Beta-adrenergic blockers infarction

Finally, experimental studies have established that nipradilol, another NO-releasing beta-adrenergic blocker, enhances postischemic recovery and limits infarct size (100a). Moreover, there is a clear involvement of NO in the ocular hypotensive action of nipradilol (100b). These studies should be carried out in humans before a conclusion is made. 

The necessity of PKA activation for successful preconditioning is demonstrated by the following (i) the beta-adrenergic receptor blocker alprenolol partially abolished ischemic preconditioning (Lochner et al. 1999) (ii) landiolol, a short-acting beta-blocker, blunted the infarct size limitation induced by ischemic preconditioning (Sanada et al. 2004) (iii) PKA inhibitors such as H89 (Sanada et al. 2004 Inserte et al. 2004) and Rp-cAMPs (Sanada et al. 2004) blunted ischemic and dibutyryl-cAMP-induced preconditioning. 

A study in 30 patients being evaluated for chest pain found that 2 mg/kg of a 10% intranasal solution of cocaine reduced coronary sinus flow hy about 14% and coronary artery diameter by 6 to 9%. The coronary vascular resistance increased by 22%. The addition of propranolol 400 micrograms/minute by intracoronary infusion, (to a total of 2 mg) reduced coronary sinus flow by a further 15% and increased the coronary vascular resistance by 17%. The probable reason is that the cocaine stimulates the alpha-receptors of the coronary blood vessels causing vasoconstriction. When the beta-receptors are blocked by propranolol, the resultant unopposed alpha-adrenergic stimulation may lead to enhanced coronary vasoconstriction (see also Beta blockers + Inotropes and Vasopressors , p.848). The clinical importance of these frndings is uncertain but the authors of the report suggest that beta blockers should be avoided in patients with myocardial ischaemia or infarction associated with the use of cocaine. ... 

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