Metabolism and Flow in the Hypoxic Brain

Bk, Siesjö

doi:10.1159/000114464

Cited by 21 publications

(3 citation statements)

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“…It should, namely, be borne in mind that the increase of this parameter in the CSF is one of the most sensitive indices of brain hypoxia [19]. We also noted in our patients (table II) an enhanced lactic dehydrogenase activity in the CSF in the course of induced hypotension and after return of the MAP to control val ues.…”

Section: Discussionsupporting

confidence: 73%

Brain Metabolism in Deep Controlled Hypotension in Neurosurgical Patients

Johansson

Cybulska

1985

Eur Neurol

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Changes in the lactate and pyruvate levels and lactic dehydrogenase activity in the cerebrospinal fluid were followed in 56 patients anaesthetised for neurosurgery. Mean arterial blood pressure (MAP) was reduced in these patients from about 90 to about 35 mm Hg. This allowed to safely place a clip at a brain artery aneurysm. In spite of deep hypotension, ischaemia described by other authors in such cases was never observed. Changes in lactate and pyruvate concentrations, lactate/pyruvate ratio and lactic dehydrogenase activity justify the conclusion that we were dealing with an undisturbed metabolism of the brain tissue. The levels of metabolic parameters, even when increased in hypotension, fell well within the range of physiological values. Attention is called to the fact that partial oxygen pressure in arterial blood during controlled hypotension was about 100 mm Hg, a value considered as limiting to oxygen metabolic transformation within the central nervous system in deep hypotension. We also suggest a different mechanism of passage of lactates and pyruvates through the blood-brain barrier.

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Section: Discussionsupporting

confidence: 73%

Brain Metabolism in Deep Controlled Hypotension in Neurosurgical Patients

Johansson

Cybulska

1985

Eur Neurol

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“…In some cases, this pro vided further confirmation of the observation of Macmillan and Siesjo (1972) that the intracellular pH may fall to 6.6 or 6.5 without a change in the energy charge potential (ECP) of the adenine nu cleotide pool. ECP is defined as ATP + 0.5 ADP/ ATP + ADP + AMP (Atkinson, 1968;Siesjo, 1972).…”

Section: Resultsmentioning

confidence: 99%

A³¹P Nuclear Magnetic Resonancein vivoStudy of Cerebral Ischaemia in the Gerbil

Thulborn

Boulay

Duchen

et al. 1982

J Cereb Blood Flow Metab

110

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Summary:We have used the noninvasive method of "'phosphorus nuclear magnetic resonance C'P N MR) in \'il'O to follow changes in phosphorous me tabolite concentrations and the intracellular pH in the right and left hemi spheres and in the cerebellum of gerbil brains after the occlusion of the right carotid artery, Spatial resolution over the brain was possible using surface coils. Ligation, which is known to cause ischaemia in this species in the ipsilat eral hemisphere, resulted in the diminution of phosphocreatine and adenine nucleotides and a decrease in tissue pH. Less acidification occurred in the contralateral hemisphere and in the cerebellum. The high-energy metabolite concentrations, phosphocreatine and adenosine triphosphate (ATP), declined in unison in the ischaemic region, in marked contrast to the sequence of events in skeletal muscle, in which phosphocreatine buffers against an immediate fall in ATP concentration. In a separate series of gerbils, 31p NMR spectra were followed for exactly 1 h after carotid ligation. The animals were then sacrificed and brain grey matter specific gravity was rapidly measured to assess the development of oedema. There was a clear correlation between abnormality of spectra and the presence of oedema. It cannot, however, be confidently as serted that a normal spectrum is never seen in oedematous gerbil brains. 3' P NMR spectra specific gravity and histological changes shown by light micros copy have been correlated and show that useful signals are received from a depth of at least 4 mm or more from the lO-mm diameter coil.

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“…Eklof and Siesjo (28) reported that hypotensive rats subjected to brain ischemia showed a similar reduction in the cerebral energy state and inferred that brain ischemia combined with hypotension caused a grossly inhomogenous reduction in cerebral blood flow. However, it remains uncertain whether the decreased blood flow or subsequent hypoxia in the brain could be a primary cause of cerebral energy failure, because the capillary and tissue oxygen tension sufficient to maintain adequate oxidative phosphorylation is considerably low (29). Duffy et al (20) demonstrated that the cerebral ATP level remained unchanged with a degree of hypoxia sufficient to produce a serious depression in brain function.…”

Section: Discussionmentioning

confidence: 99%

Relationship Between Cerebral Energy Failure and Free Fatty Acid Accumulation Following Prolonged Brain Ischemia

Kuwashima

Nakamura

Fujitani

et al. 1978

Japanese Journal of Pharmacology

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Abstract--Prolonged ischemia by bilateral carotid artery ligation in rats resulted in cerebral edema with a reduced energy state. Mitochondria isolated from the ischemic brain showed an impairment of oxidative phosphorylation.The ischemic brain was also characterized by a remarkable accumulation of free fatty acids known to have properties as an uncoupling factor. The major components of increased free fatty acids were palmitic, stearic, oleic and arachidonic acids. The analysis of saponified myelin and mitochondrial lipids from the ischemic brain showed a decrease in fatty acid contents.The main components of decreased fatty acids in these subcellular fractions corresponded to those of free fatty acids accumulating in the ischemic brain. These results indicate that cerebral energy failure in the ischemic brain is related to the accumulation of free fatty acids, which are derived from endogenous brain lipids.Although considerable efforts have been devoted to the study on experimental brain edema, the biochemical alterations associated with the pathogenesis still remain to be eluci dated. Current evidence suggests that cerebral swelling is accompanied by a reduction of the cerebral energy state (1-3) and an impairment of mitochondrial function (4-6). A deficiency of available energy is assumed to cause a disturbance of active ionic transport across the cell membrane, which could lead to cerebral swelling or cell damage. In a previous report (7), we showed that unilateral brain edema produced in rats by the combination of ischemia and hypoxic exposure was characterized by a considerable increase of free fatty acids in the brain. Our experiments also demonstrated that oleic and arachidonic acids, which increased markedly in the edematous brain, inhibited oxidative phosphorylation of in vitro mitochondrial preparations (7). These observations provided information for further study on the biochemical mechanism of cerebral energy failure in brain edema.In the present study, we investigated cerebral energy metabolism in another form of brain edema produced in rats by a permanent ligation of bilateral carotid arteries. This paper deals with biochemical events associated with cerebral energy failure and the free fatty acid change in the subcellular lipids of the edematous brain. MATERIALS AND METHODS Brain ischennaMale Wistar rats weighing 80-100 g were anesthetized with sodium hexobarbital (150 mg/

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Metabolism and Flow in the Hypoxic Brain

Cited by 21 publications

References 0 publications

Brain Metabolism in Deep Controlled Hypotension in Neurosurgical Patients

Brain Metabolism in Deep Controlled Hypotension in Neurosurgical Patients

A³¹P Nuclear Magnetic Resonancein vivoStudy of Cerebral Ischaemia in the Gerbil

Relationship Between Cerebral Energy Failure and Free Fatty Acid Accumulation Following Prolonged Brain Ischemia

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Metabolism and Flow in the Hypoxic Brain

Cited by 21 publications

References 0 publications

Brain Metabolism in Deep Controlled Hypotension in Neurosurgical Patients

Brain Metabolism in Deep Controlled Hypotension in Neurosurgical Patients

A31P Nuclear Magnetic Resonancein vivoStudy of Cerebral Ischaemia in the Gerbil

Relationship Between Cerebral Energy Failure and Free Fatty Acid Accumulation Following Prolonged Brain Ischemia

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A³¹P Nuclear Magnetic Resonancein vivoStudy of Cerebral Ischaemia in the Gerbil