Günther Dietze

Unveiling Extracellular Inorganic Phosphate Signals from Blood in Human Cardiac 31P NMR Spectra

31P NMR spectra of the human heart are usually contaminated by signals that originate from blood. The main blood signals are 2,3-diphosphoglycerate (2,3-DPG), which overlap and sometimes obscure the signal of myocardial inorganic phosphate used to calculate intracellular pH and to monitor metabolic changes in the heart. In this work we demonstrate, first, that even without proton decoupling the resolution of such spectra can be high enough to evaluate intracellular inorganic phosphate of myocardium in about 70% of the spectra and, second, that extracellular inorganic phosphate from blood contributes a signal in the chemical shift region of the 2-phosphate signal of 2,3-DPG.

Localized phosphorus NMR spectroscopy: A comparison of the FID, DRESS, CRISIS/CODEX, and STEAM methods in vitro and in vivo using a surface-coil

The FID, DRESS, CRISIS/CODEX, and STEAM techniques for localized 31P NMR spectroscopy were compared using a Siemens Magnetom SP63 1.5 T whole-body imager and a surface-coil, 80 mm in diameter, acting as transmitter and receiver coil. The comparison was performed with phantom experiments and human in vivo investigations on the calf muscle. The phantom experiments which used the same volume size showed a comparable signal-to-noise ratio for FID and DRESS, while the two fully localized techniques showed a reduction in signal-to-noise ratio to 76% for CRISIS/CODEX and 31% for STEAM. The in vivo measurements confirm the phantom results and reveal that CRISIS/CODEX gains a 2.5 fold higher signal-to-noise ratio than STEAM under the same conditions.

Spin-echo methods for the determination of 31P transverse relaxation times of the ATP NMR signals in vivo

31P magnetic resonance spectroscopy (MRS) examinations of the calf muscles of healthy volunteers were performed to determine T2 of the coupled ATP signals by use of the Hahn spin-echo and the frequency-selective spin-echo method. Additional measurements with the J-coupling refocused double echo are presented. The most reliable determination of T2 relaxation times is possible with the frequency-selective spin echo. The other methods yield substantially wrong results. Theoretical explanations are given how J-coupling and pulse-angle deviations affect the signals and therefore the T2 determinations. The calculations for a weakly coupled homonuclear AX spin system are shown because they demonstrate most of the relevant facts. In addition, some important results for a homonuclear AMX spin system, which the ATP is considered to be, are given.

31P/1H WALTZ-4 broadband decoupling at 1.5 T: different versions of the composite pulse and consequences when using a surface coil.

Two derivatives of the wideband alternating-phase low-power technique for zero-residual splitting (WALTZ)-4 decoupling sequence for broadband decoupling named WALTZ-4a and WALTZ-4b were compared for their proton decoupling performance in 31P nuclear magnetic resonance (NMR) spectroscopy using a Siemens Magnetom SP 1.5 T whole-body imager. Version WALTZ-4a originally implemented by the manufacturer doubles and triples the transmitter amplitude of the 90 degrees pulse to achieve the 180 degrees and 270 degrees flip angle required for one composite pulse R in the WALTZ sequence. WALTZ-4b follows the sequence reported from Shaka et al. and leaves the transmitter amplitude constant but increases the durations of the 180 degrees and 270 degrees pulses. The decoupling performance of WALTZ-4b is superior because it requires less transmitter power and, therefore, it is advantageous in all in vivo studies where a low specific absorption rate is desired. When WALTZ-4 is used in combination with a surface coil for transmission the theoretically required flip angles cannot be achieved in the entire sensitive volume of the coil. The decoupling performance was therefore investigated at lower and higher flip angles. Again, WALTZ-4b is advantageous and provides, in certain ranges that are off-resonant from the decoupling frequency, a good decoupling quality even for flip angles that are only 60% of the theoretically required.

Detection of monoester signals in human myocardium by 31P-MRS

Localized 3~p-NMR spectroscopy can be used to gain insight into the metabolism of the human myocardium. Typically, the signals of phosphocreatine (PCr), adenosinetriphosphate (ATP), 2,3-diphosphoglycerate (2,3-DPG), and phosphodiesters (PDE) are observed. Depending on the resolution of the spectra, the signal from inorganic phosphate (Pi) can also be observed slightly separated from the 2-DPG signal (Fig. 1). In addition, we show in this study that using an appropriate technique a phosphomonoester signal (PME) can be observed mainly in patients with hypertrophic cardiomyopathy (HCM).

Change in Chemical Shift and Splitting of 31P γ-ATP Signal in Human Skeletal Muscle During Exercise and Recovery

Proton decoupled 31P in vivo NMR spectroscopy of the human finger flexor muscles was performed during exercise and recovery using a 1.5 T whole‐body imager. Predominantly the γ‐ATP signal shows a splitting caused by different signal contributions with chemical shifts that vary independently. Studies on the human gastrocnemius and biceps femoris muscle were undertaken to investigate the appearance of the splitting in these muscles as well. In all cases more than one signal contribution was found which might represent the different muscle fibre types and their recruitment pattern following exercise. An analysis of the chemical shifts of ATP results in changes of up to 0.4 ppm and 0.1 ppm for δγ‐ and δβ‐ATP, respectively. Based solely on the chemical shifts of the ATP 31P signals the tissue pH value following exercise was determined. The result was in good agreement with the value derived from δPi.

Zur Pathogenese der koronaren HerzerkrankungOn pathogenesis of coronary heart disease

Being overweight (OW) was recognized very early as a risk factor for coronary heart disease (CHD). Its significance in the pathogenesis of CHD has been strengthened by observations showing that OW is responsible for the development of diabetes, hypertension and lipid disorders due to its induction of insulin resistance (IR). Its key role has been underlined further by recent studies indicating that OW causes endothelial dysfunction via elevated serum fatty acids, which initiates the molecular events that further the process of CHD. It is, therefore, of the utmost importance to determine its roots. The most probable reason for its high incidence is due to the genetic outfit of most people which does not permit adequate adaptation of the cerebral cortex according to the environmental changes which have occured since the early days.Being overweight (OW) was recognized very early as a risk factor for coronary heart disease (CHD). Its significance in the pathogenesis of CHD has been strengthened by observations showing that OW is responsible for the development of diabetes, hypertension and lipid disorders due to its induction of insulin resistance (IR). Its key role has been underlined further by recent studies indicating that OW causes endothelial dysfunction via elevated serum fatty acids, which initiates the molecular events that further the process of CHD. It is, therefore, of the utmost importance to determine its roots. The most probable reason for its high incidence is due to the genetic outfit of most people which does not permit adequate adaptation of the cerebral cortex according to the environmental changes which have occured since the early days. Übergewicht (ÜG) wurde schon frühzeitig als Risikofaktor für eine koronare Herzerkrankung (KHE) erkannt. Als man herausfand, dass es über eine Insulinresistenz (IR) die als Hauptrisiken betrachteten Leiden Diabetes, Hypertonie und Fettstoffwechselstörungen hervorrufen kann, wurde klar, dass es wohl eine der wichtigsten Ursachen für die heute so häufig auftretende KHE ist. Seine Schlüsselrolle in der Pathogenese der KHE wurde noch durch neueste Untersuchungen unterstrichen, die zeigten, dass das ÜG über erhöhte Serumfettsäurespiegel eine Endothelfunktionsstörung an den Gefäßen hervorruft, welche die molekularen Vorgänge in Gang setzt, die zur KHE führen. Damit kommt der Suche nach den Ursachen des ÜGS eine große Bedeutung zu. Wahrscheinlichste Ursache ist die heutige Genausstattung, die eine Anpassung der Großhirnrinde and die geänderten Umweltverhältnisse beim Gros der Menschen unmöglich macht.

Zur Pathogenese der koronaren Herzerkrankung@@@On pathogenesis of coronary heart disease

Being overweight (OW) was recognized very early as a risk factor for coronary heart disease (CHD). Its significance in the pathogenesis of CHD has been strengthened by observations showing that OW is responsible for the development of diabetes, hypertension and lipid disorders due to its induction of insulin resistance (IR). Its key role has been underlined further by recent studies indicating that OW causes endothelial dysfunction via elevated serum fatty acids, which initiates the molecular events that further the process of CHD. It is, therefore, of the utmost importance to determine its roots. The most probable reason for its high incidence is due to the genetic outfit of most people which does not permit adequate adaptation of the cerebral cortex according to the environmental changes which have occured since the early days.Being overweight (OW) was recognized very early as a risk factor for coronary heart disease (CHD). Its significance in the pathogenesis of CHD has been strengthened by observations showing that OW is responsible for the development of diabetes, hypertension and lipid disorders due to its induction of insulin resistance (IR). Its key role has been underlined further by recent studies indicating that OW causes endothelial dysfunction via elevated serum fatty acids, which initiates the molecular events that further the process of CHD. It is, therefore, of the utmost importance to determine its roots. The most probable reason for its high incidence is due to the genetic outfit of most people which does not permit adequate adaptation of the cerebral cortex according to the environmental changes which have occured since the early days. Übergewicht (ÜG) wurde schon frühzeitig als Risikofaktor für eine koronare Herzerkrankung (KHE) erkannt. Als man herausfand, dass es über eine Insulinresistenz (IR) die als Hauptrisiken betrachteten Leiden Diabetes, Hypertonie und Fettstoffwechselstörungen hervorrufen kann, wurde klar, dass es wohl eine der wichtigsten Ursachen für die heute so häufig auftretende KHE ist. Seine Schlüsselrolle in der Pathogenese der KHE wurde noch durch neueste Untersuchungen unterstrichen, die zeigten, dass das ÜG über erhöhte Serumfettsäurespiegel eine Endothelfunktionsstörung an den Gefäßen hervorruft, welche die molekularen Vorgänge in Gang setzt, die zur KHE führen. Damit kommt der Suche nach den Ursachen des ÜGS eine große Bedeutung zu. Wahrscheinlichste Ursache ist die heutige Genausstattung, die eine Anpassung der Großhirnrinde and die geänderten Umweltverhältnisse beim Gros der Menschen unmöglich macht.

Zur Pathogenese der koronaren Herzerkrankung

Being overweight (OW) was recognized very early as a risk factor for coronary heart disease (CHD). Its significance in the pathogenesis of CHD has been strengthened by observations showing that OW is responsible for the development of diabetes, hypertension and lipid disorders due to its induction of insulin resistance (IR). Its key role has been underlined further by recent studies indicating that OW causes endothelial dysfunction via elevated serum fatty acids, which initiates the molecular events that further the process of CHD. It is, therefore, of the utmost importance to determine its roots. The most probable reason for its high incidence is due to the genetic outfit of most people which does not permit adequate adaptation of the cerebral cortex according to the environmental changes which have occured since the early days.Being overweight (OW) was recognized very early as a risk factor for coronary heart disease (CHD). Its significance in the pathogenesis of CHD has been strengthened by observations showing that OW is responsible for the development of diabetes, hypertension and lipid disorders due to its induction of insulin resistance (IR). Its key role has been underlined further by recent studies indicating that OW causes endothelial dysfunction via elevated serum fatty acids, which initiates the molecular events that further the process of CHD. It is, therefore, of the utmost importance to determine its roots. The most probable reason for its high incidence is due to the genetic outfit of most people which does not permit adequate adaptation of the cerebral cortex according to the environmental changes which have occured since the early days. Übergewicht (ÜG) wurde schon frühzeitig als Risikofaktor für eine koronare Herzerkrankung (KHE) erkannt. Als man herausfand, dass es über eine Insulinresistenz (IR) die als Hauptrisiken betrachteten Leiden Diabetes, Hypertonie und Fettstoffwechselstörungen hervorrufen kann, wurde klar, dass es wohl eine der wichtigsten Ursachen für die heute so häufig auftretende KHE ist. Seine Schlüsselrolle in der Pathogenese der KHE wurde noch durch neueste Untersuchungen unterstrichen, die zeigten, dass das ÜG über erhöhte Serumfettsäurespiegel eine Endothelfunktionsstörung an den Gefäßen hervorruft, welche die molekularen Vorgänge in Gang setzt, die zur KHE führen. Damit kommt der Suche nach den Ursachen des ÜGS eine große Bedeutung zu. Wahrscheinlichste Ursache ist die heutige Genausstattung, die eine Anpassung der Großhirnrinde and die geänderten Umweltverhältnisse beim Gros der Menschen unmöglich macht.

Potential pitfall in the determination of free [Mg2+] by 31P NMR when using the β/α-ATP peak height ratio method

Recently, Clarke et al., (Clarke K, Kashiwaya Y, King MT, Gates D, Keon CA, Cross HR, Radda GK, Veech RL. The β/α peak height ratio of ATP. A measure of free [Mgfree2+] using31 P NMR, J. Biol. Chem. 1996;271:21142–21150.) reported a new method to noninvasively determine the concentration of intracellular free magnesium ([Mgfree2+]) based on the measurement of the peak height ratiohβ/α of the β- and α-ATP signals in31P NMR spectra.hβ/α varies with Mgfree2+], however, the study presented here shows thathβ/α also strongly depends on the homogeneity of the static magnetic field. For this reason, we performed at a magnetic field strength of 1.5 T31P NMR measurements of solutions that mimic intracellular medium. The magnetic field homogeneity was varied by changing the currents in the shim coils, and the effect onhβ/α is demonstrated with and without proton decoupling. In both cases,hβ/α strongly depends on the magnetic field homogeneity and can therefore lead to a pitfall in the determination of [Mgfree2+].