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Cerebral Autoregulation and Acute Ischemic Stroke
Cerebral autoregulation tightly controls blood flow to the brain by coupling cerebral metabolic demand to cerebral perfusion. In the setting of acute brain injury, such as that caused by ischemic stroke, the continued precise control of cerebral blood flow (CBF) is vital to prevent further injury. C...
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Published in: | American journal of hypertension 2012-09, Vol.25 (9), p.946-950 |
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container_title | American journal of hypertension |
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creator | JORDAN, J. Dedrick POWERS, William J |
description | Cerebral autoregulation tightly controls blood flow to the brain by coupling cerebral metabolic demand to cerebral perfusion. In the setting of acute brain injury, such as that caused by ischemic stroke, the continued precise control of cerebral blood flow (CBF) is vital to prevent further injury. Chronic as well as acute elevations in blood pressure are frequently associated with stroke, therefore, understanding the physiological response of the brain to the treatment of hypertension is clinically important. Physiological data obtained in patients with acute ischemic stroke provide no clear evidence that there are alterations in the intrinsic autoregulatory capacity of cerebral blood vessels, except perhaps in infarcted tissue. While it is likely safe to modestly reduce blood pressure by 10-15 mm Hg in most patients with acute ischemic stroke, to date, there are no controlled trial data to indicate that reducing blood pressure is beneficial. There may be subgroups, such as those with persistent large vessel occlusion, large infarcts with edema causing increased intracranial pressure or local mass effect, or chronic hypertension, in which blood pressure reduction may lead to impaired cerebral perfusion in noninfarcted tissue. |
doi_str_mv | 10.1038/ajh.2012.53 |
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While it is likely safe to modestly reduce blood pressure by 10-15 mm Hg in most patients with acute ischemic stroke, to date, there are no controlled trial data to indicate that reducing blood pressure is beneficial. There may be subgroups, such as those with persistent large vessel occlusion, large infarcts with edema causing increased intracranial pressure or local mass effect, or chronic hypertension, in which blood pressure reduction may lead to impaired cerebral perfusion in noninfarcted tissue.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1879-1905</identifier><identifier>EISSN: 1941-7225</identifier><identifier>DOI: 10.1038/ajh.2012.53</identifier><identifier>PMID: 22573015</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing Group</publisher><subject>Antihypertensive Agents - therapeutic use ; Arterial hypertension. 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Dedrick</creatorcontrib><creatorcontrib>POWERS, William J</creatorcontrib><title>Cerebral Autoregulation and Acute Ischemic Stroke</title><title>American journal of hypertension</title><addtitle>Am J Hypertens</addtitle><description>Cerebral autoregulation tightly controls blood flow to the brain by coupling cerebral metabolic demand to cerebral perfusion. In the setting of acute brain injury, such as that caused by ischemic stroke, the continued precise control of cerebral blood flow (CBF) is vital to prevent further injury. Chronic as well as acute elevations in blood pressure are frequently associated with stroke, therefore, understanding the physiological response of the brain to the treatment of hypertension is clinically important. Physiological data obtained in patients with acute ischemic stroke provide no clear evidence that there are alterations in the intrinsic autoregulatory capacity of cerebral blood vessels, except perhaps in infarcted tissue. While it is likely safe to modestly reduce blood pressure by 10-15 mm Hg in most patients with acute ischemic stroke, to date, there are no controlled trial data to indicate that reducing blood pressure is beneficial. There may be subgroups, such as those with persistent large vessel occlusion, large infarcts with edema causing increased intracranial pressure or local mass effect, or chronic hypertension, in which blood pressure reduction may lead to impaired cerebral perfusion in noninfarcted tissue.</description><subject>Antihypertensive Agents - therapeutic use</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cerebrovascular Circulation - physiology</subject><subject>Homeostasis - physiology</subject><subject>Humans</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - physiopathology</subject><subject>Medical sciences</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>Pharmacology. 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source | Oxford Journals Online |
subjects | Antihypertensive Agents - therapeutic use Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cerebrovascular Circulation - physiology Homeostasis - physiology Humans Hypertension - drug therapy Hypertension - physiopathology Medical sciences Neuropharmacology Neuroprotective agent Pharmacology. Drug treatments Stroke - physiopathology |
title | Cerebral Autoregulation and Acute Ischemic Stroke |
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