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...
متن کاملCooling for Acute Ischemic Brain Damage
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 کاملAnimal models of hypoxic-ischemic brain damage in the newborn.
Controversy continues over which animal model to use as a reflection of human disease states. With respect to perinatal brain disorders, scientists must contend with a disease in evolution. In that regard, the perinatal brain is at risk during a time of extremely rapid development and maturation, involving processes that are required for normal growth. Interfering with these processes, as part ...
متن کاملInhibition of TRPC6 degradation suppresses ischemic brain damage in rats.
Brain injury after focal cerebral ischemia, the most common cause of stroke, develops from a series of pathological processes, including excitotoxicity, inflammation, and apoptosis. While NMDA receptors have been implicated in excitotoxicity, attempts to prevent ischemic brain damage by blocking NMDA receptors have been disappointing. Disruption of neuroprotective pathways may be another avenue...
متن کاملPathogenic mechanisms in ischemic damage: a computational study.
The pathogenesis of penumbral tissue infarction during acute ischemic stroke is controversial. This peri-infarct tissue may subsequently die, or survive and recuperate, and its preservation has been a prime goal of recent therapeutic trials in acute stroke. Two major hypotheses currently under consideration are that penumbral tissue is recruited into an infarct by cortical spreading depression ...
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ژورنال
عنوان ژورنال: Neuropharmacology
سال: 2008
ISSN: 0028-3908
DOI: 10.1016/j.neuropharm.2008.01.005