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Open AccessJournal ArticleDOI

Experimental brain infarcts in cats. II. Ischemic brain edema.

F J Schuier, +1 more
- 01 Nov 1980 - 
- Vol. 11, Iss: 6, pp 593-601
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TLDR
It is concluded that the early ischemic brain edema following middle cerebral artery occlusion is of the cytotoxic type, that it develops at a flow rate below 10–15 ml/100 g/min, and that it is not strictly correlated with the energy state of the brain.
Abstract
In cats, the early development of ischemic brain edema was studied 1 to 4 hours after transorbital occlusion of the left middle cerebral artery (MCA). Two groups of animals were compared: those in which blood flow in the territory of the MCA decreased below the threshold of 10--15 ml/100 g/min (critical ischemia) and those in which it remained above this level (non-critical ischemia). In animals with critical ischemia, water content in the cortex of the MCA territory increased from 80.7 +/- 0.4 to 83.0 +/- 0.3 vol. % (means +/- SE) within 4 h. Edema was associated with an increase in tissue osmolality by 16--22 mosm/kg w.w., and a rise of sodium from 262 +/- 9 to 454 +/- 13 meq/kg d.w. and a decrease of potassium from 442 +/- 20 to 305 +/- 32 meq/kg d.w. The sodium/potassium ratio rose from 0.60 +/- 0.03 to 1.55 +/- 0.17. The water and electrolyte disturbances were accompanied by a major shift of extracellular fluid into the intracellular compartment, as evidenced by the increase in cortical impedance from 282 to 660 ohm/cm within 2 h. According to the Maxwell equation, this reflects a narrowing of the extracellular space from 19.8 to 11.4%. Brain volume was continuously monitored using an induction transducer; swelling began within a few minutes of vascular occlusion, and it continued throughout the 4 h observation period. During this time the blood-brain barrier remained intact as evidenced by the absence of Evans blue staining. Edema was associated with disturbances of the energy producing metabolism, but there was no strict correlation with either lactate or the concentration of high energy phosphates. In animals without critical ischemia, i.e. in which blood flow remained above 10--15 ml/100 g/min, edema was absent despite a distinct deterioration of the energy state of the brain. Edema was also absent in the border zone, in the territory of the posterior cerebral artery and in the contralateral hemisphere of animals with both critical and non-critical ischemia. It is concluded that the early ischemic brain edema following middle cerebral artery occlusion is of the cytotoxic type, that it develops at a flow rate below 10--15 ml/100 g/min, and that it is not strictly correlated with the energy state of the brain.

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Citations
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Journal ArticleDOI

Early detection of regional cerebral ischemia in cats: comparison of diffusion- and T2-weighted MRI and spectroscopy.

TL;DR: Diffusion‐weighted hyperintensity in ischemic tissues may be temperature‐related, due to rapid accumulation of diffusion‐restricted water in the intracellular space (cytotoxic edema) resulting from the breakdown of the transmembrane pump and/or to microscopic brain pulsations.
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Viability thresholds and the penumbra of focal ischemia.

TL;DR: It is suggested that the limited survival of the penumbra is due to periinfarct depolarizations, which result in repeated episodes of tissue hypoxia, because the increased metabolic workload is not coupled to an adequate increase of collateral blood supply.
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Diffusion-weighted MR imaging of acute stroke: correlation with T2-weighted and magnetic susceptibility-enhanced MR imaging in cats.

TL;DR: Data indicate that diffusion-weighted MR images more accurately reflect early-onset pathophysiologic changes induced by acute cerebral ischemia than do T2- Weighted spin-echo images.
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Edema and brain trauma

TL;DR: Findings suggest that cytotoxic and vasogenic brain edema are two entities which can be targeted simultaneously or according to their temporal prevalence following traumatic brain injury.
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Brain oedema in focal ischaemia: molecular pathophysiology and theoretical implications

TL;DR: A new theory is suggested suggesting that ischaemia-induced capillary dysfunction can be attributed to de novo synthesis of a specific ensemble of proteins that determine osmotic and hydraulic conductivity in Starling's equation, and whose expression is driven by a distinct transcriptional program.
References
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Journal ArticleDOI

Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia.

TL;DR: The hypothesis that electrical failure in ischemia may be directly associated with a massive release of intracellular K+ or with a critical degree of extracellular acidosis is tested and the concept of an ischemic penumbra during which the neurons remain structurally intact but functionally inactive is supported.
Journal ArticleDOI

Cerebral carbohydrate metabolism during acute hypoxia and recovery.

TL;DR: Levels of ATP, ADP, AMP and phosphocreatine were normal or near normal even when convulsions and respiratory collapse appeared imminent and Glycogen decreased and lactate rose markedly in hypoxia.
Journal ArticleDOI

Extracellular potassium activity, evoked potential and tissue blood flow. Relationships during progressive ischaemia in baboon cerebral cortex.

TL;DR: The data suggest that 3 stages may be identified in the disturbance of K+ homeostasis produced by progressive ischaemia, with an inverse relationship between flow and Ke with persisting high Ke levels, suggesting complete loss of K- clearance.
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