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

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

Moderate unilateral cerebral ischemia was produced by microembolism in 24 adult cats. Two million plastic microspheres with a diameter of 15 +/- 5 microns were injected into the left common carotid artery via the lingual artery. The physiological and metabolic responses to embolism were accessed by electrocorticography and by determining the cerebral energy state. Embolism caused an immediate slowing and voltage reduction of the ipsilateral electrocorticogram with a gradual recovery after 30 to 60 min. Some animals also had an immediate and short depression of the contralateral electrocorticogram. In spite of the market functional suppression, metabolites of the cerebral energy-producing metabolism in most of the animals changed only slightly. In the embolized hemisphere pyruvate increased from 0.06 to 0.10 mumol/g and lactate from 1.9 to 4.6 mumol/g within 5 min after embolization and remained at this level during the 4 h observation period. Phosphocreatine, adenosine triphosphate and the energy charge of the adenylate pool remained uncharged during this period. However, there was a slight increase of ATP in the non-embolized hemisphere during the early postembolic period. In two animals, the initial slowing of the electrocorticogram recurred and spread to the contralateral hemisphere, followed by bilateral flattening after a few hours. This delayed functional deterioration was accomplished by complete loss of energy-rich phosphates. These animals also had a progressive increase of cerebrospinal fluid (CSF) pressure and considerable brain swelling with cerebellar herniation after 4 h. It is concluded that unilateral cerebral embolism in the above concentration leads only to a slight increase of anerobic glycolysis without significant perturbation of the cerebral energy state, unless progressive brain swelling with cerebrellat herniation supervenes. This supports previous findings, that brain edema and not initial ischemia is the main pathogenetic factor for tissue damage in cerebral microembolism.
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PMID:The effect of mild microembolic injury on the energy metabolism of the cat brain. 615 90

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

The effect of asphyxia on seizures was determined in neonatal dogs. In normoxic (paralyzed and ventilated) neonatal dogs, bicuculline-induced seizures produced significant elevations of arterial blood pressure, PO2, glucose, lactate, and epinephrine. Cerebral blood flow increased severalfold; brain glucose, adenosine triphosphate (ATP), and phosphocreatine (PCr) did not decrease significantly. In contrast, seizures during asphyxia were associated with hypoxia, hypotension, hypercarbia, and acidosis. Significant cerebral ischemia developed. Brain glucose, ATP, and PCr were significantly depleted. Complete oxygen deprivation during neonatal seizures exhausts brain energy stores, which leads to cessation of seizure activity.
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PMID:Physiologic and metabolic alterations associated with seizures in normoxic and asphyxiated neonatal dogs. 647 9

Pentoxifylline 0.3--30 mg/kg was given intravenously to six dogs under nitrous oxide anesthesia. Cerebral blood flow was measured with a sagittal sinus outflow technique, cerebral oxygen consumption was calculated from the a-v difference, and metabolite levels were determined in biopsies of cerebral cortex. Pentoxifylline failed to influence cerebral blood flow or oxygen consumption. There was no increase in cerebral levels of phosphocreatine, ATP or total adenine nucleotides; the only significant effect was higher glucose levels in dogs given pentoxifylline (4.49 +/- 0.39 mumol/g vs 2.21 +/- 0.18 mumol/g). The latter has previously been reported to be deleterious during cerebral ischemia. Pentoxifylline thus failed to have any significant influence upon cerebral blood flow or metabolism in the dog likely to be of benefit during cerebral hypoxia or ischemia.
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PMID:Pentoxifylline does not change cerebral blood flow or metabolism in the dog. 679 17

The cerebral metabolic responses to perinatal hypoglycemia (blood glucose less than or equal to 1 mmol/l) combined with asphyxia were studied in paralyzed, lightly anesthetized newborn dogs. No major differences in heart rate, blood pressure or arterial acid-base balance between control and hypoglycemic animals occurred either prior to or during asphyxia. The electroencephalogram, unaltered by hypoglycermia alone, became isoelectric at the same intervals in both groups following respiratory arrest. Intravenous carbon black infusion at 5 min of asphyxia demonstrated no relationship between blood glucose level and cerebral perfusion (p > 0.05), whereas a positive correlation did exist between systemic blood pressure and cerebral perfusion (p < 0.01). During asphyxia, anaerobic glycolysis in brain was less enhanced in hypoglycemic dogs, resulting in a more rapid exhaustion of high-energy phosphate reserves (phosphocreatine, ATP and ADP). Thus, the cerebral metabolic responses to asphyxia superimposed upon hypoglycemia were the direct consequence of insufficient cerebral glucose stores coupled with deficient circulating glucose to brain. These metabolic disturbances were no more the result of cerebral ischemia than that which occurs during asphyxia alone. The findings also suggest that systemic physiological monitoring may be an inadequate means of appraising cerebral homeostasis during combined hypoglycemia ad hypoxia.
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PMID:Cerebral metabolism during hypoglycemia dn asphyxia in newborn dogs. 689 22

The low cerebral energy requirements of most mammals at birth reflect an immaturity of the central nervous system, and it has been suggested that energy demands in fetuses are even less well developed than in newborns. Furthermore, fetal cerebral energy requirements are presumed to be met predominantly or exclusively by anaerobic glycolysis. To clarify these issues, we investigated cerebral oxidative metabolism in 9-, 14-, 16-, and 19-day-old chick embryos and in newly hatched peeps. Animals were decapitated and quick-frozen in liquid Freon 0--5 min post-mortem. Forebrain extracts were prepared and assayed for ATP, phosphocreatine, glucose, and lactate. Alterations in these metabolites post-decapitation were used to calculate cerebral metabolic rates (delta similar to P) and rates of maximal anaerobic glycolysis (delta lactate). Rates of lactate accumulation during cerebral ischemia increased progressively from embryonic day 9 through hatching. Cerebral metabolic rates were not different in 9-, 14-, and 15-day-old embryos, but increased steadily thereafter. The extent to which total cerebral energy utilization could be derived from anaerobic glycolysis (delta lactate/delta similar to P) increased from a low at day 9 (0.29) to a maximum at day 16 (0.78). The data suggest that, despite the low cerebral metabolic activity of the chick embryo, at no time during development is anaerobic glycolysis capable of entirely supporting the energy needs of the developing brain.
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PMID:Ontogeny of cerebral oxidative metabolism in the chick embryo. 706 56

Cerebral ischemia was induced in cats using bilateral carotid artery occlusion coupled with hemorrhagic hypotension. Thirty minutes of ischemia, which depleted levels of ATP and phosphocreatine throughout the cerebral cortex, was followed by 2-4 hours of recirculation. During the recovery period, cortical perfusion and NADH fluorescence were monitored through a cranial window. Postischemic perfusion, as indicated by transit time, was initially higher than control, but declined to subnormal levels by 60 minutes. NADH fluorescence transients, induced by brief anoxia, also decreased steadily during recirculation, indicating a failure of oxidation-reduction capability. The disappearance of anoxic-NADH transients usually preceded the decline of flow, suggesting that O2 delivery was not the factor limiting redox reactions. Furthermore, tissue levels of NADH, which were nearly normal after 2-4 hours of recirculation, did not indicate tissue hypoxia. In spite of normalization of NADH, resynthesis of high energy phosphates were severely impaired. The degree of ATP recovery varied widely in different cortical regions; however, there were two general groups of ATP values--one at 5% and the other at 70% of control levels. In the energy-depleted areas, NADH levels were normal, but the total pool of NAD (NADH + NAD+) and the tissue content of K+ were 43% lower than control. In contrast, the NAD pool and K+ content were only slightly diminished in the regions with greater ATP restitution. The results suggest that postischemic resynthesis of ATP may be limited not by inadequate delivery of O2, but rather by defective production of NADH.
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PMID:Factors limiting regeneration of ATP following temporary ischemia in cat brain. 706 95

Glucose was infused intravenously into cats prior to cerebral ischemia. Brain concentrations of glucose, measured in 7 regions, were elevated 2.5-fold compared to those of non-infused animals. Ischemia of 15 or 30 minutes duration caused a greater accumulation of lactic acid in the brain of glucose-infused animals. Post-ischemic restitution of cerebral ATP, phosphocreatine, and lactate during 90 minutes of recirculation was severely impaired in the brain of animals pretreated with glucose compared to untreated animals. Thus, excess lactic acidosis may be a major factor interfering with metabolic restitution following cerebral ischemia.
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PMID:Deleterious effect of glucose pretreatment on recovery from diffuse cerebral ischemia in the cat. II. Regional metabolite levels. 741 63

In order to investigate changes in energy metabolism, neurotransmitters, and membrane disorder accompanying incomplete cerebral ischemia, a bilateral common carotid artery occlusion model of spontaneously hypertensive rats was utilized. We measured concentrations of ATP, phosphocreatine (PCr), lactate (Lac), glucose (Glu), acetylcholine (ACh), choline (Ch), and gamma-aminobutyric acid (GABA) in both the cerebral cortex and the subcortical regions after 1 h ischemia, 2 h ischemia, and 2 h reflow following 2 h ischemia, and then examined changes in concentrations of these substances during and after incomplete cerebral ischemia. Also, examined were interrelations of changes in these substance levels during ischemia. In the cerebral cortex, levels of ATP, PCr, Glu, and ACh decreased, and levels of Lac, Ch, and GABA increased during ischemia. After recirculation, levels of ATP, PCr, Ch, and GABA tended to return to the normal range. On the other hand, the Lac level remained in the ischemic range and the Glu level rose and greatly exceeded the normal range. With regard to ACh, most animals showed normal levels but some exceeded the normal range. Changes in the subcortical regions were qualitatively the same as those in the cerebral cortex during and after ischemia (except with Glu), but only smaller in degrees. Glu levels remained unchanged during ischemia. Correlation of the levels of these substances in the cerebral cortex was examined using normal and ischemic values. A high correlation was generally observed between ATP and other substance levels. The relations between ATP and either PCr or Glu levels were linear. The relation between ATP and ACh levels was logarithmic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in brain energy metabolism, neurotransmitters, and choline during and after incomplete cerebral ischemia in spontaneously hypertensive rats. 773 55


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