Para-[18F]fluorobenzylguanidine kinetics in a canine coronary artery occlusion model

Clifford R. Berry; Pradeep K. Garg; Timothy R. DeGrado; Peter Hellyer; William Weber; Sudha Garg; Bernard Hansen; Michael R. Zalutsky; R. Edward Coleman

doi:10.1016/S1071-3581(96)90004-5

Para-[¹⁸F]fluorobenzylguanidine kinetics in a canine coronary artery occlusion model

Clifford R. Berry, Pradeep K. Garg, Timothy R. DeGrado, Peter Hellyer, William Weber, Sudha Garg, Bernard Hansen, Michael R. Zalutsky, R. Edward Coleman

Radiology

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

Abstract

Background. The kinetics of para-[¹⁸F]fluorobenzylguanidine ([¹⁸F]PFBG) were investigated in a canine coronary artery occlusion model. Methods and Results. Five dogs were imaged by positron emission tomography (PET) before and after complete surgical ligation of the left anterior descending coronary artery. PET studies included a 10-minute dynamic [¹³N]NH3 perfusion scan, followed 1 hour later by 3-hour dynamic [¹⁸F]PFBG scanning. [¹⁸F]PFBG and [¹³N]NH3 images demonstrated homogeneous myocardial uptake/perfusion before infarction. One hundred eighty minutes after [¹⁸F]PFBG administration, myocardial accumulation was decreased by 60% (day 2, 0.0065% ± 0.0015% injected dose/ml) and 58% (day 16, 0.0069% ± 0.003% injected dose/ml) compared with a similar myocardial region of interest from the preinfarction (0.0160/0 ± 0.005% injected dose/ml) study. Myocardial accumulation of [¹³N]NH3 at 9 minutes showed a 52% (day 2) and 7% (day 16) decrease compared with the preinfarction study. The accumulation of [¹⁸F]PFBG in the infarction was decreased significantly at 120 and 180 minutes on all postinfarction studies (p = 0.01). In three dogs a significant decrease in the myocardial norepinephrine concentration was documented in the area of infarction (237 ± 94 ng/gm) versus the noninfarcted (1018 ± 48 ng/gm) myocardium (p = 0.001). Conclusions. A decreased accumulation of [¹⁸F]PFBG was observed in the area of myocardial infarct in this canine model. The magnitude of the decrease in [¹⁸F]PFBG was larger than that seen with [¹³N]NH₃, on day 16 after infarction, suggesting reperfusion and persistent sympathetic neuronal dysfunction.

Original language	English (US)
Pages (from-to)	119-129
Number of pages	11
Journal	Journal of Nuclear Cardiology
Volume	3
Issue number	2
DOIs	https://doi.org/10.1016/S1071-3581(96)90004-5
State	Published - 1996

Keywords

Canine
Myocardial
Para-[F]fluorobenzylguanidine

ASJC Scopus subject areas

Radiology Nuclear Medicine and imaging
Cardiology and Cardiovascular Medicine

Access to Document

10.1016/S1071-3581(96)90004-5

Cite this

@article{dcca041d7467492d90f158314f0595b5,

title = "Para-[18F]fluorobenzylguanidine kinetics in a canine coronary artery occlusion model",

abstract = "Background. The kinetics of para-[18F]fluorobenzylguanidine ([18F]PFBG) were investigated in a canine coronary artery occlusion model. Methods and Results. Five dogs were imaged by positron emission tomography (PET) before and after complete surgical ligation of the left anterior descending coronary artery. PET studies included a 10-minute dynamic [13N]NH3 perfusion scan, followed 1 hour later by 3-hour dynamic [18F]PFBG scanning. [18F]PFBG and [13N]NH3 images demonstrated homogeneous myocardial uptake/perfusion before infarction. One hundred eighty minutes after [18F]PFBG administration, myocardial accumulation was decreased by 60% (day 2, 0.0065% ± 0.0015% injected dose/ml) and 58% (day 16, 0.0069% ± 0.003% injected dose/ml) compared with a similar myocardial region of interest from the preinfarction (0.0160/0 ± 0.005% injected dose/ml) study. Myocardial accumulation of [13N]NH3 at 9 minutes showed a 52% (day 2) and 7% (day 16) decrease compared with the preinfarction study. The accumulation of [18F]PFBG in the infarction was decreased significantly at 120 and 180 minutes on all postinfarction studies (p = 0.01). In three dogs a significant decrease in the myocardial norepinephrine concentration was documented in the area of infarction (237 ± 94 ng/gm) versus the noninfarcted (1018 ± 48 ng/gm) myocardium (p = 0.001). Conclusions. A decreased accumulation of [18F]PFBG was observed in the area of myocardial infarct in this canine model. The magnitude of the decrease in [18F]PFBG was larger than that seen with [13N]NH3, on day 16 after infarction, suggesting reperfusion and persistent sympathetic neuronal dysfunction.",

keywords = "Canine, Myocardial, Para-[F]fluorobenzylguanidine",

author = "Berry, {Clifford R.} and Garg, {Pradeep K.} and DeGrado, {Timothy R.} and Peter Hellyer and William Weber and Sudha Garg and Bernard Hansen and Zalutsky, {Michael R.} and Coleman, {R. Edward}",

note = "Funding Information: From the Departments of Anatomy, Physiological Sciences, and Ra-diology, North Carolina State University, College of Veterinary Medicine, Raleigh, and the Department of Radiology, Duke Uni-versity Medical Center, Durham, N.C. Supported by grant DE-FG05-89ER60789 from the Department of Energy and the State of North Carolina. Reprint requests: Clifford R. Berry, Department of Anatomy, Physi-ological Sciences and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606. Copyright {\textcopyright} 1996 by American Society of Nuclear Cardiology. 1071-3581/96/$5.00 +0 43/1/70927",

year = "1996",

doi = "10.1016/S1071-3581(96)90004-5",

language = "English (US)",

volume = "3",

pages = "119--129",

journal = "Journal of Nuclear Cardiology",

issn = "1071-3581",

publisher = "Springer New York",

number = "2",

}

TY - JOUR

T1 - Para-[18F]fluorobenzylguanidine kinetics in a canine coronary artery occlusion model

AU - Berry, Clifford R.

AU - Garg, Pradeep K.

AU - DeGrado, Timothy R.

AU - Hellyer, Peter

AU - Weber, William

AU - Garg, Sudha

AU - Hansen, Bernard

AU - Zalutsky, Michael R.

AU - Coleman, R. Edward

N1 - Funding Information: From the Departments of Anatomy, Physiological Sciences, and Ra-diology, North Carolina State University, College of Veterinary Medicine, Raleigh, and the Department of Radiology, Duke Uni-versity Medical Center, Durham, N.C. Supported by grant DE-FG05-89ER60789 from the Department of Energy and the State of North Carolina. Reprint requests: Clifford R. Berry, Department of Anatomy, Physi-ological Sciences and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606. Copyright © 1996 by American Society of Nuclear Cardiology. 1071-3581/96/$5.00 +0 43/1/70927

PY - 1996

Y1 - 1996

N2 - Background. The kinetics of para-[18F]fluorobenzylguanidine ([18F]PFBG) were investigated in a canine coronary artery occlusion model. Methods and Results. Five dogs were imaged by positron emission tomography (PET) before and after complete surgical ligation of the left anterior descending coronary artery. PET studies included a 10-minute dynamic [13N]NH3 perfusion scan, followed 1 hour later by 3-hour dynamic [18F]PFBG scanning. [18F]PFBG and [13N]NH3 images demonstrated homogeneous myocardial uptake/perfusion before infarction. One hundred eighty minutes after [18F]PFBG administration, myocardial accumulation was decreased by 60% (day 2, 0.0065% ± 0.0015% injected dose/ml) and 58% (day 16, 0.0069% ± 0.003% injected dose/ml) compared with a similar myocardial region of interest from the preinfarction (0.0160/0 ± 0.005% injected dose/ml) study. Myocardial accumulation of [13N]NH3 at 9 minutes showed a 52% (day 2) and 7% (day 16) decrease compared with the preinfarction study. The accumulation of [18F]PFBG in the infarction was decreased significantly at 120 and 180 minutes on all postinfarction studies (p = 0.01). In three dogs a significant decrease in the myocardial norepinephrine concentration was documented in the area of infarction (237 ± 94 ng/gm) versus the noninfarcted (1018 ± 48 ng/gm) myocardium (p = 0.001). Conclusions. A decreased accumulation of [18F]PFBG was observed in the area of myocardial infarct in this canine model. The magnitude of the decrease in [18F]PFBG was larger than that seen with [13N]NH3, on day 16 after infarction, suggesting reperfusion and persistent sympathetic neuronal dysfunction.

AB - Background. The kinetics of para-[18F]fluorobenzylguanidine ([18F]PFBG) were investigated in a canine coronary artery occlusion model. Methods and Results. Five dogs were imaged by positron emission tomography (PET) before and after complete surgical ligation of the left anterior descending coronary artery. PET studies included a 10-minute dynamic [13N]NH3 perfusion scan, followed 1 hour later by 3-hour dynamic [18F]PFBG scanning. [18F]PFBG and [13N]NH3 images demonstrated homogeneous myocardial uptake/perfusion before infarction. One hundred eighty minutes after [18F]PFBG administration, myocardial accumulation was decreased by 60% (day 2, 0.0065% ± 0.0015% injected dose/ml) and 58% (day 16, 0.0069% ± 0.003% injected dose/ml) compared with a similar myocardial region of interest from the preinfarction (0.0160/0 ± 0.005% injected dose/ml) study. Myocardial accumulation of [13N]NH3 at 9 minutes showed a 52% (day 2) and 7% (day 16) decrease compared with the preinfarction study. The accumulation of [18F]PFBG in the infarction was decreased significantly at 120 and 180 minutes on all postinfarction studies (p = 0.01). In three dogs a significant decrease in the myocardial norepinephrine concentration was documented in the area of infarction (237 ± 94 ng/gm) versus the noninfarcted (1018 ± 48 ng/gm) myocardium (p = 0.001). Conclusions. A decreased accumulation of [18F]PFBG was observed in the area of myocardial infarct in this canine model. The magnitude of the decrease in [18F]PFBG was larger than that seen with [13N]NH3, on day 16 after infarction, suggesting reperfusion and persistent sympathetic neuronal dysfunction.

KW - Canine

KW - Myocardial

KW - Para-[F]fluorobenzylguanidine

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U2 - 10.1016/S1071-3581(96)90004-5

DO - 10.1016/S1071-3581(96)90004-5

M3 - Article

C2 - 8799237

AN - SCOPUS:0029664918

SN - 1071-3581

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