Detection of cardiomyocyte death in a rat model of ischemia and reperfusion using 99m Tc-labeled annexin V

Junichi Taki, Takahiro Higuchi, Atsuhiro Kawashima, Jonathan F. Tait, Seigo Kinuya, Akira Muramori, Ichiro Matsunari, Kenichi Nakajima, Norihisa Tonami, H. William Strauss

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

There is increasing evidence that cell death after myocardial ischemia and reperfusion may begin as apoptosis rather than necrosis. To determine the time course, location, and extent of this process, we studied groups of rats after a 20-min interval of coronary occlusion and reperfusion. Methods: After thoracotomy, the left coronary artery was occluded for 20 min. After release and before study, groups of animals were allowed to recover for various intervals: 0.5 h (n = 6), 1.5 h (n = 7), 6 h (n = 7), 1 d (n = 8), 3 d (n = 8), or 2 wk (n = 5). At the time of study, the rats were injected with 99m Tc-annexin V (80-150 MBq). One hour later, to verify the area at risk, 201 Tl (0.74 MBq) was injected intravenously just after the left coronary artery reocclusion and the rats were sacrificed 1 min later. Dual-tracer autoradiography was performed to assess 99m Tc-annexin V uptake and the area at risk. Results: Extensive 99m Tc-annexin V uptake was observed in the mid myocardium after 0.5-1.5 h of reperfusion. The area of annexin uptake had expanded in the subendocardial and subepicardial layers at 6 h after reperfusion and then gradually lessened over 3 d. At 0.5 and 1.5 h of reperfusion, 99m Tc-annexin V uptake ratios were 7.36 ± 2.95 and 6.34 ± 2.24 (mean ± SD), respectively. The uptake ratios gradually decreased at 6 h, 1 d, 3 d, and 2 wk after reperfusion (4.65 ± 1.93, 3.27 ± 0.92 [P < 0.01 vs. 0.5 h], 1.84 ± 0.55 [P < 0.001 vs. 0.5 h, P < 0.005 vs. 1.5 h], and 1.65 ± 0.31 [P < 0.001 vs. 0.5 h, P < 0.005 vs. 1.5 h], respectively). Conclusion: These data indicate that annexin binding commences soon after ischemia and reperfusion in the mid myocardium within the area at risk and expands to include the subendocardial and subepicardial layers at 6 h after reperfusion, followed by gradual reduction of activity over 3 d.

Original languageEnglish
Pages (from-to)1536-1541
Number of pages6
JournalJournal of Nuclear Medicine
Volume45
Issue number9
Publication statusPublished - Sep 1 2004
Externally publishedYes

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Cardiac Myocytes
Reperfusion
Ischemia
Annexins
Myocardial Reperfusion
Coronary Vessels
Myocardium
Group Processes
Time and Motion Studies
Coronary Occlusion
Thoracotomy
Autoradiography
Myocardial Ischemia
technetium Tc 99m annexin V
Cell Death
Necrosis
Apoptosis

Keywords

  • Tc-annexin V
  • Apoptosis
  • Ischemia
  • Reperfusion

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

Cite this

Taki, J., Higuchi, T., Kawashima, A., Tait, J. F., Kinuya, S., Muramori, A., ... Strauss, H. W. (2004). Detection of cardiomyocyte death in a rat model of ischemia and reperfusion using 99m Tc-labeled annexin V Journal of Nuclear Medicine, 45(9), 1536-1541.

Detection of cardiomyocyte death in a rat model of ischemia and reperfusion using 99m Tc-labeled annexin V . / Taki, Junichi; Higuchi, Takahiro; Kawashima, Atsuhiro; Tait, Jonathan F.; Kinuya, Seigo; Muramori, Akira; Matsunari, Ichiro; Nakajima, Kenichi; Tonami, Norihisa; Strauss, H. William.

In: Journal of Nuclear Medicine, Vol. 45, No. 9, 01.09.2004, p. 1536-1541.

Research output: Contribution to journalArticle

Taki, J, Higuchi, T, Kawashima, A, Tait, JF, Kinuya, S, Muramori, A, Matsunari, I, Nakajima, K, Tonami, N & Strauss, HW 2004, ' Detection of cardiomyocyte death in a rat model of ischemia and reperfusion using 99m Tc-labeled annexin V ', Journal of Nuclear Medicine, vol. 45, no. 9, pp. 1536-1541.
Taki, Junichi ; Higuchi, Takahiro ; Kawashima, Atsuhiro ; Tait, Jonathan F. ; Kinuya, Seigo ; Muramori, Akira ; Matsunari, Ichiro ; Nakajima, Kenichi ; Tonami, Norihisa ; Strauss, H. William. / Detection of cardiomyocyte death in a rat model of ischemia and reperfusion using 99m Tc-labeled annexin V In: Journal of Nuclear Medicine. 2004 ; Vol. 45, No. 9. pp. 1536-1541.
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abstract = "There is increasing evidence that cell death after myocardial ischemia and reperfusion may begin as apoptosis rather than necrosis. To determine the time course, location, and extent of this process, we studied groups of rats after a 20-min interval of coronary occlusion and reperfusion. Methods: After thoracotomy, the left coronary artery was occluded for 20 min. After release and before study, groups of animals were allowed to recover for various intervals: 0.5 h (n = 6), 1.5 h (n = 7), 6 h (n = 7), 1 d (n = 8), 3 d (n = 8), or 2 wk (n = 5). At the time of study, the rats were injected with 99m Tc-annexin V (80-150 MBq). One hour later, to verify the area at risk, 201 Tl (0.74 MBq) was injected intravenously just after the left coronary artery reocclusion and the rats were sacrificed 1 min later. Dual-tracer autoradiography was performed to assess 99m Tc-annexin V uptake and the area at risk. Results: Extensive 99m Tc-annexin V uptake was observed in the mid myocardium after 0.5-1.5 h of reperfusion. The area of annexin uptake had expanded in the subendocardial and subepicardial layers at 6 h after reperfusion and then gradually lessened over 3 d. At 0.5 and 1.5 h of reperfusion, 99m Tc-annexin V uptake ratios were 7.36 ± 2.95 and 6.34 ± 2.24 (mean ± SD), respectively. The uptake ratios gradually decreased at 6 h, 1 d, 3 d, and 2 wk after reperfusion (4.65 ± 1.93, 3.27 ± 0.92 [P < 0.01 vs. 0.5 h], 1.84 ± 0.55 [P < 0.001 vs. 0.5 h, P < 0.005 vs. 1.5 h], and 1.65 ± 0.31 [P < 0.001 vs. 0.5 h, P < 0.005 vs. 1.5 h], respectively). Conclusion: These data indicate that annexin binding commences soon after ischemia and reperfusion in the mid myocardium within the area at risk and expands to include the subendocardial and subepicardial layers at 6 h after reperfusion, followed by gradual reduction of activity over 3 d.",
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T1 - Detection of cardiomyocyte death in a rat model of ischemia and reperfusion using 99m Tc-labeled annexin V

AU - Taki, Junichi

AU - Higuchi, Takahiro

AU - Kawashima, Atsuhiro

AU - Tait, Jonathan F.

AU - Kinuya, Seigo

AU - Muramori, Akira

AU - Matsunari, Ichiro

AU - Nakajima, Kenichi

AU - Tonami, Norihisa

AU - Strauss, H. William

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N2 - There is increasing evidence that cell death after myocardial ischemia and reperfusion may begin as apoptosis rather than necrosis. To determine the time course, location, and extent of this process, we studied groups of rats after a 20-min interval of coronary occlusion and reperfusion. Methods: After thoracotomy, the left coronary artery was occluded for 20 min. After release and before study, groups of animals were allowed to recover for various intervals: 0.5 h (n = 6), 1.5 h (n = 7), 6 h (n = 7), 1 d (n = 8), 3 d (n = 8), or 2 wk (n = 5). At the time of study, the rats were injected with 99m Tc-annexin V (80-150 MBq). One hour later, to verify the area at risk, 201 Tl (0.74 MBq) was injected intravenously just after the left coronary artery reocclusion and the rats were sacrificed 1 min later. Dual-tracer autoradiography was performed to assess 99m Tc-annexin V uptake and the area at risk. Results: Extensive 99m Tc-annexin V uptake was observed in the mid myocardium after 0.5-1.5 h of reperfusion. The area of annexin uptake had expanded in the subendocardial and subepicardial layers at 6 h after reperfusion and then gradually lessened over 3 d. At 0.5 and 1.5 h of reperfusion, 99m Tc-annexin V uptake ratios were 7.36 ± 2.95 and 6.34 ± 2.24 (mean ± SD), respectively. The uptake ratios gradually decreased at 6 h, 1 d, 3 d, and 2 wk after reperfusion (4.65 ± 1.93, 3.27 ± 0.92 [P < 0.01 vs. 0.5 h], 1.84 ± 0.55 [P < 0.001 vs. 0.5 h, P < 0.005 vs. 1.5 h], and 1.65 ± 0.31 [P < 0.001 vs. 0.5 h, P < 0.005 vs. 1.5 h], respectively). Conclusion: These data indicate that annexin binding commences soon after ischemia and reperfusion in the mid myocardium within the area at risk and expands to include the subendocardial and subepicardial layers at 6 h after reperfusion, followed by gradual reduction of activity over 3 d.

AB - There is increasing evidence that cell death after myocardial ischemia and reperfusion may begin as apoptosis rather than necrosis. To determine the time course, location, and extent of this process, we studied groups of rats after a 20-min interval of coronary occlusion and reperfusion. Methods: After thoracotomy, the left coronary artery was occluded for 20 min. After release and before study, groups of animals were allowed to recover for various intervals: 0.5 h (n = 6), 1.5 h (n = 7), 6 h (n = 7), 1 d (n = 8), 3 d (n = 8), or 2 wk (n = 5). At the time of study, the rats were injected with 99m Tc-annexin V (80-150 MBq). One hour later, to verify the area at risk, 201 Tl (0.74 MBq) was injected intravenously just after the left coronary artery reocclusion and the rats were sacrificed 1 min later. Dual-tracer autoradiography was performed to assess 99m Tc-annexin V uptake and the area at risk. Results: Extensive 99m Tc-annexin V uptake was observed in the mid myocardium after 0.5-1.5 h of reperfusion. The area of annexin uptake had expanded in the subendocardial and subepicardial layers at 6 h after reperfusion and then gradually lessened over 3 d. At 0.5 and 1.5 h of reperfusion, 99m Tc-annexin V uptake ratios were 7.36 ± 2.95 and 6.34 ± 2.24 (mean ± SD), respectively. The uptake ratios gradually decreased at 6 h, 1 d, 3 d, and 2 wk after reperfusion (4.65 ± 1.93, 3.27 ± 0.92 [P < 0.01 vs. 0.5 h], 1.84 ± 0.55 [P < 0.001 vs. 0.5 h, P < 0.005 vs. 1.5 h], and 1.65 ± 0.31 [P < 0.001 vs. 0.5 h, P < 0.005 vs. 1.5 h], respectively). Conclusion: These data indicate that annexin binding commences soon after ischemia and reperfusion in the mid myocardium within the area at risk and expands to include the subendocardial and subepicardial layers at 6 h after reperfusion, followed by gradual reduction of activity over 3 d.

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