Adenosine and ischemic brain damage
نویسندگان
چکیده
منابع مشابه
Mechanisms of ischemic brain damage.
In the United States stroke is the third leading cause of death and the leading cause of disability. Brain injury following stroke results from the complex interplay of multiple pathways including excitotoxicity, acidotoxicity, ionic imbalance, peri-infarct depolarization, oxidative and nitrative stress, inflammation and apoptosis. There are very few treatments for stroke and the development of...
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Pharmacologic inactivation or genetic deletion of adenosine A2A receptors protects ischemic neurons in adult animals, but studies in neonatal hypoxia-ischemia (H-I) are inconclusive. The present study in neonatal piglets examined the hypothesis that A2A receptor signaling after reoxygenation from global H-I contributes to injury in highly vulnerable striatal neurons where A2A receptors are enri...
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Objective: To report results of a randomized pilot clinical feasibility trial of endovascular cooling in patients with ischemic stroke. Methods: Forty patients with ischemic stroke presenting within 12 hours of symptom onset were enrolled in the study. An endovascular cooling device was inserted into the inferior vena cava of those randomized to hypothermia. A core body temperature of 33 °C was...
متن کاملIschemic brain damage and memory impairment: a commentary.
Studies in humans and monkeys have identified structures in the medial temporal lobe essential for memory (the hippocampal region, i.e., the dentate gyrus, the hippocampus, and the subicular complex, and the adjacent perirhinal, entorhinal, and parahippocampal cortices). Additional work has revealed that for both species, damage limited to the hippocampal region produces less severe memory impa...
متن کاملMetabolic stages, mitochondria and calcium in hypoxic/ischemic brain damage.
Cerebral hypoxia/ischemia leads to mitochondrial dysfunction due to lack of oxygen leaving the glycolytic metabolism as a main pathway for ATP production. Inhibition of mitochondrial respiration thus triggers generation of lactate and hydrogen ions (H+), and furthermore dramatically reduces ATP generation leading to disregulation of cellular ion metabolism with subsequent intracellular calcium ...
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ژورنال
عنوان ژورنال: Japanese Journal of Pharmacology
سال: 1990
ISSN: 0021-5198
DOI: 10.1016/s0021-5198(19)32939-7