Abstract
Background: To determine whether mild to moderate ischemia that is not severe enough to induce myocardial infarction will cause myocardial cell damage or apoptosis, the 99mTc-Annexin-V (Tc-A) uptake was studied in groups of rats with various intervals of coronary occlusion and reperfusion times. Methods and Results: After left coronary artery occlusion for 15 min (n=23), 10 min (n=23), or 5min (n=12), Tc-A (80-150 MBq) was injected at 0.5, 1.5, 6, or 24 h after reperfusion. One hour later, to verify the area at risk, 201Tl (0.74 MBq) was injected just after left coronary artery re-occlusion and the rats were killed 1 min later. Dual tracer autoradiography was performed to assess Tc-A uptake and area at risk. In all 5-min occlusion and reperfusion models, no significant Tc-A uptake was observed in the area at risk. Tc-A uptake ratios in the 15-min and 10-min ischemia models were 4.46±3.16 and 2.02±0.47 (p=0.078) at 0.5 h after reperfusion, 3.49±1.78 and 1.47±0.11 (p<0.05) at 1.5h after reperfusion, 1.60±0.43 and 1.34±0.23 (p=0.24) at 6h after reperfusion, 1.50±0.33 and 1.28±0.33 (p=0.099) at 24 h after reperfusion, respectively. With 15-min ischemia, in 3 of the 5 rats there were a few micro-foci of myocardial cell degeneration and cell infiltration in less than 1% of the ischemic area at 24 h after reperfusion. No significant histological change was observed in rats with 10-min or 5-min ischemia. Conclusion: The data indicate that Tc-A binding depends on the severity of ischemia even without a significant amount of histological change or infarction.
| Original language | English |
|---|---|
| Pages (from-to) | 1141-1146 |
| Number of pages | 6 |
| Journal | Circulation Journal |
| Volume | 71 |
| Issue number | 7 |
| DOIs | |
| Publication status | Published - Jul 4 2007 |
| Externally published | Yes |
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Keywords
- Tc-Annexin- V
- Apoptosis imaging
- Myocardial ischemia
- Reperfusion
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
99mTc-Annexin-V uptake in a rat model of variable ischemic severity and reperfusion time. / Taki, Junichi; Higuchi, Takahiro; Kawashima, Atsuhiro; Tait, Jonathan F.; Muramori, Akira; Matsunari, Ichiro; Nakajima, Kenichi; Vanderheyden, Jean Luc; Strauss, H. William.
In: Circulation Journal, Vol. 71, No. 7, 04.07.2007, p. 1141-1146.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - 99mTc-Annexin-V uptake in a rat model of variable ischemic severity and reperfusion time
AU - Taki, Junichi
AU - Higuchi, Takahiro
AU - Kawashima, Atsuhiro
AU - Tait, Jonathan F.
AU - Muramori, Akira
AU - Matsunari, Ichiro
AU - Nakajima, Kenichi
AU - Vanderheyden, Jean Luc
AU - Strauss, H. William
PY - 2007/7/4
Y1 - 2007/7/4
N2 - Background: To determine whether mild to moderate ischemia that is not severe enough to induce myocardial infarction will cause myocardial cell damage or apoptosis, the 99mTc-Annexin-V (Tc-A) uptake was studied in groups of rats with various intervals of coronary occlusion and reperfusion times. Methods and Results: After left coronary artery occlusion for 15 min (n=23), 10 min (n=23), or 5min (n=12), Tc-A (80-150 MBq) was injected at 0.5, 1.5, 6, or 24 h after reperfusion. One hour later, to verify the area at risk, 201Tl (0.74 MBq) was injected just after left coronary artery re-occlusion and the rats were killed 1 min later. Dual tracer autoradiography was performed to assess Tc-A uptake and area at risk. In all 5-min occlusion and reperfusion models, no significant Tc-A uptake was observed in the area at risk. Tc-A uptake ratios in the 15-min and 10-min ischemia models were 4.46±3.16 and 2.02±0.47 (p=0.078) at 0.5 h after reperfusion, 3.49±1.78 and 1.47±0.11 (p<0.05) at 1.5h after reperfusion, 1.60±0.43 and 1.34±0.23 (p=0.24) at 6h after reperfusion, 1.50±0.33 and 1.28±0.33 (p=0.099) at 24 h after reperfusion, respectively. With 15-min ischemia, in 3 of the 5 rats there were a few micro-foci of myocardial cell degeneration and cell infiltration in less than 1% of the ischemic area at 24 h after reperfusion. No significant histological change was observed in rats with 10-min or 5-min ischemia. Conclusion: The data indicate that Tc-A binding depends on the severity of ischemia even without a significant amount of histological change or infarction.
AB - Background: To determine whether mild to moderate ischemia that is not severe enough to induce myocardial infarction will cause myocardial cell damage or apoptosis, the 99mTc-Annexin-V (Tc-A) uptake was studied in groups of rats with various intervals of coronary occlusion and reperfusion times. Methods and Results: After left coronary artery occlusion for 15 min (n=23), 10 min (n=23), or 5min (n=12), Tc-A (80-150 MBq) was injected at 0.5, 1.5, 6, or 24 h after reperfusion. One hour later, to verify the area at risk, 201Tl (0.74 MBq) was injected just after left coronary artery re-occlusion and the rats were killed 1 min later. Dual tracer autoradiography was performed to assess Tc-A uptake and area at risk. In all 5-min occlusion and reperfusion models, no significant Tc-A uptake was observed in the area at risk. Tc-A uptake ratios in the 15-min and 10-min ischemia models were 4.46±3.16 and 2.02±0.47 (p=0.078) at 0.5 h after reperfusion, 3.49±1.78 and 1.47±0.11 (p<0.05) at 1.5h after reperfusion, 1.60±0.43 and 1.34±0.23 (p=0.24) at 6h after reperfusion, 1.50±0.33 and 1.28±0.33 (p=0.099) at 24 h after reperfusion, respectively. With 15-min ischemia, in 3 of the 5 rats there were a few micro-foci of myocardial cell degeneration and cell infiltration in less than 1% of the ischemic area at 24 h after reperfusion. No significant histological change was observed in rats with 10-min or 5-min ischemia. Conclusion: The data indicate that Tc-A binding depends on the severity of ischemia even without a significant amount of histological change or infarction.
KW - Tc-Annexin- V
KW - Apoptosis imaging
KW - Myocardial ischemia
KW - Reperfusion
UR - http://www.scopus.com/inward/record.url?scp=34347247614&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34347247614&partnerID=8YFLogxK
U2 - 10.1253/circj.71.1141
DO - 10.1253/circj.71.1141
M3 - Article
C2 - 17587725
AN - SCOPUS:34347247614
VL - 71
SP - 1141
EP - 1146
JO - Circulation Journal
JF - Circulation Journal
SN - 1346-9843
IS - 7
ER -