This study was to evaluate myocardial cell and mitochondrial viability with99mTc-MIBI. In vivo studY

185Mbq 99mTc-MIBI was injected intravnously intorabbits 2-5 min after reperfusion preceded 20 min （Group A） or 3h （Group B） of LADocclusion. In Group B

relative sestamibi activity of ischemic myocardiam andmyocardial ATP contents was significantly lower than Group A; and a significantlypositive correlation between SDH and subcellular sestamibi distribution （r=0.88

P<0.001） was found. In vitro study

the capacity of mitochondria preparation tosequester sestamibi was examined after 20 min as percent of total 99mTc activity. Itwas 9.70 ± 2.59%

10.05 ± 2.00% and only 3.89 ± 1.48% in nonischemic

reversible andirreversble damaged myocardium respectively. After addition of succinate

increasedto 50.27± 12.04%

52.70± 10.97% and 6.08± 3.26%

respectively was observed.Myocardial 99mTc-MIBI mainly localized within mitochondria. Myocardial kinetics of99mTc sestamibi was significantly affected by myocardial metabolism and viability.