The role of catecholamines in ischemic preconditioning is unclear. Accordingly, the effects of tyramine-induced norepinephrine release and α 1 - receptor blockade were examined. Ischemic preconditioning with a 5-minute coronary occlusion 10 minutes before a 30-minute ischemic interval resulted in only 7.7±3.1% infarction of the risk area, significantly less than that in control rabbits with isolated 30-minute coronary occlusions (34.4±3.2%, P < .01). Intravenous infusion of tyramine 10 minutes before 30 minutes of ischemia also protected the heart from infarction to an extent similar to that seen with ischemic preconditioning (6.9±2.4% infarction). This protection observed with tyramine infusion was eliminated by α 1 -receptor blockade with BE 2254 (36.8±2.6% infarction) but was unaffected by β- blockade with propranolol (10.5±2.4% infarction). Furthermore, the protection was unaffected when the tyramine-induced hypertension was attenuated by allowing blood to flow into a volume reservoir (3.9±0.8% infarction, P < .01 vs control value). The nonselective adenosine-receptor blocker PD 115,199 also eliminated tyramine-induced protection (40.2±5.6% infarction), indicating that adenosine is involved in adrenergic-mediated protection. BE 2254 could not block ischemic preconditioning (3.9±1.1% infarction, P < .01 vs control value). Therefore, catecholamine release before prolonged ischemia can protect the heart from infarction via the α 1 - receptor, but adenosine receptor stimulation is also involved. α-Adrenergic stimulation does not appear to be critical to the protection observed after ischemic preconditioning.
Thornton, J. D., Daly, J. F., Cohen, M. V., Yang, X. M., & Downey, J. M. (1993). Catecholamines can induce adenosine receptor-mediated protection of the myocardium but do not participate in ischemic preconditioning in the rabbit. Circulation Research, 73(4), 649–655. https://doi.org/10.1161/01.RES.73.4.649