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.