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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vivo 31P nuclear magnetic resonance spectroscopy was used to monitor the time course of intracellular pH in cat cerebral cortex subjected to global cerebral ischemia under control and hyperglycemic pretreatment conditions. Transient (16 minutes) global cerebral ischemia was induced in 14 cats using an inflatable cervical cuff combined with systemic arterial hypotension. Six cats were pretreated with infusion of 1.5 g/kg glucose prior to ischemia. Relative concentrations of high-energy phosphate metabolites and intracellular pH were continuously monitored before, during, and for 2 hours after cerebral reperfusion. During ischemia, intracellular pH fell to the same level and followed a similar time course in both groups. However, during initial reperfusion in the hyperglycemic group, there was a severe further decline (p less than 0.003) in intracellular pH. We suggest that the increased neurologic deficit and mortality found in hyperglycemic animals subjected to cerebral ischemia may be attributed to this transient severe tissue acidosis.
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PMID:Intracellular acidosis during and after cerebral ischemia: in vivo nuclear magnetic resonance study of hyperglycemia in cats. 362 52

Phosphorus-31 magnetic resonance (31P MR) spectroscopy was used to obtain serial in vivo measurements of cerebral adenosine triphosphate (ATP), phosphocreatine (PCr), inorganic phosphate (Pi), and intracellular pH levels in rats during temporary global cerebral ischemia and reperfusion. Three groups of 4 rats each that recovered from permanent bilateral vertebral artery occlusion were placed in a MR spectrometer and subjected to remotely controlled bilateral carotid artery occlusion lasting 6, 15, or 30 minutes followed by 1 hour of reperfusion. Four additional rats that developed systemic hypotension (2 during a 6-minute occlusion and 2 during a 15-minute occlusion) were also studied. 31P MR spectra were obtained in each rat before, during, and after ischemia. Rats in which MR spectra showed metabolic recovery underwent a second occlusion followed by reperfusion and sacrifice. In the 12 normotensive rats, metabolic alterations began within 3 minutes after the onset of global ischemia. By the end of the occlusion period, cerebral ATP had decreased by 20 to 100% in 10 rats and PCr had decreased by 15 to 75% in all 12; Pi increased by 25 to 240%. The mean intracellular pH decreased from 7.33 to 6.9 +/- 0.6. The degree of metabolic deterioration during ischemia was not related to the duration of occlusion. During reperfusion, ATP, PCr, Pi, and intracellular pH returned to normal in 4 rats; 5 rats had partial metabolic recovery, and 3 had minimal or transient metabolic recovery followed by progressive deterioration. All rats that developed systemic hypotension had a decrease in ATP, PCr, and intracellular pH and an increase in Pi during the initial occlusion. Each had transient partial recovery in ATP during reperfusion, and 2 had slight recovery of PCr. The onset of hypotension was followed by depletion of these metabolites, progressive increase in Pi, and progressive intracellular acidosis. All rats that deteriorated metabolically after reversal of carotid occlusion died by the end of the reperfusion period or soon after. The 8 rats that recovered from the first occlusion were subjected to a second period of ischemia, during which each rat showed severe depletion of metabolites. During the second reperfusion, only 1 rat showed significant metabolic recovery, which lasted only 30 minutes and was followed by progressive deterioration. Severe global cerebral ischemia was associated with a progressive decline in both ATP and PCr, whereas less complete ischemia seemed to be characterized by stabilization or recovery of ATP and continued depression of PCr.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sequential in vivo measurement of cerebral intracellular metabolites with phosphorus-31 magnetic resonance spectroscopy during global cerebral ischemia and reperfusion in rats. 369 5

The study was performed to elucidate whether the biological plasticity of the brain is reduced with advancing age. Both glucose and energy metabolism in the brain cortex of male Wistar rats aged 6, 12, 24 and 30 months were investigated under normal conditions and in 12 and 24 months old rats under complete cerebral ischemia. Under physiological conditions, glucose, fructose-1,6-phosphate and ATP decreased from 6 to 12 months of age whereas pyruvate, malate and creatine phosphate fell from 12 to 30 months of age. It was concluded that glucose and energy metabolism in brain cortex may be slightly reduced with normal aging. Complete cerebral ischemia caused server reduction in cortical glucose, pyruvate, citrate, alpha-ketoglutarate, malate, oxaloacetate, ATP and creatine phosphate and an increase in fructose-1,6-phosphate, lactate, succinate and AMP. Differences between 12 and 24 month old animals became obvious. It is concluded that aged animals as compared to adult animals are not capable of reacting sufficiently to stress conditions. The biological capacity of the brain is assumed to be reduced with aging.
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PMID:[Biologic plasticity of the aging brain]. 376 73

Fluosol-DA (Perfluorochemical Blood Substitute) was investigated in a previous study and found to provide some protection from ischemia and possible usefulness in limiting the size of infarction. In the present study, larger doses over longer periods of acute focal cerebral ischemia were used. Twenty four cats had transorbital ligation of the middle cerebral artery (MCA). The 12 experimental animals were given 20% Fluosol-DA. The control group of 12 received isotonic saline solution. Twenty-four hours after the MCA occlusion, the cats were perfused with saline and phosphate-buffered formalin. The brains were removed and immersed in 10% formalin for 2 weeks. The results of macroscopic and histological examination suggested that, although Fluosol-DA did not provide complete protection from ischemic injury to the brains of the cats treated, it may have helped to slow the development of the pathological changes.
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PMID:Modification of cerebral ischemia with Fluosol. 396 63

The energy state of the brain during and after transient cerebral ischemia was examined in rats by in vivo measurement of 31P-nuclear magnetic resonance (NMR) spectra using a topical magnetic resonance spectrometer. EEGs and regional CBF (rCBF) were monitored on the same ischemic models. Immediately after the induction of ischemia, the height of the ATP and phosphocreatine peaks in the spectrum began to decrease with a concurrent increase of the inorganic phosphate (Pi) peak. The calculated pH from the chemical shift of Pi decreased during ischemia. The EEG pattern became flat immediately after ischemic induction. The rCBF decreased below the sensitivity level of the measuring instrument. With 30-min ischemia, the 31P-NMR spectrum returned to a normal pattern rapidly after recirculation. However, recovery of the EEG was delayed. The rCBF after recirculation showed postischemic hyperemia followed by hypoperfusion. In cases of 120-min ischemia, none of the spectra showed recovery. Thus, we could investigate the dynamic process of pathophysiological changes occurring in the ischemic brain in vivo.
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PMID:In vivo studies of energy metabolism in experimental cerebral ischemia using topical magnetic resonance. Changes in 31P-nuclear magnetic resonance spectra compared with electroencephalograms and regional cerebral blood flow. 398 22

Phosphatic metabolite (perchloric acid extractable) concentrations of cerebral tissues were analyzed by phosphorus-31 nuclear magnetic resonance (P-31 NMR) spectroscopy following external perfusion of the isolated rat brain (30 min or 60 min) under the following conditions: (a) constant perfusion pressure with either fluorocarbon- or erythrocyte-based medium, and (b) constant perfusate flow rate (3 ml/min) with the erythrocyte-based medium. Metabolite concentrations of control perfused brains were compared with those in nonperfused controls to provide a basis for detecting any qualitative or quantitative changes in cerebral metabolite composition. Metabolic responses of perfused brains to ischemia (incomplete ischemia, 83% reduction in flow for 10 min; transient complete ischemia for 1.5 or 2 min) were evaluated immediately after the ischemic episode and at selected time points during reperfusion (3 and 15 min). Alterations in cerebral metabolite levels induced by hypoxia were analyzed using a nonperfused rat brain model. Irrespective of the perfusion method employed, the phosphatic metabolites of control perfused rat brains were identical quantitatively to those of the nonperfused controls. Cerebral ischemia resulted in significantly increased levels of ADP, AMP + IMP, Pi, fructose 1,6-diphosphate, and glycerol 3-phosphate (global ischemia only), whereas ATP and phosphocreatine (PCr) levels declined significantly. The magnitude of these changes varied with the severity of the ischemia; however, following 15 min of control reperfusion metabolite levels had reverted to preischemic values. Significant perturbations in tissue phosphoethanolamine (3.84 delta resonance) content were evident at various time points during ischemia and postischemic recovery, which varied according to the perfusion conditions. In contrast to the changes observed in response to ischemia, hypoxia affected only cerebral high-energy phosphate levels. ATP and PCr levels were reduced, while a concomitant, essentially equimolar, increase in Pi and ADP was observed. The present studies indicate that in terms of phosphatic metabolites, the control equilibrated isolated perfused rat brain is quantitatively and qualitatively indistinguishable from the nonperfused rat brain in vivo regardless of the perfusion conditions (constant flow versus constant pressure). The metabolic responses to ischemia and hypoxia, as measured by P-31 NMR, were consistent with the pattern of changes reported elsewhere. Overall, P-31 NMR spectroscopic evaluation of the intact rat brain provides a potential experimental context for dynamic measures of cerebral metabolism under exogenously controlled conditions. Th
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PMID:P-31 nuclear magnetic resonance analysis of brain: II. Effects of oxygen deprivation on isolated perfused and nonperfused rat brain. 609 45

Effects of perfluorochemical (PFC) and glycerol on energy metabolism in cerebral ischaemia were examined by the sequential measurements of in vivo 31P-NMR spectrum using topical magnetic resonance (TMR). Experimental cerebral ischaemia was induced in forty-five Wistar rats by a four-vessel occlusion method. The 31P-NMR spectrum and the EEG were monitored during preischaemic and ischaemic periods and after circulation was restored for various periods up to 240 min. There were several peaks in the 31P-NMR spectrum of the preischaemic rat brain; beta-ATP, alpha-ATP, gamma-ATP, phosphocreatine (PCr), phosphodiesters, inorganic phosphate (Pi) and sugar phosphate. As soon as the ischaemia was induced, PCr and ATP decreased and Pi increased. The chemical shift of the increased Pi peak decreased, showing acidosis of the brain tissue. After circulation was restored following the 30 min ischaemia, recovery of the 31P-NMR spectrum occurred within 30 min in all sixteen untreated rats. Recovery of the 31P-NMR spectrum was induced by recirculation only in half of the six rats in the untreated 60 min ischaemia group. None of the six rats in the untreated group showed recovery of the spectrum after 120 min ischaemia. When 20% Fluosol-DA was administered at a dose of 20 ml/kg before the induction of ischaemia, all eight rats showed recovery of the spectrum after 120 min ischaemia. Moreover, four of six rats treated with both PFC and glycerol showed temporary recovery even after 240 min ischaemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Measurements of in vivo energy metabolism in experimental cerebral ischaemia using 31P-NMR for the evaluation of protective effects of perfluorochemicals and glycerol. 615 9

Metabolic changes in the ischemic brains of cats were investigated in vivo with high energy phosphate compounds as parameters by using a topical magnetic resonance (TMR) spectrometer. The experimental focal cerebral ischemia was made in four cats by modifying the method of O'Brien and Waltz. The stem of left middle cerebral artery was exposed and set the occlusive device 5-7 days before the in vivo measurement. 31P-NMR spectrum was taken under general anesthesia with Ketamine HCI and with decreased blood flow. The following points must be considered in obtaining 31P-TMR spectrum in a cat brain: Firstly, as much muscle as possible must be removed from the detective area because it contains phosphate compounds. Our experiment showed that bone and blood had little or no effect on the 31P-TMR spectrum. Secondly, although same procedure was repeated, it was difficult to obtain constant ischemic lesion; in site and size. The detective area in setting was not changed in the particular area. However there was a possibility of the detective area also including various non-ischemic regions. Thirdly, 31P-TMR spectrum had several peaks in a cat brain; which were sugar phosphate, inorganic phosphate, phosphodiesters, phosphocreatine, gamma-, alpha-, beta-ATP in the pre-occlusive conditions. These peaks did not appear in clear volume separation with one another. We drew the perpendicular line from through between two neighbour peaks to the horizontal base line and artificially divided two peaks. The area of each peak did not represent correctly the density of each component. Fourthly, unnecessary components were rationalistically excluded from the 'raw' spectrum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Research on experimental cerebral infarction in cats with in vivo TMR (topical magnetic resonance) approach]. 646 7

Effects of new antihypoxic agent (bifemelane) on survival and brain metabolism were studied in acute cerebral ischemia induced by bilateral carotid artery ligation in mongolian gerbils and SHR. Either 10 mg/kg or 30 mg/kg body weight of bifemelane solved in distilled water was intraperitoneally administered 1 hr in gerbils and 1.5 hrs in SHR prior to carotid ligation, and same amount of vehicle was also given in similar manner for control animals. Brain tissue metabolites such as lactate, pyruvate and ATP were determined by using the enzymatic technique in the ischemic brain frozen in situ 1 hr after carotid ligations in SHR. Mean survival times following carotid ligations were 186 +/- 255 min (+/- SD) in control gerbils, 429 +/- 455 min in those with 10 mg/kg of bifemelane, and 310 +/- 429 min in those with 30 mg/kg respectively, its difference between control and 10 mg/kg group being significant (P less than 0.05). Supratentorial lactate concentrations in the ischemic brains of SHR were substantially the same among the groups, whereas ATP levels were 0.62 +/- 0.24 mM/kg in control animals, 1.10 +/- 0.67 mM/kg in rats with 10 mg/kg of the drug, and 1.13 +/- 0.42 mM/kg in those with 30 mg/kg, respectively. In animals with a high dose pretreatment, the reduction of ATP was significantly smaller than that in control (P less than 0.02), indicating that this agent prevents a decline of high energy phosphate in the ischemic brain although anaerobic metabolites increase similarly in animals of all experiment groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Protective effects of 4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride (bifemelane) on acutely induced cerebral ischemia in Mongolian gerbils and spontaneously hypertensive rats (SHR)]. 651 31

Respiratory activity of isolated rat brain mitochondria was measured following in vitro exposure to oxygen radicals. The radicals were generated by hypoxanthine and xanthine oxidase in the presence of a suitable iron chelate and caused a severe inhibition of respiration stimulated by phosphate plus ADP (with malate + glutamate as substrate). The damage could be prevented by catalase or high concentrations of mannitol, but not by superoxide dismutase. A similar effect was observed when hypoxanthine and xanthine oxidase were replaced by glucose and glucose oxidase or by hydrogen peroxide. Most of the findings indicate that the hydroxyl radical is the damaging agent. It is concluded that brain mitochondria exposed to oxygen radicals in vitro show an inhibition of respiratory activity similar to that reported by other investigators as occurring in mitochondria in vivo following transient cerebral ischemia. Therefore, oxygen radicals may contribute to this type of cell damage.
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PMID:Respiratory activity of isolated rat brain mitochondria following in vitro exposure to oxygen radicals. 684 68


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