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TitleMechanisms of Cerebral Hypoxia and Stroke [electronic resource] / edited by George Somjen
ImprintBoston, MA : Springer US, 1988
Connect tohttp://dx.doi.org/10.1007/978-1-4684-5562-5
Descript XII, 474 p. online resource

SUMMARY

The articles and short communications in this volume are based on papers preยญ sented to the Symposium on Cerebral Hypoxia and Stroke held in Budapest in August of 1987. Besides participants at the meeting, three scientists who were invited but could not attend have also contributed chapters to this volume. A synopsis of the general discussion at the conference and a review chapter conclude this volume. To the readers of this book it will not be news that stroke is a worldwide problem. Efforts to cope with this often devastating condition are worldwide also, as attested by the international membership of the conference. It has been said of oxygen deficiency that it not only stops the machine, it also wrecks the machinery. The paramount question in stroke research is this: why can't the brain be restarted after a hypoxic episode in much the same manner as a motor car can when its gas tank is refilled after it stalled because it ran out of fuel? Participants at the Symposium had been requested in advance of the meeting to especially consider a series of specific questions in relation to this general problem. Among these specific questions were: the mechanism of synaptic blockade in hypoxic brain tissue; the transition from reversible to irreversible arrest of function; the nature of postischemic (delayed) cell death; the possible basic differences in the consequences of hypoxia and ischemia; and actual and potential approaches to the prevention and treatment of cell damage in hypoxia and stroke


CONTENT

Adaptation in Diving Vertebrates -- Inborn resistance to hypoxia and the O2-dependence of metabolism -- Brain vulnerability and survival during anoxia: protective strategies of hypoxia-resistant vertebrates -- General Pathology -- Early and late neuronal damage following cerebral ischemia -- Selective neuronal cell death after transient forebrain ischemia in the mongolian gerbil -- Possible implications of ischemic damage to dentate hilar somatostatin neurons in the rat -- Regulation of glutamate receptors in hippocampus after cerebral ischemia -- Role of edema in the pathophysiology of ischemic injury -- Acidosis-related brain damage immediate and delayed events -- Pathology of ischaemic brain damage: implications for therapy -- Ischemic damage of rat hippocampus and basal ganglia: light microscopical and biochemical changes -- Pathophysiology -- Physiological aspects of brain ischaemia in the experimental primate and man -- The dependency of cerebral ischemic damage on duration and severity of ischemia: studies of single cell activity and multimodality evoked responses -- Microcirculation and metabolism in reversible and irreversible cerebral ischemia -- Cerebral blood flow and its responsiveness to CO2 after traumatic and ischemic brain injuries -- The correlation between electrophysiological parameters (EEG, DC potential and tissue available O2) and regional metabolites (pH, ATP, glucose, NADH, K) after 45 min middle cerebral artery occlusion and 3 hours recirculation in cats -- Cerebral hypoxia during repetitive seizures -- Microcirculation, NAD/NADH fluorescence, extracellular potassium and glucose metabolism changes in focal cerebral ischemia -- Neurons, glia and ions in hypoxia, hypercapnia and acidosis -- Effects of anoxia on nerve cell function -- Reversible synaptic blockade caused by hypoxia of moderate degree in hippocampal tissue slices -- Anoxia reversibly inactivates hippocampal calcium currents -- Reversibility of neuronal function of hippocampal slice during deprivation of oxygen and/or glucose -- The effect of hypoxia on hippocampal neurones and its prevention by Ca2+-antagonists -- Anoxia in CA1 pyramidal cells: ionic and metabolic factors contributing to recovery of ion transport and synaptic transmission -- Long-term inhibition of synaptic transmission and macromolecular synthesis following anoxia in the rat hippocampal slice: interaction between Ca2+ and NMDA receptors -- Early alterations in striatal and hippocampal impedance and extracellular amino acids by cardiac arrest in freely moving rats -- Susceptibility to spreading depression and anoxia: regional differences and drug control -- Blood flow and metabolism in cortical spreading depression -- Dynamics of volatile buffers in brain cells during spreading depression -- The role of spreading depression-like hypoxic depolarization in irreversible neuron damage, and its prevention -- NMDA antagonists inhibit cortical spreading depression, but accelerate the onset of neuronal depolarization induced by asphyxia -- Does Leaoโ{128}{153}s spreading depression cause irreversible brain damage? -- Electrophysiological and biochemical events in the isolated perfused rat brain under ischemia and reperfusion -- Neurotransmitter modulation of neuronal damage following cerebral ischemia: Effects on protein ubiquitination -- Detection of free radicals in cerebral tissue and their relation to cerebral hypoxia/ischemia -- Pharmacology -- The limits of reversibility from ischemic cerebral insult and our method of prolonging cerebral survival -- Excitatory amino acid neurotransmission and protection against ischaemic brain damage -- Excitatory amino acid and purinergic transmitter involvement in ischemia-induced selective neuronal death -- Protection of hippocampal neurons from โ{128}{156}ischemicโ{128}{157} insult in vitro by acidic amino acid antagonists -- Magnesium inhibits ischemia-induced calcium accumulation in hilar neurones: possible effect of NMDA-receptor -- Dopamine and the susceptibility of striatal neurons to ischemia -- Effects of flunarizine on normal and injured rat cerebral cortex -- Improvement of postischemic cell damage and energy metabolism in the rat by flunarizine and emopamil -- Discrimination between vascular and direct effects on cerebral parenchyma of emopamil -- Prophylaxis and therapy of hypoxic and ischemic brain: effects of monosialoganglioside GM1 -- Adenosine neuromodulation of selectively vulnerable CA1 neurons -- The nucleoside-transport inhibitor, mioflazine, increases recovery of hippocampal synaptic transmission and energy-rich metabolites after normothermic global ischemia -- Glutamine protects neuronal function against hypoxia in vitro -- Cerebroprotective effect of histamine receptor blockers in hypoxia-induced experimental brain edema -- Drug effects on cerebral extracellular ionic derangement during ischemic hypoxia -- Discussion and Conclusions -- General discussion: a synopsis -- Basic mechanisms in cerebral hypoxia and stroke: background, review and conclusions -- Author index


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