Harmen Reyngoudt1,2, Suna Turk1,2, and Pierre G. Carlier1,2
1NMR Laboratory, Institute of Myology, Paris, France, 2CEA, DRF, I²BM, MIRCen, Paris, France
Synopsis
The finding of an alkaline Pi pool has been established with
31P-NMRS in healthy resting skeletal muscle and the dystrophic muscle of GMRD dogs
and DMD patients. The pH values corresponding to this Pi pool corresponds
better with extracellular pH. Intracellular pH, however, can also be measured
with 1H-NMRS, using carnosine. In a group of DMD patients, we
observed that pH determined with 31P-NMRS were systematically increased,
whereas this was not always the case for pH based on the measurement of carnosine, revealing
two groups in dystrophic muscle: (1) pH elevated with 31P and 1H and (2) pH
only elevated with 31P.
Purpose
Quantitative
nuclear magnetic resonance imaging (NMRI) and phosphorus NMR spectroscopy (
31P-NMRS)
have been used to investigate the mechanisms of Duchenne muscular dystrophy
(DMD), the most common muscle-wasting disorder. Splitting of the inorganic
phosphate (P
i) peak, showing a second P
i peak (P
i,b)
upfield from Pi (P
i,a) was shown in healthy resting
skeletal muscle [1] as well as in skeletal muscle of GRMD (Golden
Retriever muscular dystrophy) dogs, the canine model for DMD [2], and in upper limb skeletal muscle of DMD
patients [3], reflecting a more alkaline P
i pool.
The pH values observed for P
i,b were too alkaline to correspond to
healthy tissue (pH around 7.0), and corresponded better to pH values found in
interstitial or extracellular space. Intracellular pH, however, can also be
measured with proton NMRS (
1H-NMRS), exploiting the two imidazole
protons of carnosine (Fig. 1) [4]. In resting muscle, carnosine is
exclusively found in the cytosol, suggesting pH calculated with
1H-NMRS
might be different from pH calculated with
31P-NMRS in suffering
muscle cells. The aim of this work was to perform both
1H-NMRS and
31P-NMRS
at rest in DMD patients and healthy controls.
Methods
Data was acquired in 18 DMD patients (all male,
10 ± 2 yrs), as well as in 7 healthy controls (4 male, 31 ± 4 yrs) on a 3T
Siemens Prisma system using a body matrix coil for quantitative NMRI, a
dual-tuned 31P-1H surface coil for 31P-NMRS or
a 15-channel volume knee coil for 1H-NMRS. 1H-NMRS data
was obtained using a PRESS sequence with a TR of 3000 ms and a TE of 30 ms.
Voxels were positioned in the gastrocnemius medialis muscle and voxel size
depended on muscle size. Two 1H-NMR spectra were acquired: one
water-suppressed (central frequency at 8.0 ppm, 64 averages) and one
unsuppressed water spectrum (central frequency at 4.7 ppm, 16 averages). 31P-NMRS
data was obtained from a non-localized excitation (TR = 4000 ms, 64 averages)
with the coil wrapped around the calf (Fig. 1). NMRS data was processed with
the AMARES [5] algorithm from jMRUI using
optimized prior knowledge (Fig. 2,3). Additionally, an MSME sequence with 17
echoes was acquired which was processed using in-house python code, extracting
water T2 and fat fraction values based on the tri-exponential model
of Azzabou et al. [6]. Kruskal-Wallis tests for
comparisons of groups and Spearman correlation analysis was performed (with P = 0.05 as significance level).Results
Fig. 4a shows that pH values derived from 31P-NMRS
were systematically increased in DMD patients. While there is good agreement
between 1H and 31P pH determination in normal subjects
(group A), discrepancies can be observed in DMD patients. Whereas all have
alkaline pH when determined by 31P-NMRS, there are DMD subjects with
normal intracellular pH as calculated from the carnosine resonance (group B),
the others have an increased (intracellular) pH measured by the two methods
(group C), as illustrated in Fig. 4a. Interestingly, the carnosine
intracellular pH was never found alkaline in absence of concurrent Pi
pH elevation. The same observation can be made for the relation between 1H
derived pH and water T2. Abnormal intracellular pH is hardly ever
associated with normal water T2 values (Fig. 4b). Elevated 31P-derived
pH values are observed in both the presence and absence of elevated water T2
(Fig. 4c). Data of the three groups are summarized in Table 1.Discussion
While pH alterations in the dystrophic muscle
had been described long ago, the mechanism for the prominence of an alkaline Pi
resonance in dystrophic muscle was still being debated. It may reflect cell pH dysregulation
in leaky damaged myocytes or an increased volume fraction of the interstitium,
impossible to distinguish using 31P-NMRS. Magnetization transfer
experiments have indicated that, at least partly, the alkaline Pi
pool was in exchange with ATP, and consequently originating from cells. The
combined 1H and 31P approach used here identified that
the two proposed mechanisms can exist. In muscles where 1H and 31P
pH estimates are in agreement, the lesional mechanisms predominate. When 1H
and 31P measures are discordant, it indicates that the alkaline Pi
pool is extracellular, with an increased interstitial volume fraction being possibly
related to fibrotic changes. Consequently, it will be worth investigating
whether carnosine-based intracellular pH may provide an early indicator of
dystrophic myocytes to therapy, as opposed to the 31P-NMRS-based pH,
whose origin cannot be ascertained and may reflect predominantly the extent of chronic
degenerative changes in dystrophic muscles.Conclusion
Contrary to 31P-NMRS, carnosine 1H-NMRS
can be used as a biomarker to assess specifically the intramyocytic pH changes
in Duchenne patients.Acknowledgements
No acknowledgement found.References
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