The role of
catecholamines in ischemic preconditioning is unclear. Accordingly, the effects of
tyramine-induced
norepinephrine release and alpha 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 alpha 1-receptor blockade with
BE 2254 (36.8 +/- 2.6%
infarction) but was unaffected by beta-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 alpha 1-receptor, but
adenosine receptor stimulation is also involved. alpha-
Adrenergic stimulation does not appear to be critical to the protection observed after ischemic preconditioning.