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

The neurologic outcomes following incomplete cerebral ischemia in rats treated by fasting, nonfasting, or glucose administration (6 ml/kg of 50% glucose solution intraperitoneal) were compared. Rats were anesthetized with 1.4% inspired isoflurane in air and incomplete ischemia was produced by temporary unilateral carotid occlusion and hypotension of 30 mmHg for 30 min. The rats were recovered and neurologic outcome was scored every 8 h for 3 days using a 6-point scale ranging from 0 (normal) to 5 (death associated with stroke). Brain histopathology was scored using a four-point scale on 19 of 30 rats surviving the 3-day postischemic neurologic examination and was correlated with neurologic deficit scores. Fasted rats had plasma glucose concentrations of 79 +/- 7 mg/100 ml (mean +/- SE) during ischemia and a significantly better neurologic outcome (P less than 0.001) than glucose-loaded rats (plasma glucose = 496 +/- 43 mg/100 ml). Nonfasted rats had blood glucose values (292 +/- 28 mg/100 ml) and deficit scores not significantly different from fasted but better than glucose-loaded rats (P = 0.054). Brain histology showed the greatest neuronal damage in caudate followed by hippocampus and cortical tissue. Histopathologic evaluation showed a correlation of r = 0.87 (P less than 0.01) with neurologic outcome. In separate experiments brain samples were collected at the end of the ischemic period in each of the experimental groups and regional tissue lactate and brain phosphocreatine and adenosinetriphosphate (ATP) concentrations were measured. Ischemic tissue lactate was similar in fasted, nonfasted, and glucose-loaded rats in caudate and hippocampus but was significantly higher in glucose loaded rats in cortical and thalamic tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brain lactate and neurologic outcome following incomplete ischemia in fasted, nonfasted, and glucose-loaded rats. 235 19

The energy metabolism of the brain was measured in three types of ischemic models in the cat using phosphorus-31 magnetic resonance spectroscopy. The cerebral ischemia was produced as follows. In Group 1, two balloons were inflated in the left subclavian artery and the brachiocephalic trunk. In Group 2, the left middle cerebral artery was occluded through a transorbital approach. A combination of the two was employed in Group 3. Phosphorus-31 magnetic resonance spectra were obtained serially during 2 hours of ischemia. Immediately after occlusion, peaks of phosphocreatine and adenosine triphosphate decreased, whereas the peak of inorganic phosphate increased and split in two. Intracellular pH determined by chemical shift of the inorganic phosphate peak decreased. These changes were more pronounced in Group 3 when compared with the other groups. Histological study showed no infarction in Group 1 and infarcted areas in Groups 2 and 3. The size of the infarcted area in Group 3 was larger than that in Group 2. These results suggest that the model of middle cerebral artery occlusion potentiated with the occlusion of the brachiocephalic trunk and the left subclavian artery by balloon catheters is a reliable stroke model and that phosphorus-31 magnetic resonance spectroscopy is useful to understand the pathophysiological state of cerebral ischemia in vivo.
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PMID:Phosphorus-31 magnetic resonance spectroscopy of cerebral ischemia in cats. 238 42

Image-guided 31P and 1H magnetic resonance localized spectroscopy was performed on patients with brain tumors, temporal lobe epilepsy, chronic brain stroke, and deep white matter lesions. Absolute molar concentrations of metabolites, peak area ratios, and pH were obtained. The important findings were that 31P metabolite concentrations were significantly reduced in tumors, infarcts, and deep white matter lesions. Similarly, 1H metabolite intensities were reduced in chronic stroke. In the seizure foci of epilepsy patients, in tumors, and in chronic stroke, the pH was more alkaline than the normal pH. Peak area ratios were altered in tumors (reduction of phosphocreatine/inorganic phosphate (PCr/Pi) and in chronic stroke (large increases in Cr/NAA and Cho/NAA). Finally, the spectroscopic imaging technique offers a versatile alternative to the "single point" techniques, producing spectra or images of the spatial distribution of individual 31P metabolites.
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PMID:Clinical MRS studies of the brain. 255 86

The effects of acute volume and/or pressure loading on myocardial metabolic and mechanical function were studied in 13 dogs. Volume loads were applied by shunting the abdominal aorta to the vena cava using polyethylene tubing (5 mm inner diameter). A plastic regulator allowed shunts to be opened or closed. Dogs were heparinized (100 units/kg) to prevent shunts from clotting. To study the effects of pressure loading, a norepinephrine infusion (1 microgram/kg/min) was administered. Mechanical function of the heart was evaluated using heart rate X systolic blood pressure (HR X SBP), cardiac output (CO), pressure X volume work (systolic blood pressure X stroke volume); (P X V), and oxygen consumption (MVO2) to estimate external myocardial work. Metabolic function was evaluated by 31P NMR. Phosphocreatine/adenosine triphosphate (PCr/ATP) ratios were used to estimate the bioenergetic regulation of oxidative phosphorylation during increased work load. HR X SBP, CO, P X V, and MVO2 were correlated with PCr/ATP. Although there was some variability, generally volume loading was associated with an increase in HR X SBP, CO, P X V, and MVO2 accompanied by no change, or small increases or small decreases in PCr/ATP throughout the loading period. These data indicate that the heart bioenergetics are quite stable during volume and/or pressure loading and that 31P spectroscopy methods can document this stability and tight metabolic regulation during in vivo loading conditions.
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PMID:In vivo myocardial bioenergetics during acute volume and/or pressure loading in a canine model: a 31P NMR study. 261 95

During perinatal asphyxia, cerebral blood flow is markedly reduced in the gray and white matter of the telencephalon. Since previous work has implicated prostaglandins in the control of blood flow, we tested the hypothesis that a thromboxane synthesis inhibitor would improve cerebral blood flow and blunt the metabolic alterations that accompany asphyxia. Forty-three newborn beagles 2-7 days old were anesthetized, ventilated, and randomized to insult (5 minutes of asphyxia) or no insult and received treatment with either the thromboxane synthesis inhibitor CGS 13080 (CIBA-GEIGY Corp.) (0.06 mg/kg/hr i.v. infusion) or saline. Cerebral blood flow was measured in 25 pups. Pups received treatment 30 minutes before insult or no insult. In pups randomized to insult and receiving saline, cerebral blood flow increased during insult in the medulla but decreased elsewhere. Pups randomized to insult and treated with thromboxane synthesis inhibitor had increased cerebral blood flow during insult in all cerebral regions studied. In addition, these pups experienced a significantly higher incidence of intraventricular hemorrhage than did pups randomized to insult and receiving saline. In other experiments with 18 pups, brain extracts were prepared for proton nuclear magnetic resonance spectral analysis of high-energy phosphorylated compounds and lactate levels. In pups exposed to insult and receiving saline, mean +/- SD phosphocreatine concentration fell from 1.9 +/- 0.1 to 0.4 +/- 0.1 mmol/kg, lactate concentration increased from 2.0 +/- 0.5 to 3.3 +/- 0.4 mmol/kg, and the calculated pH fell 0.8 units. There were no differences between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1989 Jun
PMID:Thromboxane synthesis inhibitor in a beagle pup model of perinatal asphyxia. 272 50

We investigated the effect of mild whole-body hyperthermia before and after 16 minutes of global cerebral ischemia on metabolic recovery during recirculation in cats using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy. Hyperthermia (temperature 40.6 +/- 0.2 degrees C) was induced greater than or equal to 1 hour before ischemia and was maintained during 1.5-2 hours of recirculation in nine cats; four cats were subjected to hyperthermia without cerebral ischemia, six to hyperthermia during recirculation (after return of intracellular pH to preischemic values), and 14 to normothermic ischemia and recirculation. Our data indicate that preischemic hyperthermia results in an intracellular cerebral pH during recirculation significantly lower than that in normothermic cats. In hyperthermic cats beta-ATP and phosphocreatine (PCr) concentrations and the ratio of PCr to inorganic phosphate failed to return to preischemic levels during recirculation in contrast to normothermic cats. Hyperthermia without ischemia and hyperthermia during recirculation had no significant effect on intracellular pH. Thus, preischemic hyperthermia has a detrimental effect on metabolic recovery after transient global cerebral ischemia.
Stroke 1988 Dec
PMID:Effect of mild hyperthermia on recovery of metabolic function after global cerebral ischemia in cats. 320 11

Dihydropyridine calcium channel blockers such as nicardipine are under evaluation for treating acute cerebral ischemia because they may increase cerebral blood flow by causing vasodilation and because they may be cytoprotective in part by limiting production of arachidonic acid metabolites. We demonstrated in a previous study that nicardipine improves postischemic neuronal function, as measured by somatosensory evoked potentials, without reducing the extent of light-microscopic CA-1 hippocampal histologic damage. To characterize further the effect of nicardipine on global ischemic injury, we administered the drug beginning 24 hours before 30 minutes of four-vessel ischemia in Wistar rats. We then measured hippocampal ATP, phosphocreatine, and glucose contents immediately and 2 hours after ischemia, and measured learning ability (working and reference errors) on an eight-arm radial maze beginning 30 days after ischemia. To gain insight into the possible mechanism of action, we measured production of arachidonic acid metabolites (eicosanoids: TXB2 and 6-keto-PGF1 alpha) and hemispheric and hippocampal cerebral blood flow by the [14C]butanol indicator fractionation technique immediately and 2 hours after ischemia. Nicardipine was associated with fewer working errors (p less than 0.02) but no difference in reference errors. The drug had no effect on energy metabolites, cerebral blood flow, or eicosanoids immediately after ischemia, but ATP, phosphocreatine, and cerebral blood flow all returned to normal levels significantly more rapidly during reperfusion in treated rats. Nicardipine improves behavioral, electrophysiologic, and mitochondrial function after ischemia without preventing cellular damage and improves postischemic reperfusion. The drug's positive effect appears to occur during reperfusion.
Stroke 1988 Apr
PMID:Efficacy and mechanism of action of a calcium channel blocker after global cerebral ischemia in rats. 336 73

Progressive cerebral ischemia was induced in seven anesthetized hyperglycemic rats by carotid artery ligation and hemorrhagic hypotension. Phosphorus metabolites, intracellular pH, and lactate in the brain were monitored by 31P and 1H magnetic resonance spectroscopy. Under conditions in which blood flow was low, phosphocreatine (PCr) concentration and intracellular pH decreased and the concentration of lactate increased. The decrease in ATP was approximately one-third that of PCr until only 25% PCr remained, after which ATP was lost more rapidly than PCr. These changes were interpreted in terms of three regions observed by the magnetic resonance coil, one of complete ischemia, one of partial ischemia, and one of perfusion sufficient to maintain normal metabolite levels. The extent of the three regions was estimated quantitatively. Broadening and splitting of the inorganic phosphorus (Pi) peak into two components provided further evidence of distinct populations of cells, one very acidic and another less so. Apparent intracellular buffering capacity was calculated as 23.6 +/- 1.3 mumol lactate/g wet wt/pH.
Stroke 1988 May
PMID:Metabolic changes during experimental cerebral ischemia in hyperglycemic rats, observed by 31P and 1H magnetic resonance spectroscopy. 336 94

Eight cats were subjected to graded hemorrhagic hypotension following bilateral carotid ligation to produce incomplete global cerebral ischemia. Three additional cats served as controls. The somatosensory evoked potential (SEP) and direct cortical response (DCR) were monitored in all animals and in each case, the cortical component of the SEP was abolished during progressive ischemia while the morphology of the DCR was well-preserved but with reduced amplitude. Determinations of adenosine triphosphate (ATP), phosphocreatine (PCr), and lactate levels in cerebral cortex and white matter were made in five experimental cats and the three controls. At the time of failure of the cortical SEP, PCr was dramatically reduced and lactate moderately elevated in the white matter while ATP remained unchanged. Cortical lactate was only mildly elevated and PCr and ATP were unchanged accounting for preservation of the DCR. In this model of global ischemia, abolition of the cortical SEP is due to a block of stimulus conduction in white matter projection pathways. A hypothesis to explain the observed metabolic changes is presented and correlation is made to clinical situations.
Stroke
PMID:Comparison of the somatosensory evoked potential and the direct cortical response following severe incomplete global ischemia: selective vulnerability of the white matter conduction pathways. 381 Jul 28

Graded transient cerebral hemispheral ischemia was produced in nitrous oxide-anesthetized Wistar rats by a procedure combining unilateral common carotid artery occlusion; elevation of intracranial pressure to 40-45 mm Hg by infusion of mock cerebrospinal fluid; and maintenance of arterial blood pressure at 100-110 mm Hg by controlled hemorrhage. Cerebral perfusion pressure was thus reduced into the ischemic range ipsilateral to carotid occlusion but remained 55-70 mm Hg contralaterally. Regional cerebral blood flow, measured autoradiographically, fell by 85-90% in the ischemic dorsolateral and lateral neocortex, hippocampus and lateral striatum, but remained at 71% of control or higher contralaterally. Metabolite assay revealed a gradient of energy depletion, with profound reductions in ATP and phosphocreatine and marked elevations of lactate in lateral neocortex, lateral striatum, hippocampus and lateral thalamus. Importantly, dorsolateral neocortex proved to be a penumbral zone, with marked lactate elevation comparable to that of lateral cortex, yet only intermediate degrees of ATP and PCr reduction. Contralateral structures were metabolically unaffected apart from mild increases in lactate. The advantages of this focal ischemia model include the consistent topographic distribution of ischemia and its regional gradations of intensity; the avoidance of painstaking intracranial microsurgery and of systemic complications; preservation of intact energy state of the contralateral hemisphere; ease of reversibility of ischemia; and lack of seizures. The consistent metabolic penumbral zone is a unique feature of the model.
Stroke
PMID:Graded focal cerebral ischemia in the rat by unilateral carotid artery occlusion and elevated intracranial pressure: hemodynamic and biochemical characterization. 400 62


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