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1 Bristol Heart Institute,
We have used mitochondrial entrapment of
2-deoxy-D-[3H]glucose (2-DG) to
demonstrate that recovery of Langendorff-perfused rat hearts from
ischemia is accompanied by reversal of the mitochondrial permeability transition (MPT). In hearts loaded with 2-DG before 40 min
of ischemia and 25 min of reperfusion, 2-DG entrapment [expressed as 105 × (mitochondrial
2-[3H]DG dpm per unit
citrate synthase)/(total heart
2-[3H]DG dpm/g wet
wt)] increased from 11.1 ± 1.3 (no ischemia,
n = 4) to 32.5 ± 1.9 (n = 6;
P < 0.001). In other experiments,
2-DG was loaded after 25 min of reperfusion to determine whether some mitochondria that had undergone the MPT during the initial phase of
reperfusion subsequently "resealed" and thus no longer took up
2-DG. The reduction of 2-DG entrapment to 20.6 ± 2.4 units (n = 5) confirmed that this was the
case. Pyruvate (10 mM) in the perfusion medium increased recovery of
left ventricular developed pressure from 57.2 ± 10.3 to 98.9 ± 10.8% (n = 6;
P < 0.05) and reduced entrapment of
2-DG loaded preischemically and postischemically to 23.5 ± 1.5 (n = 4;
P < 0.001) and 10.5 ± 0.5 (n = 4;
P < 0.01) units, respectively. The
presence of pyruvate increased tissue lactate content at the end of
ischemia and decreased the effluent pH during the initial phase
of reperfusion concomitant with an increase in lactate output. We
suggest that pyruvate may inhibit the MPT by decreasing
pHi and scavenging free radicals,
thus protecting hearts from reperfusion injury.
rat; reperfusion injury; apoptosis; deoxyglucose; pHi
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