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Vol. 294, Issue 2, 451-457, August 2000
Department of Pharmacology and Toxicology, Medical College of
Wisconsin, Milwaukee, Wisconsin (R.M.F., A.K.H., G.J.G.); and Toray
Industries, Kanagawa, Japan (H.N.)
We examined the role of the sarcolemmal and mitochondrial ATP-sensitive
potassium (KATP) channel in a rat model of myocardial infarction after stimulation with the selective 
1-opioid
receptor agonist TAN-67. Hearts were subjected to 30 min of regional
ischemia and 2 h of reperfusion. Infarct size was expressed as a
percentage of the area at risk. TAN-67 significantly reduced
infarct size/area at risk (29.6 ± 3.3) versus control (63.1 ± 2.3). The sarcolemmal-selective KATP channel antagonist
HMR 1098, administered 10 min before TAN-67, did not significantly
attenuate cardioprotection (26.0 ± 7.3) at a dose (3 mg/kg) that
had no effect in the absence of TAN-67 (56.3 ± 4.3). Pretreatment
with the mitochondrial selective antagonist 5-hydroxydecanoic acid
(5-HD) 5 min before the 30-min occlusion completely abolished
TAN-67-induced cardioprotection (54.3 ± 2.7), but had no effect
in the absence of TAN-67 (62.6 ± 4.1), suggesting the involvement
of the mitochondrial KATP channel. Additionally, we
examined the antiarrhythmic effects of TAN-67 in the presence or
absence of 5-HD and HMR 1098 during 30 min of ischemia. Control animals
had an average arrhythmia score of 10.40 ± 2.41. TAN-67 significantly reduced the arrhythmia score during 30 min of ischemia (2.38 ± 0.85). 5-HD and HMR 1098 in the absence of TAN-67
produced an insignificant decrease in the arrhythmia score (8.80 ± 2.56 and 4.20 ± 1.07, respectively). 5-HD administration
before TAN-67 treatment abolished its antiarrhythmic effect (4.71 ± 1.11). However, HMR 1098 did not abolish TAN-67-induced protection
against arrhythmias (1.67 ± 0.80). These data suggest that
1-opioid receptor stimulation is cardioprotective
against myocardial ischemia and sublethal arrhythmias and suggest a
role for the mitochondrial KATP channel in mediating these
cardioprotective effects.
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