Durchblutung und Sauerstoffaufnahme des Gehirns

Hirsch, Hans Joachim; Schneider, Max

doi:10.1007/978-3-642-48664-7_5

Cited by 4 publications

(1 citation statement)

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“…The experimental works previously done by many investigators demonstrated that the normothermic brain can not revive after more than 10 min of complete arrest of cerebral circulation (4). Although the failure of the restoration of the neuronal function was considered to be neuronal death occured within this time limit, recent observations may intoduce another concept.…”

Section: Introductionmentioning

confidence: 99%

Biochemical and Electrophysiological Aspects of Neuronal Recovery after Prolonged Ischemia of the Cat

Satô

Hossmann

Kobayashi

1971

Neurol. Med. Chir.(Tokyo)

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Complete cerebral ischemia of 30 min duration was produced in normothermic cats by clamping the innominate and the left subclavian arteries and simultaneously lowering the systemic blood pressure. After ischemia the brain were recirculated with blood for periods of 15 to 2 hrs. The suppression and recovery of the neuronal function during and after ischemia were assessed in the sensorimotor cortex by recording the spontaneous EEG and the pyramidal response after stimulation of the cortex; by measuring the concentration of energy metabolites, such as phosphocreatine, adenosine triphosphate, glucose, and lactate, and by measuring the DNP-stimulated ATP-ase activity of isolated mitochondria in the brain. The EEG was suppressed 11 ± 1.4 seconds after the onset of ischemia and the pyramidal response after 240±38 seconds. At the end of ischemia, the enregy rich phosphates were completely exhausted, the glucose content had fallen to 4 % of the control value, and lactate increased 23 fold. The DNP-stimulated ATP-ase activity declined 22% of the control value. The ultrastructural alteration of the sensorimotor cortex was minimum at the end of ischemia.Recovery of the pyramidal response started 3 to 6 min after restoring the blood flow and was completed within 2 hrs; the EEG reappeared after 1 to 2 hrs. The functional recovery was related to the restoration of the energy rich phosphates and glucose-levels and to the simultaneous reduction of the accummulated lactate. Under the potimal conditions, CrP and glucose were normalized within 30 min and lactate was reduced to 127% of the control value within 2 hrs after the end of ischemia. The ATP concentration, and DNP-stimulated ATP-ase activity, however, returned only to 72% and less than 90% respectively, even when spontaneous EEG activity reappeared. The mitochondrial swelling which was observed as one of the structural changes of the sensorimotor cortex taken at this time,

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Section: Introductionmentioning

confidence: 99%