Circulation, Vol 86, 295-301, Copyright © 1992 by American Heart Association
T Toyo-oka, K Nagayama, J Suzuki and T Sugimoto
Background. It might be possible to estimate the metabolic derangement of
cardiac muscle by topical nuclear magnetic resonance spectroscopy (MRS) in
vivo without killing the animal. Methods and Results. By use of topical 1H-
and 31P-MRS focused on the heart of Syrian hamsters with or without
cardiomyopathy (CM; BIO 14.6 strain), the chemical constituents were
measured in vivo nondestructively and repetitively at several stages of
development of CM. A phantom experiment and two- dimensional plot of chain
methylenes (CH2) of lipid/water ratio by 1H- MRS versus creatine phosphate
(CP)/[beta-P]ATP ratio by 31P-MRS indicated that signal cross talk from the
adjacent organs was negligible. Even before the onset of clinical or
pathological manifestation of CM (7 weeks after birth), CH2/water ratio by
1H-MRS was lower in the CM group (7.3 +/- 0.7%) than in control (11.8 +/-
2.0%, p less than 0.05), and it decreased further at the hypertrophic stage
(17 weeks, 4.1 +/- 0.7%, p less than 0.05) and the congestive stage (27
weeks, 4.3 +/- 0.9%, p less than 0.05). In contrast, the CP/[beta-P]ATP
ratio by 31P-MRS started to decrease at the hypertrophic stage (1.90 +/-
0.18 versus 2.52 +/- 0.24, p less than 0.05) and decreased further at the
congestive stage to 1.53 +/- 0.18 (p less than 0.01). These in vivo MRS
data were confirmed by both biochemical assay and in vitro MRS analysis in
heavy water after the animals were killed. Conclusions. A combination of
topical 1H-MRS and 31P-MRS in vivo is promising for the noninvasive and
sensitive assessment of cardiac muscle metabolism. Comparison of these MRS
studies and biochemical analysis suggested not only the modification of
water, lipid, CP, or ATP contents but also the reduction of flexibility or
fluidity of lipids in cardiomyopathic heart.
ARTICLES
Noninvasive assessment of cardiomyopathy development with simultaneous measurement of topical 1H- and 31P-magnetic resonance spectroscopy
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
This article has been cited by other articles:
![]() |
T. Toyo-Oka, T. Kawada, J. Nakata, H. Xie, M. Urabe, F. Masui, T. Ebisawa, A. Tezuka, K. Iwasawa, T. Nakajima, et al. Translocation and cleavage of myocardial dystrophin as a common pathway to advanced heart failure: A scheme for the progression of cardiac dysfunction PNAS, May 11, 2004; 101(19): 7381 - 7385. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Kawada, M. Nakazawa, S. Nakauchi, K. Yamazaki, R. Shimamoto, M. Urabe, J. Nakata, C. Hemmi, F. Masui, T. Nakajima, et al. Rescue of hereditary form of dilated cardiomyopathy by rAAV-mediated somatic gene therapy: Amelioration of morphological findings, sarcolemmal permeability, cardiac performances, and the prognosis of TO-2 hamsters PNAS, January 22, 2002; 99(2): 901 - 906. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Sakamoto, K. Ono, M. Abe, G. Jasmin, T. Eki, Y. Murakami, T. Masaki, T. Toyo-oka, and F. Hanaoka Both hypertrophic and dilated cardiomyopathies are caused by mutation of the same gene, delta -sarcoglycan, in hamster: An animal model of disrupted dystrophin-associated glycoprotein complex PNAS, December 9, 1997; 94(25): 13873 - 13878. [Abstract] [Full Text] [PDF] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1992 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |