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The pasting properties of rice starch (RS) with high concentration (10%, w/w) were investigated in the presence or absence of pullulan (PUL) using a rapid visco-analyzer (RVA). Addition of pullulan resulted in the reduction of peak viscosity, trough viscosity, final viscosity, and setback value of RS. Furthermore, an interesting phenomenon, i.e. a small viscosity peak appeared in the RVA curves of RS-PUL mixtures, was observed. It indicated that addition of pullulan might suppress the gelatinization of starch granules by maintaining the integration of some granules. The scanning electron microscope (SEM) observation of samples suggested that starch granules could be wrapped by a thin membrane composed of pullulan and/or pullulan-amylose associations. The coating ability of pullulan and/or the possible molecular interactions between pullulan and amylose could be responsible for these results.

The1H nuclear magnetic resonance (NMR) myoglobin (Mb) Val E11 signal provides a unique opportunity to assess the functional role of Mb in the cell. On CO infusion in perfused myocardium, the MbO2signal at −2.76 parts per million (ppm) gradually disappears, whereas the corresponding MbCO signal emerges at −2.26 ppm, reflecting the state of Mb inhibition. Up to 76.8% MbCO saturation, myocardial O2consumption (MV˙o2) remains constant, whereas the rate-pressure product (RPP) has already dropped to 92% of the control level. At 87.6% MbCO saturation, the lactate formation rate has increased by a factor of two, and MV˙o2begins to decline. However, the ratio CO/O2is still 1/10, well below the inhibition threshold for cytochrome oxidase activity. The MV˙o2decline in the face of an adequate O2supply and an unperturbed high-energy phosphate level implies that Mb may play a role in directly regulating respiration, mediated potentially by a shift in NADH/NAD. Although nitrite inhibits Mb, nitrite also directly affects the myocardial function.

Nitrite oxidation of oxymyoglobin in perfused rat myocardium under nonlimiting oxygen produces a detectable 1H nuclear magnetic resonance metmyoglobin (metMb) signal at -3.9 ppm. When the myocardium is perfused with < 10 mM nitrite, the 1H nuclear magnetic resonance MbO2 gamma CH3 Val E11 signal does not change intensity and the metMb reporter signal at -3.9 ppm is undetectable. However the rate pressure product decreases by 26% from the control level. Phosphocreatine, myocardial oxygen consumption, Pi, ATP, and pH remain constant. With > 10 mM infused nitrite, myoglobin (Mb) oxidation becomes apparent. As the MbO2 gamma CH3 Val E11 signal intensity decreases, the metMb signal intensity at -3.9 ppm increases. At the same time the 31P high-energy phosphate signals, rate pressure product, and lactate formation exhibit significant alterations. Myocardial oxygen consumption, however, remains constant. The data indicate that Mb oxidation does not limit myocardial respiration but does reduce energy production. Pulse-recovery experiments further demonstrate that a transient perfusion with 2 mM infused nitrite depresses the contractile function, which does not recover during reperfusion with oxygenated, nitrite-free buffer. The findings support the view that either Mb mediates energy coupling or nitrite directly uncouples energy production in myocardium. They also reveal a glimpse of the intracellular reductase activity that maintains the Mb in the Fe (II) state.