Myocardial kinetics of Tc-99m glucarate in low flow, hypoxia, and aglycemia

D. R. Okada, G. Johnson, Zhonglin Liu, S. D. Hocherman, B. A. Khaw, K. Y. Pak, Robert D. Okada

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Background. Technetium-99m glucarate is a myocardial infarct-avid imaging agent. Recent conflicting and inconclusive reports have suggested that the agent may be taken up by ischemic but viable myocardium. The purposes of this study were (1) to determine conclusively whether there is Tc-99m glucarate uptake in ischemic viable myocardium and (2) to investigate the potential mechanisms for such uptake by studying components of ischemia, namely, low flow, hypoxia, and aglycemia. Methods and Results. Rat hearts were isolated and perfused in a modified Langendorff preparation with a crytalloid perfusate. Tc-99m glucarate was studied in control (n = 6), low-flow (n = 5), hypoxic (n = 5), and aglycemic (n = 5) conditions. The experimental protocol consisted of 20-minute baseline (12 mL/min flow) and 20-minute treatment (low flow at 1 mL/min, hypoxia, or aglycemia), followed by tracer uptake (20 minute) and washout (20 minutes). Activity was monitored with a sodium iodide detector. The tracer was delivered continuously over a 20-minute uptake period. The injected dose was 150 μCi (5.6 MBq). Hemodynamics were monitored throughout. Triphenyltetrazolium chloride staining was used to assess myocardial viability. There was no evidence of myocardial necrosis. Low flow tended to delay tracer uptake compared with control for the first 10 minutes, but this did not reach statistical significance. Low flow increased end fractional retention significantly compared with control (mean ± SEM, 59.0% ± 0.9% peak vs 41.2% ± 1.4%, respectively; P < .05). Hypoxia resulted in a trend toward increased uptake; however, this was significant only at one early time point during the uptake phase. Retention in the hypoxia group was similar to control. Tc-99m glucarate uptake was significantly increased in aglycemia from 16 minutes to peak compared with control (1.36% ± 0.71% injected dose per gram vs 0.91% ± 0.37% injected dose per gram, respectively; P < .05). Aglycemia produced significantly higher end fractional retention compared with control (51.6% ± 1.8% peak vs 41.2% ± 1.4%, respectively; P < .05). Conclusions. Tc-99m glucarate myocardial retention is increased in the setting of ischemia, even in the absence of necrosis. This increased retention is not due to hypoxia. Furthermore, the retention is only partially explained by tissue hypoglycemia. Thus low flow per se appears to have a role in this increased retention, probably as a result of delayed flow-dependent washout.

Original languageEnglish (US)
Pages (from-to)168-176
Number of pages9
JournalJournal of Nuclear Cardiology
Volume10
Issue number2
DOIs
StatePublished - Mar 2003
Externally publishedYes

Fingerprint

Myocardium
Necrosis
Ischemia
Sodium Iodide
Technetium
Hypoglycemia
Hemodynamics
Myocardial Infarction
technetium Tc 99m glucarate
Hypoxia
Staining and Labeling
triphenyltetrazolium

Keywords

  • Aglycemia
  • Hypoxia
  • Ischemia
  • Kinetics
  • Myocardium
  • Technetium-99m glucarte

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Okada, D. R., Johnson, G., Liu, Z., Hocherman, S. D., Khaw, B. A., Pak, K. Y., & Okada, R. D. (2003). Myocardial kinetics of Tc-99m glucarate in low flow, hypoxia, and aglycemia. Journal of Nuclear Cardiology, 10(2), 168-176. https://doi.org/10.1067/mnc.2003.1

Myocardial kinetics of Tc-99m glucarate in low flow, hypoxia, and aglycemia. / Okada, D. R.; Johnson, G.; Liu, Zhonglin; Hocherman, S. D.; Khaw, B. A.; Pak, K. Y.; Okada, Robert D.

In: Journal of Nuclear Cardiology, Vol. 10, No. 2, 03.2003, p. 168-176.

Research output: Contribution to journalArticle

Okada, DR, Johnson, G, Liu, Z, Hocherman, SD, Khaw, BA, Pak, KY & Okada, RD 2003, 'Myocardial kinetics of Tc-99m glucarate in low flow, hypoxia, and aglycemia', Journal of Nuclear Cardiology, vol. 10, no. 2, pp. 168-176. https://doi.org/10.1067/mnc.2003.1
Okada, D. R. ; Johnson, G. ; Liu, Zhonglin ; Hocherman, S. D. ; Khaw, B. A. ; Pak, K. Y. ; Okada, Robert D. / Myocardial kinetics of Tc-99m glucarate in low flow, hypoxia, and aglycemia. In: Journal of Nuclear Cardiology. 2003 ; Vol. 10, No. 2. pp. 168-176.
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abstract = "Background. Technetium-99m glucarate is a myocardial infarct-avid imaging agent. Recent conflicting and inconclusive reports have suggested that the agent may be taken up by ischemic but viable myocardium. The purposes of this study were (1) to determine conclusively whether there is Tc-99m glucarate uptake in ischemic viable myocardium and (2) to investigate the potential mechanisms for such uptake by studying components of ischemia, namely, low flow, hypoxia, and aglycemia. Methods and Results. Rat hearts were isolated and perfused in a modified Langendorff preparation with a crytalloid perfusate. Tc-99m glucarate was studied in control (n = 6), low-flow (n = 5), hypoxic (n = 5), and aglycemic (n = 5) conditions. The experimental protocol consisted of 20-minute baseline (12 mL/min flow) and 20-minute treatment (low flow at 1 mL/min, hypoxia, or aglycemia), followed by tracer uptake (20 minute) and washout (20 minutes). Activity was monitored with a sodium iodide detector. The tracer was delivered continuously over a 20-minute uptake period. The injected dose was 150 μCi (5.6 MBq). Hemodynamics were monitored throughout. Triphenyltetrazolium chloride staining was used to assess myocardial viability. There was no evidence of myocardial necrosis. Low flow tended to delay tracer uptake compared with control for the first 10 minutes, but this did not reach statistical significance. Low flow increased end fractional retention significantly compared with control (mean ± SEM, 59.0{\%} ± 0.9{\%} peak vs 41.2{\%} ± 1.4{\%}, respectively; P < .05). Hypoxia resulted in a trend toward increased uptake; however, this was significant only at one early time point during the uptake phase. Retention in the hypoxia group was similar to control. Tc-99m glucarate uptake was significantly increased in aglycemia from 16 minutes to peak compared with control (1.36{\%} ± 0.71{\%} injected dose per gram vs 0.91{\%} ± 0.37{\%} injected dose per gram, respectively; P < .05). Aglycemia produced significantly higher end fractional retention compared with control (51.6{\%} ± 1.8{\%} peak vs 41.2{\%} ± 1.4{\%}, respectively; P < .05). Conclusions. Tc-99m glucarate myocardial retention is increased in the setting of ischemia, even in the absence of necrosis. This increased retention is not due to hypoxia. Furthermore, the retention is only partially explained by tissue hypoglycemia. Thus low flow per se appears to have a role in this increased retention, probably as a result of delayed flow-dependent washout.",
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AU - Okada, D. R.

AU - Johnson, G.

AU - Liu, Zhonglin

AU - Hocherman, S. D.

AU - Khaw, B. A.

AU - Pak, K. Y.

AU - Okada, Robert D.

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N2 - Background. Technetium-99m glucarate is a myocardial infarct-avid imaging agent. Recent conflicting and inconclusive reports have suggested that the agent may be taken up by ischemic but viable myocardium. The purposes of this study were (1) to determine conclusively whether there is Tc-99m glucarate uptake in ischemic viable myocardium and (2) to investigate the potential mechanisms for such uptake by studying components of ischemia, namely, low flow, hypoxia, and aglycemia. Methods and Results. Rat hearts were isolated and perfused in a modified Langendorff preparation with a crytalloid perfusate. Tc-99m glucarate was studied in control (n = 6), low-flow (n = 5), hypoxic (n = 5), and aglycemic (n = 5) conditions. The experimental protocol consisted of 20-minute baseline (12 mL/min flow) and 20-minute treatment (low flow at 1 mL/min, hypoxia, or aglycemia), followed by tracer uptake (20 minute) and washout (20 minutes). Activity was monitored with a sodium iodide detector. The tracer was delivered continuously over a 20-minute uptake period. The injected dose was 150 μCi (5.6 MBq). Hemodynamics were monitored throughout. Triphenyltetrazolium chloride staining was used to assess myocardial viability. There was no evidence of myocardial necrosis. Low flow tended to delay tracer uptake compared with control for the first 10 minutes, but this did not reach statistical significance. Low flow increased end fractional retention significantly compared with control (mean ± SEM, 59.0% ± 0.9% peak vs 41.2% ± 1.4%, respectively; P < .05). Hypoxia resulted in a trend toward increased uptake; however, this was significant only at one early time point during the uptake phase. Retention in the hypoxia group was similar to control. Tc-99m glucarate uptake was significantly increased in aglycemia from 16 minutes to peak compared with control (1.36% ± 0.71% injected dose per gram vs 0.91% ± 0.37% injected dose per gram, respectively; P < .05). Aglycemia produced significantly higher end fractional retention compared with control (51.6% ± 1.8% peak vs 41.2% ± 1.4%, respectively; P < .05). Conclusions. Tc-99m glucarate myocardial retention is increased in the setting of ischemia, even in the absence of necrosis. This increased retention is not due to hypoxia. Furthermore, the retention is only partially explained by tissue hypoglycemia. Thus low flow per se appears to have a role in this increased retention, probably as a result of delayed flow-dependent washout.

AB - Background. Technetium-99m glucarate is a myocardial infarct-avid imaging agent. Recent conflicting and inconclusive reports have suggested that the agent may be taken up by ischemic but viable myocardium. The purposes of this study were (1) to determine conclusively whether there is Tc-99m glucarate uptake in ischemic viable myocardium and (2) to investigate the potential mechanisms for such uptake by studying components of ischemia, namely, low flow, hypoxia, and aglycemia. Methods and Results. Rat hearts were isolated and perfused in a modified Langendorff preparation with a crytalloid perfusate. Tc-99m glucarate was studied in control (n = 6), low-flow (n = 5), hypoxic (n = 5), and aglycemic (n = 5) conditions. The experimental protocol consisted of 20-minute baseline (12 mL/min flow) and 20-minute treatment (low flow at 1 mL/min, hypoxia, or aglycemia), followed by tracer uptake (20 minute) and washout (20 minutes). Activity was monitored with a sodium iodide detector. The tracer was delivered continuously over a 20-minute uptake period. The injected dose was 150 μCi (5.6 MBq). Hemodynamics were monitored throughout. Triphenyltetrazolium chloride staining was used to assess myocardial viability. There was no evidence of myocardial necrosis. Low flow tended to delay tracer uptake compared with control for the first 10 minutes, but this did not reach statistical significance. Low flow increased end fractional retention significantly compared with control (mean ± SEM, 59.0% ± 0.9% peak vs 41.2% ± 1.4%, respectively; P < .05). Hypoxia resulted in a trend toward increased uptake; however, this was significant only at one early time point during the uptake phase. Retention in the hypoxia group was similar to control. Tc-99m glucarate uptake was significantly increased in aglycemia from 16 minutes to peak compared with control (1.36% ± 0.71% injected dose per gram vs 0.91% ± 0.37% injected dose per gram, respectively; P < .05). Aglycemia produced significantly higher end fractional retention compared with control (51.6% ± 1.8% peak vs 41.2% ± 1.4%, respectively; P < .05). Conclusions. Tc-99m glucarate myocardial retention is increased in the setting of ischemia, even in the absence of necrosis. This increased retention is not due to hypoxia. Furthermore, the retention is only partially explained by tissue hypoglycemia. Thus low flow per se appears to have a role in this increased retention, probably as a result of delayed flow-dependent washout.

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KW - Hypoxia

KW - Ischemia

KW - Kinetics

KW - Myocardium

KW - Technetium-99m glucarte

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