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
SN - 0895-7061
VL - 2
SP - 486
EP - 492
JO - American Journal of Hypertension
JF - American Journal of Hypertension
IS - 6 Pt 1
ER -