Pathophysiology of stroke

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Standard

Pathophysiology of stroke. / Strandgaard, S; Paulson, O B.

I: Journal of Cardiovascular Pharmacology, Bind 15 Suppl 1, 1990, s. S38-42.

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Harvard

Strandgaard, S & Paulson, OB 1990, 'Pathophysiology of stroke', Journal of Cardiovascular Pharmacology, bind 15 Suppl 1, s. S38-42.

APA

Strandgaard, S., & Paulson, O. B. (1990). Pathophysiology of stroke. Journal of Cardiovascular Pharmacology, 15 Suppl 1, S38-42.

Vancouver

Strandgaard S, Paulson OB. Pathophysiology of stroke. Journal of Cardiovascular Pharmacology. 1990;15 Suppl 1:S38-42.

Author

Strandgaard, S ; Paulson, O B. / Pathophysiology of stroke. I: Journal of Cardiovascular Pharmacology. 1990 ; Bind 15 Suppl 1. s. S38-42.

Bibtex

@article{8fa690d60c4c46d5b186ad0801d79380,
title = "Pathophysiology of stroke",
abstract = "Therapeutic intervention in acute ischemic stroke must be directed at salvaging damaged, but viable, tissue. Ideally, treatment should start in the initial phase when the ischemic tissue still retains a potential for recovery. Furthermore, ischemic stroke may be associated with {"}chronic threatening ischemia,{"} in which there is ischemic, but viable, tissue with collateral circulation distal to a stenosed or occluded artery. In chronic threatening ischemia, therapeutic manipulation may improve the clinical situation. Since cerebral vasomotor function is impaired or abolished in acute stroke and chronic threatening ischemia, vasodilator therapy tends to {"}steal{"} blood away from the lesion. Vasoconstrictors, by decreasing perfusion in healthy parts of the brain, may improve perfusion in ischemic tissue; it has, however, proved difficult to gain clinical benefit from this therapeutic modality. Converting-enzyme inhibitors may have a place in the management of ischemic stroke as they tend to shift cerebral autoregulation toward lower pressures. Calcium antagonists given acutely in stroke may create a steal effect. Despite this, clinical trials indicate that calcium-antagonist treatment may improve the outcome of stroke patients, possibly by an action on the ischemia-threatened brain cells.",
keywords = "Animals, Brain/metabolism, Brain Ischemia/physiopathology, Cerebral Hemorrhage/physiopathology, Cerebrovascular Disorders/drug therapy, Humans",
author = "S Strandgaard and Paulson, {O B}",
year = "1990",
language = "English",
volume = "15 Suppl 1",
pages = "S38--42",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams & Wilkins",

}

RIS

TY - JOUR

T1 - Pathophysiology of stroke

AU - Strandgaard, S

AU - Paulson, O B

PY - 1990

Y1 - 1990

N2 - Therapeutic intervention in acute ischemic stroke must be directed at salvaging damaged, but viable, tissue. Ideally, treatment should start in the initial phase when the ischemic tissue still retains a potential for recovery. Furthermore, ischemic stroke may be associated with "chronic threatening ischemia," in which there is ischemic, but viable, tissue with collateral circulation distal to a stenosed or occluded artery. In chronic threatening ischemia, therapeutic manipulation may improve the clinical situation. Since cerebral vasomotor function is impaired or abolished in acute stroke and chronic threatening ischemia, vasodilator therapy tends to "steal" blood away from the lesion. Vasoconstrictors, by decreasing perfusion in healthy parts of the brain, may improve perfusion in ischemic tissue; it has, however, proved difficult to gain clinical benefit from this therapeutic modality. Converting-enzyme inhibitors may have a place in the management of ischemic stroke as they tend to shift cerebral autoregulation toward lower pressures. Calcium antagonists given acutely in stroke may create a steal effect. Despite this, clinical trials indicate that calcium-antagonist treatment may improve the outcome of stroke patients, possibly by an action on the ischemia-threatened brain cells.

AB - Therapeutic intervention in acute ischemic stroke must be directed at salvaging damaged, but viable, tissue. Ideally, treatment should start in the initial phase when the ischemic tissue still retains a potential for recovery. Furthermore, ischemic stroke may be associated with "chronic threatening ischemia," in which there is ischemic, but viable, tissue with collateral circulation distal to a stenosed or occluded artery. In chronic threatening ischemia, therapeutic manipulation may improve the clinical situation. Since cerebral vasomotor function is impaired or abolished in acute stroke and chronic threatening ischemia, vasodilator therapy tends to "steal" blood away from the lesion. Vasoconstrictors, by decreasing perfusion in healthy parts of the brain, may improve perfusion in ischemic tissue; it has, however, proved difficult to gain clinical benefit from this therapeutic modality. Converting-enzyme inhibitors may have a place in the management of ischemic stroke as they tend to shift cerebral autoregulation toward lower pressures. Calcium antagonists given acutely in stroke may create a steal effect. Despite this, clinical trials indicate that calcium-antagonist treatment may improve the outcome of stroke patients, possibly by an action on the ischemia-threatened brain cells.

KW - Animals

KW - Brain/metabolism

KW - Brain Ischemia/physiopathology

KW - Cerebral Hemorrhage/physiopathology

KW - Cerebrovascular Disorders/drug therapy

KW - Humans

M3 - Review

C2 - 1695301

VL - 15 Suppl 1

SP - S38-42

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

ER -

ID: 279620735