The Clinical Problem: How Much Anoxia-Ischemia Damages the Brain?

Plum, Fred

doi:10.1001/archneur.1973.00490300021001

Cited by 33 publications

(11 citation statements)

References 8 publications

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“…Zones of greater metabolic activity may require more substrate to maintain structural integrity. 6 ' 7 Thus gray matter, with its greater metabolic activity, might be expected to be particularly sensitive to ischemia. Some histopathologic studies have supported this notion, 8 but correlated blood flow data have been lacking.…”

Section: Recovery Of Functionmentioning

confidence: 99%

Differential regional vulnerability in transient focal cerebral ischemia.

Marcoux¹,

Morawetz²,

Crowell³

et al. 1982

Stroke

211

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Section: Recovery Of Functionmentioning

confidence: 99%

Differential regional vulnerability in transient focal cerebral ischemia.

Marcoux¹,

Morawetz²,

Crowell³

et al. 1982

Stroke

211

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“…Observations dealing with the consequences of complete brain ischemia are most variable and sometimes controversial, regarding both the duration of ischemia and the susceptibility of the particular structures of the central nervous system and of the particular types of cells and the character of the consequent cell lesion [Weinberger et al, 1940;Olsson and Hossmann, 1971;Hossmann and Hossmann, 1973;Plum, 1973;Hossmann and Zimmermann, 1974;Marshall et al, 1975;Nemoto et al, 1977;Pulsinelli and Brierley, 19791. Moreover, in the past decade it has been convincingly demonstrated that both energetic metabolism and various energy-dependent biophysical activities of the nerve cell (ie, ECoG, inspiratory activity of the phrenic nerve), may be completely restored to normal after complete cerebral ischemia lasting up to 60 min [Hossmann and Zimmermann, 1974;Samoilov and Semenov, 1979;Pluta and Kapukinski, 19801.…”

Section: Introductionmentioning

confidence: 99%

Ultrastructural changes in the sensomotor cortex of the rabbit after complete 30‐min brain ischemia

Pluta

Gajkowska

1984

J of Neuroscience Research

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Experiments were performed on rabbits in which complete 30-min brain ischemia was induced. Electron-microscopic studies revealed higher susceptibility to ischemia of the motor cortex than the sensory cortex, which was manifested by a higher number of damaged nerve cells in the former than in the latter. Ultrastructural abnormalities of motor cortex neurons, including the presence of numerous vesicular structures in the cell nuclei, swelling of mitochondria, and an increase in the number of intracytoplasmic fibrillary structures appeared 3 h after blood recirculation and became more intensive after 6 h.

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“…The permissible duration of brain ischemia without sustaining irreversible damage is disputed, but is recognized to be short by Plum, 14 Brierley et al, 15 and Hossmann and Kleihues. 16 Less clear are the mechanisms accounting for brain vulnerability.…”

Section: Discussionmentioning

confidence: 99%

Energy Metabolism During Brain Ischemia

Yatsu

Lee

Liao

1975

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Energy Metabolism During Brain Ischemia• The permissible duration of brain ischemia without sustaining damage is short. Less clear are the mechanisms accounting for the vulnerability of brain to ischemic insults. Neurochemical factors implicated include impairment of energy synthesis by mitochondria and of energy-dependent processes such as synaptic transmission, ATPase activity, membrane conductance and altered protein and lipid synthesis. To clarify the vulnerability of energy metabolism, we investigated energy availability and synthesis in our model of global cerebral ischemia. Our studies evaluated in vitro mitochondrial ATP synthesis and the in vivo quantitation of the cortical adenylate pool. Results of our investigations support a growing body of evidence showing the energy state to be relatively stable to ischemia. We conclude that an energy-dependent process of brain is primarily vulnerable to ischemia. 5 Our investigations confirm and extend these observations by correlating simultaneous in vitro and in vivo parameters of energy metabolism with functional recovery. In our model of global ischemia, 6 ischemia was created by combining systemic hypotension with hypoxia of varying periods followed by circulatory restoration. Energy metabolism was evaluated with in vitro mitochondrial ATP synthesis and the in vivo cortical adenylate pool. Additional Key Methods BRAIN ISCHEMIA AND RECOVERYRandom-bred New Zealand white rabbits weighing between 4 and 5 kg were used. The rabbits were given a rapid-acting anesthesia, Ketamine (cyclohexylamine), intubated, and paralyzed with succinylcholine. Ventilation was performed mechanically with a Harvard pump. Two dural electrodes were implanted to record the electroencephalogram. The femoral artery was catheterized for constant blood pressure recording and the collection of blood for gases and pH measurements. A detailed description of procedures and the dosage of various pharmacological agents used have been

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The Clinical Problem: How Much Anoxia-Ischemia Damages the Brain?

Cited by 33 publications

References 8 publications

Differential regional vulnerability in transient focal cerebral ischemia.

Differential regional vulnerability in transient focal cerebral ischemia.

Ultrastructural changes in the sensomotor cortex of the rabbit after complete 30‐min brain ischemia

Energy Metabolism During Brain Ischemia

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