Pathophysiological basis for the application of noradrenergic transmission blockade in the therapy of cerebral ischemic accidents
Stoica, E.
Neurologie et Psychiatrie 22(3): 193-201
1984
ISSN/ISBN: 0259-6326 PMID: 6387873 Document Number: 229657
Many clinical and experimental data demonstrate that, cerebral ischemia induces both a systemic discharge of catecholamines (CA) and a release of such neurotransmitters from the ischemic brain tissue. By activating cerebral oxygen and glucose consumption and by disrupting the blood-brain barrier thus, promoting cerebral edema, the systemic and cerebral CA discharge may aggravate the metabolic and hemodynamic disorders produced by cerebral ischemia. The drugs which depress the noradrenergic transmission either by reducing the central tonus of sympathetic nervous system or by blocking .alpha. or .beta. adrenergic receptors may counteract the deleterious effects of CA discharge and offer at least a partial protection against cerebral ischemia. The decline in cerebrovascular mortality and the reduction in the incidence of stroke noticed in the last 3 decades seem to be a good support for the applications of such a therapy since the above-mentioned trend has been at least partly ascribed to the broader use of antihypertensive armamentarium which includes many drugs which depress noradrenergic transmission (.alpha.-methyldopa, clonidine, reserpine, propranolol).