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Ischemic cascadeThe ischemic (ischaemic) cascade is a series of biochemical reactions that take place in the brain and other aerobic tissues after seconds to minutes of ischemia (inadequate blood supply).[1] This is typically secondary to stroke, injury, or cardiac arrest due to heart attack. Most ischemic neurons that die do so due to the activation of chemicals produced during and after ischemia.[2] The ischemic cascade usually goes on for two to three hours but can last for days, even after normal blood flow returns.[3] Additional recommended knowledgeA cascade is a series of events in which one event triggers the next, in a linear fashion. Thus "ischemic cascade" is actually a misnomer, since in it, events are not always linear: in some cases, they are circular, and sometimes one event can cause or be caused by multiple other events.[4] In addition, cells receiving different amounts of blood may go through different chemical processes. Despite these facts, the ischemic cascade can be generally characterized as follows:
The fact that the ischemic cascade involves a number of steps has led doctors to suspect that neuroprotectants such as calcium channel blockers or glutamate antagonists could be produced to interrupt the cascade at a single one of the steps, blocking the downstream effects. Though initial trials for such neuroprotective drugs led many to be hopeful, until recently, human clinical trials with neuroprotectants such as NMDA receptor antagonists were unsuccessful. However, NXY-059, the disulfonate derivative of the radical-scavenging spintrap phenylbutylnitrone, has been reported to give neuroprotection in Phase III human trials.[7] References
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This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Ischemic_cascade". A list of authors is available in Wikipedia. |
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