Treatment of acute focal cerebral ischemia with propranolol.

Abstract

Propranolol's potential as a protective agent against tissue injury has been noted in experimental myocardial, renal and early acute focal cerebral ischemia. The purpose of the present investigation was to study further the effects of racemic (d,l) propranolol on blood-brain barrier permeability, morphological changes, cortical electrical activity, and regional cerebral blood flow (rCBF) in experimental focal cerebral ischemia. Thirty adult cats, anesthetized with nitrous oxide, underwent 6 hours of right middle cerebral artery (MCA) occlusion. Fifteen cats were untreated. Fifteen cats were given a continuous infusion of racemic propranolol (1 mg/kg/hr) for 7 hours beginning 1 hour before MCA occlusion and a 4 mg/kg bolus immediately before occlusion, both directly into the right carotid artery. Right Sylvian rCBF did not significantly differ in the treated and untreated groups. Carbon filling defects and vital dye (i.e., Evans blue and fluorescein) extravasation were less severe in the propranolol treated animals. Light microscopic findings demonstrated no difference in infarct size between the two groups. The findings suggest that at doses given, racemic propranolol does not exert a protective effect upon cerebral tissue subjected to 6 hours of incomplete ischemia.

Pre‐stroke use of beta‐blockers does not affect ischaemic stroke severity and outcome

“…Brain injury was reduced and outcome improved after middle cerebral artery occlusion in mice lacking beta 2 ‐adrenergic receptors [13], or pretreated either with the non‐selective beta‐adrenergic blockers propranolol and carvedilol [2,14] or the selective beta 2 ‐adrenergic blocker ICI 118551 [13]. Other studies failed to demonstrate neuroprotective effects after middle cerebral artery occlusion in cats pretreated with propranolol [15,16]. In rodents, the beta 2 ‐adrenergic agonist clenbuterol displayed neuroprotective effects in focal brain ischaemia, an action that appeared to be dependent on the release of nerve growth factor by astrocytes [6–8].…”

Analytic Review: Ischemic Cerebrovascular Disease: Diagnosis and Management

“…Many vasodilating drugs have been tried in hopes of improving flow to the ischemic brain. Although of possible value theoretically, these drugs have not been shown to be clinically useful in acute strokes, and there is concern that they might lead to a steal of blood away from ischemic brain [3,4,18,26,55,56]. Ischemic areas of brain lose the ability to autoregulate blood flow, and as a result flow becomes dependent on perfusion pressure.…”