CATECHOLAMINES CAN INDUCE ADENOSINE RECEPTOR-MEDIATED PROTECTION OF THE MYOCARDIUM BUT DO NOT PARTICIPATE IN ISCHEMIC PRECONDITIONING IN THE RABBIT

The role of catecholamines in ischemic preconditioning is unclear. Acc ordingly, the effects of tyramine-induced norepinephrine release and a lpha1-receptor blockade were examined. Ischemic preconditioning with a 5-minute coronary occlusion 10 minutes before a 30 -minute ischemic i nterval resulted in only 7.7+/-3.1% infarction of the risk area, signi ficantly less than that in control rabbits with isolated 30-minute cor onary occlusions (34.4+/-3.2%, P<.01). Intravenous infusion of tyramin e 10 minutes before 30 minutes of ischemia also protected the heart fr om infarction to an extent similar to that seen with ischemic precondi tioning (6.9+/-2.4% infarction). This protection observed with tyramin e infusion was eliminated by alpha1-receptor blockade with BE 2254 (36 .8+/-2.6% infarction) but was unaffected by beta-blockade with propran olol (10.5+/-2.4% infarction). Furthermore, the protection was unaffec ted 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 115,19 9 also eliminated tyramine-induced protection (40.2+/-5.6% infarction) , indicating that adenosine is involved in adrenergic-mediated protect ion. BE 2254 could not block ischemic preconditioning (3.9+/-1.1% infa rction, P<.01 vs control value). Therefore, catecholamine release befo re prolonged ischemia can protect the heart from infarction via the al pha1-receptor, but adenosine receptor stimulation is also involved. Al pha-Adrenergic stimulation does not appear to be critical to the prote ction observed after ischemic preconditioning.