities. The first reports on position emission tomography (PET) scans in CNS lupus patients show decreased glucose uptake in the brain. The cerebral blood flow decreases during active diffuse and focal CNS lupus. The blood-brain barrier is somewhat more frequently impaired in diffuse CNS lupus. Intrathecal IgG and IgM production is observed in 25-66% of all CNS lupus patient. Various specificities of autoantibodies have been observed in CNS lupus. Of these, anticardiolipin (ACA) antibodies show a well-documented association with focal involvement of the CNS in SLE. These antibodies could cause thrombosis by interfering with the protein C pathway of fibrinolysis. In addition, they are associated with endocardial and valvular heart disease, which is often observed in SLE and which could cause embolism. The relation between ACA and diffuse CNS lupus is not yet clear. Low-avidity anti-DNA antibodies are also found in CNS lupus, possibly because of their cross-reaction with cardiolipin. Antineuronal antibodies and lymphocytotoxic antibodies have been associated with diffuse CNS lupus and abnormalities on neuropsychological testing. However, the population of these antibodies is rather heterogeneous and it has not been possible to assess a common target antigen. Therefore, it is still obscure whether there is also a second immune-mediated mechanism responsible for the development of the diffuse form of CNS lupus.
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PMID:Diagnosis and pathogenesis of CNS lupus. 186 69

To find out whether the high blood glucose values sometimes found in the first stage of ischemic stroke have any prognostic value, we considered 76 patients hospitalized within 24 h of an acute cerebral infarction, documented by CT brain scan and/or necropsy, whose fasting blood glucose was recorded before any treatment was given. The patients were sorted into 3 groups: diabetics, normoglycemic non-diabetics and hyperglycemic nondiabetics. On the CT findings cases with large cortical and/or subcortical infarcts were analyzed separately from those with lacunar infarcts. The clinical symptoms on admission proved to be more severe (p less than 0.02) and 30-day mortality higher (p less than 0.02) among the hyperglycemic non-diabetics, who also showed a highly significant (p less than 0.00001) preponderance of large cortical and subcortical infarcts over lacunar infarcts. Multivariate analysis, which took account of variables of known relevance to the prognosis of cerebral infarction (age, sex, arterial hypertension, severity of the clinical pattern, type of brain lesion), confirmed the statistically discriminant power, in terms of mortality, of belonging to the hyperglycemic nondiabetic group. The results of the study confirm that hyperglycemia at stroke onset in nondiabetic patients is an adverse prognostic factor and suggest that it may be a reaction to stress, depending on the size of the infarcted area.
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PMID:Hyperglycemia at ischemic stroke onset as prognostic factor. 187 6

Vascular diseases of the brain (functional transient and ischemic apoplexy, circulatory encephalopathy) in 79 patients were treated by UHF electromagnetic field of millimetric wave range. 14 patients entered the control group. The treatment results are indicative of clear-cut trend to a decrease of arterial pressure, normalization of blood glucose level, arrest of DIC syndrome development.
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PMID:[Experience with using extremely high frequency radiotherapy of the millimeter wave range in cerebrovascular disorders]. 188 82

Hyperglycemia is often associated with an increased frequency of cerebrovascular disease and exacerbation of neuronal injury in focal ischemic cerebral infarction. We used a combination of high-field proton MR imaging and 1H and 31P MR spectroscopy to investigate whether hyperglycemia would adversely influence cerebral metabolism and eventual infarct size following unilateral occlusion of the middle cerebral artery (MCA) of cats pretreated with the calcium channel blocker nicardipine. Normoglycemic animals injected with 10 micrograms/kg of nicardipine (8 micrograms.kg-1.hr-1 maintenance dose) manifested only mild disturbances in phosphorus metabolism and cerebral pH regulation compared with untreated controls, and showed a significant reduction in infarct size 7 hr after MCA occlusion. By comparison, hyperglycemic cats (plasma glucose, 200-300 mg/dl) had significantly reduced cerebral high-energy phosphates, elevated lactic acid, and larger ischemic lesions in the occluded MCA territory, irrespective of whether they were treated with nicardipine. These results indicate that moderate hyperglycemia can exaggerate ischemic brain damage by enhancing formation of tissue lactic acid and impairing normal phosphorus metabolism. One implication of this study is that dextrose should not be provided to patients with acute ischemic stroke.
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PMID:Hyperglycemia augments ischemic brain injury: in vivo MR imaging/spectroscopic study with nicardipine in cats with occluded middle cerebral arteries. 188 34

This study, in biologically bred hyperglycemic diabetic rats, examined the effect of a intravenous insulin infusion (1.5 units.hr-1) on blood, plasma, and brain glucose concentrations to determine their relationship during decreasing blood and plasma glucose levels. The data were compared to saline-treated diabetic rats and saline-treated nondiabetic littermates. The volume and duration of the treatment infusion were similar in all groups. Insulin infusion in diabetic rats produced the expected reduction in blood and plasma glucose, and normoglycemia was produced within 78 +/- 37 minutes (mean +/- SD). However, once normoglycemia was achieved, brain glucose was still significantly greater by 44% than in nondiabetic rats (p = 0.015). Moreover, the ratio of brain to plasma glucose was more than 50% greater in diabetic than nondiabetic rats, irrespective of whether or not they received insulin (p less than 0.01). We conclude that measurement of blood or plasma glucose in diabetic subjects will tend to underestimate the amount of glucose in the brain and that this relationship is not influenced by acute insulin therapy.
Stroke 1991 Apr
PMID:Effects of insulin on blood, plasma, and brain glucose in hyperglycemic diabetic rats. 190


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