Optimized outer volume suppression for single-shot fast spin-echo cardiac imaging.

Among the ultrafast MRI techniques, the single-shot fast spin-echo sequence offers a robust alternative to echo planar imaging, essentially because of a much reduced sensitivity to B0 inhomogeneity. This property is particularly appealing in situations in which B0 inhomogeneities can be severe and difficult to correct, such as in cardiac imaging. With single-shot cardiac imaging, however, achieving high resolution over the necessarily large field of views without introducing back-folding artifacts is problematic. One option is to use multishot sequences. However, then issues related to cardiac gating arise. Another solution is to use, optimized presaturation slabs with quadratic phase pulses generated by the Shinnar-LeRoux algorithm. These can be set to reduce the field of view in the phase-encoding direction, resulting in a reduction in the number of phase-encoding steps. For instance, for a 1 x 2-mm spatial resolution, over a rectangular, 250 x 125-mm field of view, and using a half Fourier acquisition, an echo-train length of only 40 is required. With a 4.5-msec echo spacing, the total imaging time is approximately 180 msec. The efficacy of this solution on phantoms and volunteers is demonstrated. Multislice short-axis examinations of the whole heart, realized within a single short breath-hold of approximately 10 seconds, are shown. The possibility of investigating not only cardiac anatomy but also both contractility and myocardial perfusion is discussed.

In vivo 31P nuclear magnetic resonance spectroscopy of skeletal muscle energetics in endotoxemic rats: a prospective, randomized study.

OBJECTIVE: To identify possible alterations in the skeletal muscle high-energy phosphate metabolism at the early phase of endotoxic shock in rats. DESIGN: A prospective, randomized study of skeletal muscle energetics in endotoxemic and in control rats, by in vivo 31P nuclear magnetic resonance (NMR) spectroscopy at rest, under regional ischemia, and during reperfusion. SETTING: Biochemical NMR laboratory equipped for surgery and hemodynamic monitoring. SUBJECTS: Wistar rats were randomized to different groups. Eight rats were injected with Escherichia coli endotoxin (15 mg/kg, survival time 19 +/- 4 hrs) intraperitoneally. Seven other rats served as controls. The additional nine rats were studied for the saturation recovery pulse sequence. INTERVENTIONS: In the treatment group, endotoxin was injected 8 hrs before NMR spectroscopy. The right hind limbs were studied under anaesthesia using a surface coil NMR probe. Their high-energy phosphate contents and intracellular pH were determined by 31P NMR spectroscopy. After baseline measurements, an ischemia-reperfusion challenge was imposed on the muscle by transient clamping of the abdominal aorta. Contralateral femoral artery pressure was constantly monitored. MEASUREMENTS AND MAIN RESULTS: During the baseline period, the endotoxin-treated muscles did not show any difference in the distribution of the high-energy phosphate compounds or in intracellular pH, as compared with the controls. Ischemia resulted in a significantly faster decline of the inorganic phosphate/creatine phosphate ratio in the endotoxin-treated rats (1.35 +/- 0.17 vs. 0.51 +/- 0.06 at the end of the 38-min ischemic period). Skeletal muscle acidosis developed earlier and was deeper in the endotoxemic animals (pH: 6.94 +/- 0.02 vs. 7.02 +/- 0.03 at the end of ischemia). During reperfusion, the calculated time constants of recovery of inorganic phosphate to phosphocreatine ratios were identical between groups. CONCLUSIONS: Resting nonischemic muscles of endotoxin-treated rats show no evidence of alterations in high-energy phosphate metabolism. However, under ischemic conditions, high-energy phosphate metabolism deteriorates faster in the skeletal muscles of treated animals. These data support the hypothesis of a greater mismatch during perfusion at very low pressure between residual oxygen availability and oxygen needs in the endotoxin-treated muscle cell.

The induction of cardiac hypertrophy by catecholamines can be dissociated from their inotropic effect.

In this study, ornithine decarboxylase, the first and rate-limiting enzyme of the polyamine pathway, was used as a marker of the very early stages of cardiac hypertrophy. Our data show that ornithine decarboxylase is independently regulated by ventricular wall stress and adrenergic receptors, and support the theory that catecholamines have a pressure-independent trophic effect. The infusion of beta 2-adrenergic agonist, terbutaline, at 10(-7) mol/l, did not affect the cardiac performance of isovolumic perfused rat hearts. Despite the lack of functional changes, ornithine decarboxylase activity, as assayed in vitro by 14C-ornithine decarboxylation, was markedly increased in both left and right ventricles. Further investigation showed that ornithine decarboxylase stimulation by catecholamines, unlike ornithine decarboxylase basal activity, was dependent on the extracellular calcium level. Furthermore, passive increases in ventricular wall stress in non-beating hearts also increased left ventricular ornithine decarboxylase activity.