Effect of postconditioning on myocardial 99mTc-annexin-V uptake: Comparison with ischemic preconditioning and caspase inhibitor treatment

Junichi Taki, Takahiro Higuchi, Atsuhiro Kawashima, Makoto Fukuoka, Daiki Kayano, Jonathan F. Tait, Ichiro Matsunari, Kenichi Nakajima, Seigo Kinuya, H. William Strauss

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

99mTc-Annexin-V imaging has been proved to be feasible to detect phosphatidylserine, which externalizes on the outer cell membrane early in the process of apoptosis. To determine whether postconditioning suppresses myocardial cell damage or apoptosis, we evaluated the intensity and distribution of 99mTc-annexin-V uptake after postconditioning in a rat model of ischemia and reperfusion and compared the effect to that of ischemic preconditioning and pretreatment with caspase inhibitor. Methods: In control rats (n = 13), after thoracotomy the left coronary artery was occluded for 20 min followed by reperfusion for 30 or 90 min and injection of 99mTc-annexin-V (80-150 MBq). One hour later, to verify the area at risk, 201TI (0.74 MBq) was injected intravenously just beyond the left coronary artery reocclusion, and the rats were sacrificed 1 min later. In the groups of rats with various interventions, postconditioning (n = 11) was performed just after the reperfusion, and preconditioning (n = 11) and caspase inhibitor treatment (n = 11) were performed before ischemia. Dual-tracer autoradiography was performed to assess 99mTc-annexin-V uptake and area at risk. Results: In all control rats, intense 99mTc-annexin-V uptake was observed in the area at risk (uptake ratios at 30 or 90 min after reperfusion, 4.15 ± 1.89 and 3.70 ± 1.41, respectively). Postconditioning suppressed 99mTc-annexin-V uptake (uptake ratios at 30 or 90 min after reperfusion, 2.09 ± 0.56, P < 0.05, and 1.88 ± 0.69, P < 0.05, respectively). Preconditioning also suppressed uptake (uptake ratios at 30 and 90 min after reperfusion, 1.17 ± 0.29, P < 0.005, and 1.33 ± 0.74, P < 0.01, respectively), as did caspase inhibitor (uptake ratios at 30 and 90 min after reperfusion, 2.08 ± 0.50, P < 0.05, and 1.27 ± 0.24, P < 0.005, respectively). In all interventions, the percentage of cells positive on deoxyuride-5′- triphosphate biotin nick end labeling and histologic changes with myocardial cell degeneration and cell infiltrations were suppressed markedly. Conclusion: These data indicate that 99mTc-annexin-V imaging may be a way to monitor myocardial injury and its response to novel therapeutic interventions including postconditioning, preconditioning, and antiapoptotic therapy.

Original languageEnglish
Pages (from-to)1301-1307
Number of pages7
JournalJournal of Nuclear Medicine
Volume48
Issue number8
DOIs
Publication statusPublished - Aug 1 2007
Externally publishedYes

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Ischemic Preconditioning
Caspase Inhibitors
Annexin A5
Reperfusion
Therapeutics
Coronary Vessels
Ischemia
Apoptosis
Phosphatidylserines
Thoracotomy
Biotin
Autoradiography
Odds Ratio
Cell Membrane
Injections
Wounds and Injuries

Keywords

  • Tc-annexin-V
  • Apoptosis imaging
  • Caspase inhibitor
  • Ischemic preconditioning
  • Postconditioning

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

Cite this

Effect of postconditioning on myocardial 99mTc-annexin-V uptake : Comparison with ischemic preconditioning and caspase inhibitor treatment. / Taki, Junichi; Higuchi, Takahiro; Kawashima, Atsuhiro; Fukuoka, Makoto; Kayano, Daiki; Tait, Jonathan F.; Matsunari, Ichiro; Nakajima, Kenichi; Kinuya, Seigo; Strauss, H. William.

In: Journal of Nuclear Medicine, Vol. 48, No. 8, 01.08.2007, p. 1301-1307.

Research output: Contribution to journalArticle

Taki, J, Higuchi, T, Kawashima, A, Fukuoka, M, Kayano, D, Tait, JF, Matsunari, I, Nakajima, K, Kinuya, S & Strauss, HW 2007, 'Effect of postconditioning on myocardial 99mTc-annexin-V uptake: Comparison with ischemic preconditioning and caspase inhibitor treatment', Journal of Nuclear Medicine, vol. 48, no. 8, pp. 1301-1307. https://doi.org/10.2967/jnumed.106.037408
Taki, Junichi ; Higuchi, Takahiro ; Kawashima, Atsuhiro ; Fukuoka, Makoto ; Kayano, Daiki ; Tait, Jonathan F. ; Matsunari, Ichiro ; Nakajima, Kenichi ; Kinuya, Seigo ; Strauss, H. William. / Effect of postconditioning on myocardial 99mTc-annexin-V uptake : Comparison with ischemic preconditioning and caspase inhibitor treatment. In: Journal of Nuclear Medicine. 2007 ; Vol. 48, No. 8. pp. 1301-1307.
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abstract = "99mTc-Annexin-V imaging has been proved to be feasible to detect phosphatidylserine, which externalizes on the outer cell membrane early in the process of apoptosis. To determine whether postconditioning suppresses myocardial cell damage or apoptosis, we evaluated the intensity and distribution of 99mTc-annexin-V uptake after postconditioning in a rat model of ischemia and reperfusion and compared the effect to that of ischemic preconditioning and pretreatment with caspase inhibitor. Methods: In control rats (n = 13), after thoracotomy the left coronary artery was occluded for 20 min followed by reperfusion for 30 or 90 min and injection of 99mTc-annexin-V (80-150 MBq). One hour later, to verify the area at risk, 201TI (0.74 MBq) was injected intravenously just beyond the left coronary artery reocclusion, and the rats were sacrificed 1 min later. In the groups of rats with various interventions, postconditioning (n = 11) was performed just after the reperfusion, and preconditioning (n = 11) and caspase inhibitor treatment (n = 11) were performed before ischemia. Dual-tracer autoradiography was performed to assess 99mTc-annexin-V uptake and area at risk. Results: In all control rats, intense 99mTc-annexin-V uptake was observed in the area at risk (uptake ratios at 30 or 90 min after reperfusion, 4.15 ± 1.89 and 3.70 ± 1.41, respectively). Postconditioning suppressed 99mTc-annexin-V uptake (uptake ratios at 30 or 90 min after reperfusion, 2.09 ± 0.56, P < 0.05, and 1.88 ± 0.69, P < 0.05, respectively). Preconditioning also suppressed uptake (uptake ratios at 30 and 90 min after reperfusion, 1.17 ± 0.29, P < 0.005, and 1.33 ± 0.74, P < 0.01, respectively), as did caspase inhibitor (uptake ratios at 30 and 90 min after reperfusion, 2.08 ± 0.50, P < 0.05, and 1.27 ± 0.24, P < 0.005, respectively). In all interventions, the percentage of cells positive on deoxyuride-5′- triphosphate biotin nick end labeling and histologic changes with myocardial cell degeneration and cell infiltrations were suppressed markedly. Conclusion: These data indicate that 99mTc-annexin-V imaging may be a way to monitor myocardial injury and its response to novel therapeutic interventions including postconditioning, preconditioning, and antiapoptotic therapy.",
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T1 - Effect of postconditioning on myocardial 99mTc-annexin-V uptake

T2 - Comparison with ischemic preconditioning and caspase inhibitor treatment

AU - Taki, Junichi

AU - Higuchi, Takahiro

AU - Kawashima, Atsuhiro

AU - Fukuoka, Makoto

AU - Kayano, Daiki

AU - Tait, Jonathan F.

AU - Matsunari, Ichiro

AU - Nakajima, Kenichi

AU - Kinuya, Seigo

AU - Strauss, H. William

PY - 2007/8/1

Y1 - 2007/8/1

N2 - 99mTc-Annexin-V imaging has been proved to be feasible to detect phosphatidylserine, which externalizes on the outer cell membrane early in the process of apoptosis. To determine whether postconditioning suppresses myocardial cell damage or apoptosis, we evaluated the intensity and distribution of 99mTc-annexin-V uptake after postconditioning in a rat model of ischemia and reperfusion and compared the effect to that of ischemic preconditioning and pretreatment with caspase inhibitor. Methods: In control rats (n = 13), after thoracotomy the left coronary artery was occluded for 20 min followed by reperfusion for 30 or 90 min and injection of 99mTc-annexin-V (80-150 MBq). One hour later, to verify the area at risk, 201TI (0.74 MBq) was injected intravenously just beyond the left coronary artery reocclusion, and the rats were sacrificed 1 min later. In the groups of rats with various interventions, postconditioning (n = 11) was performed just after the reperfusion, and preconditioning (n = 11) and caspase inhibitor treatment (n = 11) were performed before ischemia. Dual-tracer autoradiography was performed to assess 99mTc-annexin-V uptake and area at risk. Results: In all control rats, intense 99mTc-annexin-V uptake was observed in the area at risk (uptake ratios at 30 or 90 min after reperfusion, 4.15 ± 1.89 and 3.70 ± 1.41, respectively). Postconditioning suppressed 99mTc-annexin-V uptake (uptake ratios at 30 or 90 min after reperfusion, 2.09 ± 0.56, P < 0.05, and 1.88 ± 0.69, P < 0.05, respectively). Preconditioning also suppressed uptake (uptake ratios at 30 and 90 min after reperfusion, 1.17 ± 0.29, P < 0.005, and 1.33 ± 0.74, P < 0.01, respectively), as did caspase inhibitor (uptake ratios at 30 and 90 min after reperfusion, 2.08 ± 0.50, P < 0.05, and 1.27 ± 0.24, P < 0.005, respectively). In all interventions, the percentage of cells positive on deoxyuride-5′- triphosphate biotin nick end labeling and histologic changes with myocardial cell degeneration and cell infiltrations were suppressed markedly. Conclusion: These data indicate that 99mTc-annexin-V imaging may be a way to monitor myocardial injury and its response to novel therapeutic interventions including postconditioning, preconditioning, and antiapoptotic therapy.

AB - 99mTc-Annexin-V imaging has been proved to be feasible to detect phosphatidylserine, which externalizes on the outer cell membrane early in the process of apoptosis. To determine whether postconditioning suppresses myocardial cell damage or apoptosis, we evaluated the intensity and distribution of 99mTc-annexin-V uptake after postconditioning in a rat model of ischemia and reperfusion and compared the effect to that of ischemic preconditioning and pretreatment with caspase inhibitor. Methods: In control rats (n = 13), after thoracotomy the left coronary artery was occluded for 20 min followed by reperfusion for 30 or 90 min and injection of 99mTc-annexin-V (80-150 MBq). One hour later, to verify the area at risk, 201TI (0.74 MBq) was injected intravenously just beyond the left coronary artery reocclusion, and the rats were sacrificed 1 min later. In the groups of rats with various interventions, postconditioning (n = 11) was performed just after the reperfusion, and preconditioning (n = 11) and caspase inhibitor treatment (n = 11) were performed before ischemia. Dual-tracer autoradiography was performed to assess 99mTc-annexin-V uptake and area at risk. Results: In all control rats, intense 99mTc-annexin-V uptake was observed in the area at risk (uptake ratios at 30 or 90 min after reperfusion, 4.15 ± 1.89 and 3.70 ± 1.41, respectively). Postconditioning suppressed 99mTc-annexin-V uptake (uptake ratios at 30 or 90 min after reperfusion, 2.09 ± 0.56, P < 0.05, and 1.88 ± 0.69, P < 0.05, respectively). Preconditioning also suppressed uptake (uptake ratios at 30 and 90 min after reperfusion, 1.17 ± 0.29, P < 0.005, and 1.33 ± 0.74, P < 0.01, respectively), as did caspase inhibitor (uptake ratios at 30 and 90 min after reperfusion, 2.08 ± 0.50, P < 0.05, and 1.27 ± 0.24, P < 0.005, respectively). In all interventions, the percentage of cells positive on deoxyuride-5′- triphosphate biotin nick end labeling and histologic changes with myocardial cell degeneration and cell infiltrations were suppressed markedly. Conclusion: These data indicate that 99mTc-annexin-V imaging may be a way to monitor myocardial injury and its response to novel therapeutic interventions including postconditioning, preconditioning, and antiapoptotic therapy.

KW - Tc-annexin-V

KW - Apoptosis imaging

KW - Caspase inhibitor

KW - Ischemic preconditioning

KW - Postconditioning

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