Interrelationship of oxidative metabolism and local perfusion demonstrated by NMR in human skeletal muscle.

Using nuclear magnetic resonance (NMR), we have examined the relationship of high-energy phosphate metabolism and perfusion in human soleus and gastrocnemius muscles. With 31P-NMR spectroscopy, we monitored phosphocreatine (PCr) decay and recovery in eight normal volunteers and four heart failure patients performing ischemic plantar flexion. By using echo-planar imaging, perfusion was independently measured by a local [inversion-recovery (T1-flow)] and a regional technique (NMR-plethysmography).

Perfusion changes in human skeletal muscle during reactive hyperemia measured by echo-planar imaging.

Muscle performance is markedly influenced by tissue perfusion. Techniques that allow quantification of microvascular flow are limited by the use of ionizing radiation. In this investigation, we apply an NMR model previously developed by Detre et al.

Alteration of Ca2+ release channel function in sarcoplasmic reticulum of pressure-overload-induced hypertrophic rat heart.

The effects of pressure-overload left ventricular hypertrophy on the Ca2+ release channel in sarcoplasmic reticulum (SR) were studied by [3H]ryanodine binding and 45Ca2+ flux measurements. The density of Ca2+ release channel in left ventricle determined by equilibrium [3H]ryanodine binding to whole homogenates was significantly lower in hypertrophy than sham (Bmax: 0.47 +/- 0.