Cerebral blood flow and its pathophysiology in hypertension

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Standard

Cerebral blood flow and its pathophysiology in hypertension. / Strandgaard, S; Paulson, O B.

I: American Journal of Hypertension, Bind 2, Nr. 6 Pt 1, 06.1989, s. 486-92.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Strandgaard, S & Paulson, OB 1989, 'Cerebral blood flow and its pathophysiology in hypertension', American Journal of Hypertension, bind 2, nr. 6 Pt 1, s. 486-92. https://doi.org/10.1093/ajh/2.6.486

APA

Strandgaard, S., & Paulson, O. B. (1989). Cerebral blood flow and its pathophysiology in hypertension. American Journal of Hypertension, 2(6 Pt 1), 486-92. https://doi.org/10.1093/ajh/2.6.486

Vancouver

Strandgaard S, Paulson OB. Cerebral blood flow and its pathophysiology in hypertension. American Journal of Hypertension. 1989 jun.;2(6 Pt 1):486-92. https://doi.org/10.1093/ajh/2.6.486

Author

Strandgaard, S ; Paulson, O B. / Cerebral blood flow and its pathophysiology in hypertension. I: American Journal of Hypertension. 1989 ; Bind 2, Nr. 6 Pt 1. s. 486-92.

Bibtex

@article{95c0090128bf43c5a656b20971d60d86,
title = "Cerebral blood flow and its pathophysiology in hypertension",
abstract = "In chronic hypertension, the lower limit of autoregulation of cerebral blood flow (CBF) is shifted towards high blood pressure with a consequent impairment of the tolerance to acute hypotension. Despite this, antihypertensive treatment in the great majority of patients prevents stroke and the risk for treatment-induced cerebral ischemia is only real in a limited number of clinical settings such as malignant hypertension, hypertension in the elderly, and hypertension associated with acute stroke. During long-term treatment adaptive hypertensive changes in CBF autoregulation may be reversible, especially in young patients. Drugs used for emergency lowering of blood pressure may be classified into four groups according to their effect on CBF and intracranial pressure: (1) drugs with no pharmacological action in the cerebral circulation; (2) cerebral vasodilators; (3) alpha-adrenergic and ganglionic blockers; and (4) angiotensin-converting enzyme (ACE) inhibitors. Oxygen saturation in the jugular venous blood is of the order of 60% to 70% and is considerably higher than in the coronary sinus. It is hypothesized that this oxygen reserve enables the brain better than the heart to take hemodynamic advantage of pressure lowering without risking tissue ischemia. This may explain why antihypertensive treatment prevents stroke but not myocardial infarction. Acute hypertensive encephalopathy is probably caused by failure of autoregulatory vasoconstriction with focal or generalized dilatation of small arteries and arterioles. This is associated with a high CBF, dysfunction of the blood-brain barrier, and the formation of brain edema that is thought to cause the clinical symptoms.",
keywords = "Animals, Antihypertensive Agents/adverse effects, Brain Diseases/etiology, Brain Ischemia/chemically induced, Cerebrovascular Circulation/drug effects, Cerebrovascular Disorders/prevention & control, Emergency Medical Services, Homeostasis/drug effects, Humans, Hypertension/complications, Myocardial Infarction/etiology, Risk Factors",
author = "S Strandgaard and Paulson, {O B}",
year = "1989",
month = jun,
doi = "10.1093/ajh/2.6.486",
language = "English",
volume = "2",
pages = "486--92",
journal = "American Journal of Hypertension",
issn = "0895-7061",
publisher = "Oxford University Press",
number = "6 Pt 1",

}

RIS

TY - JOUR

T1 - Cerebral blood flow and its pathophysiology in hypertension

AU - Strandgaard, S

AU - Paulson, O B

PY - 1989/6

Y1 - 1989/6

N2 - In chronic hypertension, the lower limit of autoregulation of cerebral blood flow (CBF) is shifted towards high blood pressure with a consequent impairment of the tolerance to acute hypotension. Despite this, antihypertensive treatment in the great majority of patients prevents stroke and the risk for treatment-induced cerebral ischemia is only real in a limited number of clinical settings such as malignant hypertension, hypertension in the elderly, and hypertension associated with acute stroke. During long-term treatment adaptive hypertensive changes in CBF autoregulation may be reversible, especially in young patients. Drugs used for emergency lowering of blood pressure may be classified into four groups according to their effect on CBF and intracranial pressure: (1) drugs with no pharmacological action in the cerebral circulation; (2) cerebral vasodilators; (3) alpha-adrenergic and ganglionic blockers; and (4) angiotensin-converting enzyme (ACE) inhibitors. Oxygen saturation in the jugular venous blood is of the order of 60% to 70% and is considerably higher than in the coronary sinus. It is hypothesized that this oxygen reserve enables the brain better than the heart to take hemodynamic advantage of pressure lowering without risking tissue ischemia. This may explain why antihypertensive treatment prevents stroke but not myocardial infarction. Acute hypertensive encephalopathy is probably caused by failure of autoregulatory vasoconstriction with focal or generalized dilatation of small arteries and arterioles. This is associated with a high CBF, dysfunction of the blood-brain barrier, and the formation of brain edema that is thought to cause the clinical symptoms.

AB - In chronic hypertension, the lower limit of autoregulation of cerebral blood flow (CBF) is shifted towards high blood pressure with a consequent impairment of the tolerance to acute hypotension. Despite this, antihypertensive treatment in the great majority of patients prevents stroke and the risk for treatment-induced cerebral ischemia is only real in a limited number of clinical settings such as malignant hypertension, hypertension in the elderly, and hypertension associated with acute stroke. During long-term treatment adaptive hypertensive changes in CBF autoregulation may be reversible, especially in young patients. Drugs used for emergency lowering of blood pressure may be classified into four groups according to their effect on CBF and intracranial pressure: (1) drugs with no pharmacological action in the cerebral circulation; (2) cerebral vasodilators; (3) alpha-adrenergic and ganglionic blockers; and (4) angiotensin-converting enzyme (ACE) inhibitors. Oxygen saturation in the jugular venous blood is of the order of 60% to 70% and is considerably higher than in the coronary sinus. It is hypothesized that this oxygen reserve enables the brain better than the heart to take hemodynamic advantage of pressure lowering without risking tissue ischemia. This may explain why antihypertensive treatment prevents stroke but not myocardial infarction. Acute hypertensive encephalopathy is probably caused by failure of autoregulatory vasoconstriction with focal or generalized dilatation of small arteries and arterioles. This is associated with a high CBF, dysfunction of the blood-brain barrier, and the formation of brain edema that is thought to cause the clinical symptoms.

KW - Animals

KW - Antihypertensive Agents/adverse effects

KW - Brain Diseases/etiology

KW - Brain Ischemia/chemically induced

KW - Cerebrovascular Circulation/drug effects

KW - Cerebrovascular Disorders/prevention & control

KW - Emergency Medical Services

KW - Homeostasis/drug effects

KW - Humans

KW - Hypertension/complications

KW - Myocardial Infarction/etiology

KW - Risk Factors

U2 - 10.1093/ajh/2.6.486

DO - 10.1093/ajh/2.6.486

M3 - Journal article

C2 - 2757806

VL - 2

SP - 486

EP - 492

JO - American Journal of Hypertension

JF - American Journal of Hypertension

SN - 0895-7061

IS - 6 Pt 1

ER -

ID: 275592193