HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Takatsu, H. Articles by Fujiwara, H. Search for Related Content PubMed PubMed Citation Articles by Takatsu, H. Articles by Fujiwara, H.

Modulation of Left Ventricular Iodine-125-MIBG Accumulation in Cardiomyopathic Syrian Hamsters Using the Renin-Angiotensin System

The Second Department of Internal Medicine, Gifu University School of Medicine, Gifu, Japan

Correspondence: For correspondence or reprints contact: Hisato Takatsu, MD, The Second Department of Internal Medicine, Gifu University School of Medicine, 40 Tsukasamachi, Gifu 500, Japan.

ABSTRACT

Genetically inbred cardiomyopathic hamsters were examined to investigate the mechanism of reduced myocardial accumulation of metaiodobenzylguanidine (MIBG) in the cardiomyopathic heart. Methods: Bio 14.6 Syrian hamsters (hypertrophic stage: n = 15, early heart failure stage: n = 17) and control F1b strain golden hamsters (n = 36) were injected with 296 kBq of [¹²⁵I] MIBG and killed 30 min or 4 hr later. Thirty-three of these hamsters were pretreated with 10 mg/kg of desipramine to determine non-neuronal MIBG accumulation. To evaluate the nonexocytotic MIBG release from nerve endings, desipramine was administered to four Bio 14.6 hamsters 15 min after [¹²⁵I]MIBG injection. To determine the role of the activated renin-angiotensin system (RAS) in MIBG washout from sympathetic nerve terminals in cardiomyopathy at early heart failure stage, 10 mg/kg/day cilazapril, an angiotensin-converting enzyme inhibitor, was given orally to 7 controls and 16 cardiomyopathic hamsters for 16 wk. Results: In the absence of desipramine pretreatment, left ventricular [¹²⁵I]MIBG accumulation 4 hr after injection was 0.376% ± 0.015 %kg dose/g (mean ± s.e.m.) in the hypertrophic hamsters (versus 0.418 ± 0.019 in controls of the same age; ns), and 0.195 ± 0.025 in early heart failure hamsters. Treatment with cilazapril partially restored MIBG accumulation in the Bio 14.6 hamsters but did not affect the controls. Conclusion: Decreased [¹²⁵I]MIBG accumulation in cardiomyopathic hamsters during the early heart failure stage is caused by neuronal release which is partially modulated by the activated RAS.

Key Words: iodine-123-metaiodobenzylguanidine • cardiomyopathy • angiotensin-converting enzyme inhibitor

This article has been cited by other articles:

				A. Igawa, T. Nozawa, N. Yoshida, N. Fujii, M. Inoue, S. Tazawa, H. Asanoi, and H. Inoue Heterogeneous cardiac sympathetic innervation in heart failure after myocardial infarction of rats Am J Physiol Heart Circ Physiol, April 1, 2000; 278(4): H1134 - H1141. [Abstract] [Full Text] [PDF]

				F Hartmann, S Ziegler, S Nekolla, M Hadamitzky, M Seyfarth, G Richardt, and M Schwaiger Regional patterns of myocardial sympathetic denervation in dilated cardiomyopathy: an analysis using carbon-11 hydroxyephedrine and positron emission tomography Heart, March 1, 1999; 81(3): 262 - 270. [Abstract] [Full Text]

				K. Sakata, M. Shirotani, H. Yoshida, and C. Kurata Comparison of effects of enalapril and nitrendipine on cardiac sympathetic nervous system in essential hypertension J. Am. Coll. Cardiol., August 1, 1998; 32(2): 438 - 443. [Abstract] [Full Text] [PDF]