Proton Magnetic Resonance Spectroscopy of the Brain during Acute Hypoxia-Ischemia and Delayed Cerebral Energy Failure in the Newborn Piglet

Penrice, J; Lorek, A; Cady, Ernest B.; Amess, PN; Wylezińska, M; Cooper, Christopher; D'Souza, Patricia; Brown, Guy C.; Kirkbride, Vincent; Edwards, A. David; Wyatt, JS; Reynolds, E. O. R.

doi:10.1203/00006450-199706000-00001

Cited by 131 publications

(104 citation statements)

References 27 publications

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“…Some animals recovered their normoxic impedance baseline while other animals had a secondary rise of impedance after the initial recovery. This behaviour corresponds to the previously described phases of primary and secondary energy losses (Penrice et al 1997). This should be due to the fact that the physiological system of each piglet responds in a slightly different way to the hypoxic insult and thus affects the timing of the physiological mechanism following hypoxia.…”

Section: High Subject Specificitymentioning

confidence: 99%

Spectroscopy study of the dynamics of the transencephalic electrical impedance in the perinatal brain during hypoxia

Seoane¹,

Lindecrantz²,

Olsson³

et al. 2005

Physiol. Meas.

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Hypoxia/ischaemia is the most common cause of brain damage in neonates. Thousands of newborn children suffer from perinatal asphyxia every year. The cells go through a response mechanism during hypoxia/ischaemia, to maintain the cellular viability and, as a response to the hypoxic/ischaemic insult, the composition and the structure of the cellular environment are altered. The alterations in the ionic concentration of the intra-and extracellular and the consequent cytotoxic oedema, cell swelling, modify the electrical properties of the constituted tissue. The changes produced can be easily measured using electrical impedance instrumentation. In this paper, we report the results from an impedance spectroscopy study on the effects of the hypoxia on the perinatal brain. The transencephalic impedance, both resistance and reactance, was measured in newborn piglets using the four-electrode method in the frequency range from 20 kHz to 750 kHz and the experimental results were compared with numerical results from a simulation of a suspension of cells during cell swelling. The experimental results make clear the frequency dependence of the bioelectrical impedance, confirm that the variation of resistance is more sensitive at low than at high frequencies and show that the reactance changes substantially during hypoxia. The resemblance between the experimental and numerical results proves the validity of modelling tissue as a suspension of cells and confirms the importance of the cellular oedema process in the alterations of the electrical properties of biological tissue. The study of the effects of hypoxia/ischaemia in the bioelectrical properties of tissue may lead to the development of useful clinical tools based on the application of bioelectrical impedance technology.

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Section: High Subject Specificitymentioning

confidence: 99%

Spectroscopy study of the dynamics of the transencephalic electrical impedance in the perinatal brain during hypoxia

Seoane¹,

Lindecrantz²,

Olsson³

et al. 2005

Physiol. Meas.

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“…The porcine model of hypoxic-ischaemic injury reproduced the metabolic derangements seen after human perinatal HI (Azzopardi et al, 1989;Martin et al, 1996;Hanrahan et al, 1996): reduced concentrations of high energy phosphates and increased Lac were observed during HI and again during a delayed phase of injury; pH i fell during HI but not during delayed energy depletion Penrice et al, 1997). The metabolic consequences of HI were variable, providing a dynamic range of injury from moderate to very severe which was precisely quantitated by MRS.…”

Section: Cerebral Energy Metabolismmentioning

confidence: 91%

“…During HI there is a decline in the cerebral concentration of high energy phosphates and an increase in cerebral lactate (Lac) concentration that recovers soon after resuscitation. However, despite restored substrate delivery, some 8 ± 12 h later a delayed phase of reduced phosphorylation potential and increased Lac concentration begins (Vannucci et al, 1994;Lorek et al, 1994;Penrice et al, 1997;Azzopardi et al, 1989;Martin et al, 1996;Hanrahan et al, 1996). The degree of delayed impairment of cerebral energy metabolism predicts the severity of later neurodevelopmental impairment in newborn human infants (Roth et al, 1992), and also the severity of histological injury in newborn piglets (Mehmet et al, 1994;Yue et al, 1996) and rat pups (Blumberg et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Relation of impaired energy metabolism to apoptosis and necrosis following transient cerebral hypoxia-ischaemia

et al. 1998

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This study investigated whether both mild and severe hypoxia-ischaemia (HI) caused significant numbers of cells to die by apoptosis in the developing brain in vivo. Newborn piglets were subjected to transient global HI and the fraction of all cells in the cingulate gyrus that were apoptotic or necrotic counted 48 h after resuscitation. The mean (S.D.) proportion of apoptotic cells was 11.9% (6.7%) (sham operated controls 4.1% (2.7%)), while 11.4% (8.4%) were necrotic (controls 0.7% (1.3%)) (P50.05). Apoptotic and necrotic cell counts were both linearly related to the severity of impaired cerebral energy metabolism measured by magnetic resonance spectroscopy (P50.05), as shown by: (1) the decline in the ratio of nucleotide triphosphates to the exchangeable phosphate pool during HI; (2) the fall in the ratio of phosphocreatine to inorganic phosphate 8 ± 48 h after HI; and (3) an increased ratio of lactate to total creatine at both these times. Thus both apoptosis and necrosis occurred in the cingulate gyrus after both severe and mild HI in vivo in proportion to the severity of the insult.

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“…Gels were electrophoretically transferred to nitrocellulose filters. Glial fibrillary acidic protein (GFAP), microtubule-associated protein (MAP-2), and the synaptic vesicle protein, SNAP-25, were analyzed in paired ipsilateral and contralateral hemispheres, and in agematched controls by Western blot, as previously described (Penrice et al, 1997). GFAP and MAP-2 were detected with mouse monoclonal antibodies from Sigma Immunochemicals (St. Louis, MO); SNAP-25 was detected with a mouse monoclonal antibody, clone SP-14, provided as a gift from Dr. Peter Davies, Albert Einstein Medical College, New York, NY).…”

Section: Measurement Of Neuronal and Glial Protein Markersmentioning

confidence: 99%

“…Reynolds and his research colleagues have championed the theory of a delayed cerebral energy failure, based initially upon research in newborn human infants: 31 P magnetic resonance spectroscopy measurements of newborn human brain have shown an early restitution of the phosphorus spectra upon resuscitation from asphyxia, followed thereafter by a secondary decline in energy status, defined as a tissue depletion of phosphocreatine, ATP, or both compounds (Azzopardi et al, 1989;Hamilton et al, 1986;Hope et al, 1984). More recently, the same research group has demonstrated a similar delayed cerebral energy failure after hypoxia-ischemia in the newborn piglet, again using magnetic resonance spectroscopy (Lorek et al, 1994;Penrice et al, 1997). In these human and animal experiments, the investigators showed that phosphocreatine/inorganic phosphorus (Pi) ratios were depressed initially by hypoxia-ischemia only to normalize in the early recovery interval.…”

mentioning

confidence: 99%

Secondary Energy Failure after Cerebral Hypoxia–Ischemia in the Immature Rat

Vannucci

Towfighi

Vannucci

2004

J Cereb Blood Flow Metab

120

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Summary:A delayed or secondary energy failure occurs during recovery from perinatal cerebral hypoxia-ischemia. The question remains as to whether the energy failure causes or accentuates the ultimate brain damage or is a consequence of cell death. To resolve the issue, 7-day postnatal rats underwent unilateral common carotid artery occlusion followed thereafter by systemic hypoxia with 8% oxygen for 2.5 hours. During recovery, the brains were quick frozen and individually processed for histology and the measurements of 1) high-energy phosphate reserves and 2) neuronal (MAP-2, SNAP-25) and glial (GFAP) proteins. Phosphocreatine (PCr) and ATP, initially depleted during hypoxia-ischemia, were partially restored during the first 18 hours of recovery, with secondary depletions at 24 and 48 hours. During the initial recovery phase (6 to 18 hours), there was a significant correlation between PCr and the histology score (0 to 3), but not for ATP. During the late recovery phase, there was a highly significant correlation between all measured metabolites and the damage score. Significant correlation also exhibited between the neuronal protein markers, MAP-2 and SNAP-25, and PCr as well as the sum of PCr and Cr at both phases of recovery. No correlation existed between the high-energy reserves and the glial protein marker, GFAP. The close correspondence of PCr to histologic brain damage and the loss of MAP-2 and SNAP-25 during both the early and late recovery intervals suggest evolving cellular destruction as the primary event, which precedes and leads to the secondary energy failure.

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Proton Magnetic Resonance Spectroscopy of the Brain during Acute Hypoxia-Ischemia and Delayed Cerebral Energy Failure in the Newborn Piglet

Cited by 131 publications

References 27 publications

Spectroscopy study of the dynamics of the transencephalic electrical impedance in the perinatal brain during hypoxia

Spectroscopy study of the dynamics of the transencephalic electrical impedance in the perinatal brain during hypoxia

Relation of impaired energy metabolism to apoptosis and necrosis following transient cerebral hypoxia-ischaemia

Secondary Energy Failure after Cerebral Hypoxia–Ischemia in the Immature Rat

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