Total cerebral ischemia: application of a new model system to studies of cerebral microcirculation.

Jackson, David; Dole, William P.; McGloin, Jack; Rosenblatt, Judah

doi:10.1161/01.str.12.1.66

Cited by 24 publications

(2 citation statements)

References 29 publications

(8 reference statements)

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“…Models of complete global cerebral ischemia in the dog include ventricular fibrillation, 10 aortic occlusion, 11 and increased intracranial pressure with controlled hemorrhage. 12 All of these models may invoke secondary effects from other organ systems, changing total intracranial sodium and factitiously altering the sodium MRS signal, which is sensitive both to the total amount (not concentration) of sodium ions and to their distribution (intracellular versus extracellular).…”

Section: Resultsmentioning

confidence: 99%

Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.

Eleff

Maruki

Monsein

et al. 1991

Stroke

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We tested the hypotheses that with the onset of cerebral ischemia, massive cellular sodium influx does not occur until adenosine triphosphate is fully depleted and that on reperfusion, neuronal sodium efflux does not occur until adenosine triphosphate is fully restored. We examined the temporal relationships among transcellular sodium, energy metabolism, and intracellular pH with sodium and phosphorus magnetic resonance spectroscopy in a new, hemodynamically stable, brain stem-sparing model of reversible, complete cerebral ischemia in eight anesthetized dogs. Inflation of a neck tourniquet after placement of glue at the tip of the basilar artery resulted in decreased blood flow to the cerebrum from 29 ±5 to 0-3 ±0.5 ml/min/100 g. Medullary blood flow was not significantly affected, and arterial blood pressure was unchanged. Sodium signal intensity decreased and did not lag behind the fall in adenosine triphosphate. After 12 minutes of ischemia, reperfusion resulted in a more rapid recovery of sodium intensity (12.4±4.8 minutes) than either adenosine triphosphate (16.5±3.7 minutes) or intracellular pH (38.9±1.8 minutes). Because intracellular sodium has a weaker signal than extracellular sodium, the decreased sodium intensity is interpreted as sodium influx and indicates that sodium influx does not require full depletion of adenosine triphosphate. Rapid recovery of sodium intensity during early reperfusion may represent sodium efflux, although increased plasma volume and sodium uptake from plasma may also contribute. If our interpretation of the sodium signal is correct, delayed recovery of adenosine triphosphate may be due to the utilization of adenosine triphosphate for the restoration of transcellular sodium gradient (Stroke 1991^2:233-241) T he application of magnetic resonance spectroscopy (MRS) to in situ brain allows the time course of ischemically perturbed cerebral bioenergetics as reflected by adenosine triphosphate (ATP), phosphocreatine, and intracellular pH 1 -2 and transcellular sodium gradient 3 to be examined. The potential interactions of brain sodium gradients, intracellular pH, and bioenergetics are many. Maintenance of a normal sodium gradient, necessary for normal neurologic function, is an ATP- Received May 25, 1990; accepted October 17, 1990. dependent process and accounts for 40% of the metabolic demand of the brain as assessed by highdose lidocaine during barbiturate coma. 4 Maintenance of a normal intracellular pH is critical for proper functioning of most enzymatic processes. With the onset of complete ischemia, intracellular pH falls as glucose stores are converted to lactic acid and ATP is hydrolyzed.5 Soon after ATP depletion, extracellular Na + activity decreases. 6 However, Na + influx may precede the sudden decrease in extracellular Na + activity as measured by microelectrodes if this early Na + influx is accompanied by sufficient water to maintain a constant sodium activity. On reperfusion, limited ATP generation may be diverted into restoring ionic gradients instead of main...

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Section: Resultsmentioning

confidence: 99%

Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.

Eleff

Maruki

Monsein

et al. 1991

Stroke

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“…Cardiac arrest produces a global cerebral ischemic injury. Early animal models of global cerebral ischemia included, among others, aortic balloon occlusion ( 29 ) and neck tourniquet insults ( 30 ). Clinically relevant models of cardiac arrest were developed more recently, and CBF was thoroughly assessed using these models.…”

Section: Alterations In Cbf After Cardiac Arrest: Animal Modelsmentioning

confidence: 99%

Alterations in Cerebral Blood Flow after Resuscitation from Cardiac Arrest

Iordanova

Clark

et al. 2017

Front. Pediatr.

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Greater than 50% of patients successfully resuscitated from cardiac arrest have evidence of neurological disability. Numerous studies in children and adults, as well as in animal models have demonstrated that cerebral blood flow (CBF) is impaired after cardiac arrest. Stages of cerebral perfusion post-resuscitation include early hyperemia, followed by hypoperfusion, and finally either resolution of normal blood flow or protracted hyperemia. At the level of the microcirculation the blood flow is heterogeneous, with areas of no flow, low flow, and increased flow. CBF directed therapies in animal models of cardiac arrest improved neurological outcome, and therefore, the alterations in CBF after cardiac arrest likely contribute to the development of hypoxic ischemic encephalopathy. Current intensive care after cardiac arrest is centered upon maintaining systemic oxygenation, normal blood pressure values for age, maintaining general homeostasis, and avoiding hyperthermia. Assessment of CBF and oxygenation is not routinely performed after cardiac arrest. Currently available and underutilized techniques to assess cerebral perfusion include transcranial doppler, near-infrared spectroscopy, and arterial spin labeling magnetic resonance imaging. Limited clinical studies established the role of CBF and oxygenation monitoring in prognostication after cardiac arrest and few studies suggest that guiding critical care post-resuscitation to mean arterial pressures above the minimal autoregulatory range might improve outcome. Important knowledge gaps thus remain in cerebral monitoring and CBF and oxygen goal-directed therapies post-resuscitation from cardiac arrest.

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Current Concepts in Brain Resuscitation

Kirsch¹

1986

Arch Intern Med

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Total cerebral ischemia: application of a new model system to studies of cerebral microcirculation.

Cited by 24 publications

References 29 publications

Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.

Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.

Alterations in Cerebral Blood Flow after Resuscitation from Cardiac Arrest

Current Concepts in Brain Resuscitation

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