Blood flow and metabolism during and after repeated partial brain ischemia in neonatal piglets.

Laptook, Abbot R.; Corbett, Ronald J. T.; Ruley, Joan I.; Olivares, Edward

doi:10.1161/01.str.23.3.380

Cited by 24 publications

(7 citation statements)

References 35 publications

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“…12 We have recently applied this technique to investigate the effects of repeated intervals of brain ischemia; the results of the 12 fed piglets represent a portion of this work. 13 The two concentric radiofrequency coils were tuned to 80 ( CBF=100A k, where A, the partition coefficient, was previously determined to equal 0.85±0.07 ml/g for neonatal piglets. MRS by peak height analysis.…”

Section: Methodsmentioning

confidence: 99%

Glucose-associated alterations in ischemic brain metabolism of neonatal piglets.

Laptook

Corbett

Arencibia-Mireles

et al. 1992

Stroke

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Background and Purpose: During global brain ischemia or hypoxia-ischemia in adults, hyperglycemia is deleterious to the brain. In contrast, similar adverse effects have not been found in neonatal animals. This investigation examined neonatal piglets to determine if there were specific alterations of ischemic brain metabolism associated with different systemic glucose concentrations and to potentially clarify the effects of hyperglycemia during ischemia in neonates.Methods: Two groups of animals (n=12 in each group) were studied during partial ischemia to compare the effects of hyperglycemia (plasma glucose concentration, 258+97 mg% [mean±SD]) with modest hypoglycemia (plasma glucose concentration, 62 ±23 mg%). A broad spectrum of cerebral blood flow reduction was achieved by combining inflation of a cervical pressure cuff with varying degrees of hemorrhagic hypotension. High-energy phosphorylated metabolites, intracellular pH, and cerebral blood flow were simultaneously measured using a magnetic resonance spectroscopic technique. Brain metabolic variables (/J-ATP, inorganic phosphorus, phosphocreatine, intracellular pH) were plotted as a function of blood flow reduction during partial ischemia for each group.Results: During ischemia values of cerebral blood flow were comparably distributed between groups and ranged from 15% to 110% of those of control. At a given reduction of cerebral blood flow, hyperglycemic piglets maintained a higher concentration of/J-ATP (p=0.011) and had a smaller increase in inorganic phosphorus (p<0.001). At cerebral blood flow <50% of control, the intracellular pH of piglets with modest hypoglycemia during partial ischemia was never reduced to <6.46, whereas intracellular pH fell as low as 5.97 for hyperglycemic animals.Conclusions: ATP preservation may account for the differing effects of glucose during ischemia in neonates compared with adults, provided that the accentuated brain acidosis is not deleterious to neonatal brain tissue. (Stroke 1992;23:1504-1511 KEY WORDS • cerebral ischemia • cerebral metabolism • glucose • nuclear magnetic resonance • pigs

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Section: Methodsmentioning

confidence: 99%

Glucose-associated alterations in ischemic brain metabolism of neonatal piglets.

Laptook

Corbett

Arencibia-Mireles

et al. 1992

Stroke

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“…This pathophysiolgic model for hypoxic–ischemic brain injury is based on characteristics of the temporal sequence of cerebral energy state in timed injury newborn animal models [14]. Primary energy failure is characterized by reductions in cerebral blood flow and, consequently, delivery of oxygen and substrates to brain tissue [14,15]. High-energy phosphorylated compounds are reduced, and brain tissue acidosis is prominent.…”

Section: What Is the Pathophysiology Of Hie?mentioning

confidence: 99%

Hypothermia for hypoxic–ischemic encephalopathy

Cotten¹,

Shankaran

2010

Expert Review of Obstetrics & Gynecology

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Moderate to severe hypoxic-ischemic injury in newborn infants, manifested as encephalopathy immediately or within hours after birth, is associated with a high risk of either death or a lifetime with disability. In recent multicenter clinical trials, hypothermia initiated within the first 6 postnatal hours has emerged as a therapy that reduces the risk of death or impairment among infants with hypoxic-ischemic encephalopathy. Prior to hypothermia, no therapies directly targeting neonatal encephalopathy secondary to hypoxic-ischemic injury had convincing evidence of efficacy. Hypothermia therapy is now becoming increasingly available at tertiary centers. Despite the deserved enthusiasm for hypothermia, obstetric and neonatology caregivers, as well as society at large, must be reminded that in the clinical trials more than 40% of cooled infants died or survived with impairment. Although hypothermia is an evidence-based therapy, additional discoveries are needed to further improve outcome after HIE. In this article, we briefly present the epidemiology of neonatal encephalopathy due to hypoxic-ischemic injury, describe the rationale for the use of hypothermia therapy for hypoxic-ischemic encephalopathy, and present results of the clinical trials that have demonstrated the efficacy of hypothermia. We also present findings noted during and after these trials that will guide care and direct research for this devastating problem. KeywordsHIE; hyperthermia; hypothermia; hypoxic-ischemic encephalopathy; neonate; perinatal asphyxia What is hypoxic-ischemic encephalopathy & what is its impact on health outcomes?Neonatal encephalopathy, or a persistently abnormal neurologic examination that includes one or more of the following: altered consciousness, abnormal muscle tone or reflexes, altered respirations, and sometimes seizures in the first postnatal hours to days -can be caused by a number of etiologies, including acute perinatal asphyxia, intracranial bleeding and stroke, injuries secondary to birth trauma, infections, metabolic disorders including hypoglycemia, and congenital brain abnormalities. Encephalopathy due to hypoxic-ischemic injuryhypoxic-ischemic encephalopathy (HIE) -is defined as brain injury caused by the combination of inadequate blood flow and oxygen delivery to the brain. Attributing neonatal encephalopathy © 2010 Expert Reviews Ltd † Author for correspondence Duke University Medical Center, Box 2739 DUMC, Durham, NC 27710, USA, Tel.: +1 919 681 4844, Fax: +1 919 681 6065 cotte010@mc.duke.edu. NIH Public Access Author ManuscriptExpert Rev Obstet Gynecol. Author manuscript; available in PMC 2011 January 1. Published in final edited form as:Expert Rev Obstet Gynecol. 2010 March 1; 5(2): 227-239. doi:10.1586/eog.10.7. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript to perinatal hypoxic-ischemic injury requires combinations of parameters indicative of metabolic acidosis in the first postnatal hours with low cord pH (<7.0), base deficit of over 12, and evidence of a need for r...

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“…HIE results from two recognized phases: primary and secondary energy failure [21, 22]. Primary energy failure occurs during the HI insult and is characterized by decreased cerebral blood flow, which in turn reduces delivery of oxygen and substrates to brain tissue [23]. Following primary energy failure, the cerebral metabolism may recover through reperfusion– reoxygenation, only to deteriorate from secondary energy failure, which is this new phase of neuronal damage, starting at about 6–24 hours after the initial injury mostly characterized by mitochondrial dysfunction, and initiation of the apoptotic cascade.…”

Section: Introductionmentioning

confidence: 99%

Therapeutic Hypothermia as a Neuroprotective Strategy in Neonatal Hypoxic-Ischemic Brain Injury and Traumatic Brain Injury

Sinha²,

Pandya³

et al. 2012

CMM

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Evidence shows that artificially lowering body and brain temperature can significantly reduce the deleterious effects of brain injury in both newborns and adults. Although the benefits of therapeutic hypothermia have long been known and applied clinically, the underlying molecular mechanisms have yet to be elucidated. Hypoxic-ischemic brain injury and traumatic brain injury both trigger a series of biochemical and molecular events that cause additional brain insult. Induction of therapeutic hypothermia seems to ameliorate the molecular cascade that culminates in neuronal damage. Hypothermia attenuates the toxicity produced by the initial injury that would normally produce reactive oxygen species, neurotransmitters, inflammatory mediators, and apoptosis. Experiments have been performed on various depths and levels of hypothermia to explore neuroprotection. This review summarizes what is currently known about the beneficial effects of therapeutic hypothermia in experimental models of neonatal hypoxic-ischemic brain injury and traumatic brain injury, and explores the molecular mechanisms that could become the targets of novel therapies. In addition, this review summarizes the clinical implications of therapeutic hypothermia in newborn hypoxic-ischemic encephalopathy and adult traumatic brain injury.

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Blood flow and metabolism during and after repeated partial brain ischemia in neonatal piglets.

Cited by 24 publications

References 35 publications

Glucose-associated alterations in ischemic brain metabolism of neonatal piglets.

Glucose-associated alterations in ischemic brain metabolism of neonatal piglets.

Hypothermia for hypoxic–ischemic encephalopathy

Therapeutic Hypothermia as a Neuroprotective Strategy in Neonatal Hypoxic-Ischemic Brain Injury and Traumatic Brain Injury

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