Continuous zirconia fibers with a nanometer ceramic structure and a tensile strength up to 2.8 GPa were fabricated by pyrolyzing polyacetylacetonatozirconium precursor fibers through a special atmosphere heat treatment. DSC‐TGA, GC‐MS, IR, SEM, and TEM were used to study the fiber transformation mechanism during heating. Results showed that special atmosphere heat treatment could make the organics in the fibers come out directly without carbonization and remove them almost entirely under 400°C, and the obtained zirconia fibers had few defects, good continuity, and high strength.

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A novel inorganic sol-gel method for preparation of high-quality zirconia fibers was proposed, with starting from the reaction between ZrOCl 2 Á 8H 2 O (ZOC) and H 2 O 2 . The spinning solution with good spinnability was obtained by controlling the mole ratio of H 2 O 2 /ZOC to 4 for reaction, and the mole ratio of Cl/Zr remained close to 1 in the reacted solution. The double chain structure of the inorganic polyzirconium molecule in the spinning solution was determined by elemental analysis and FT-IR. The precursor fibers were obtained by using a novel 30,000 rpm centrifugal spinning apparatus. Being heat-treated to 1300 C under steam atmosphere, the precursor fibers transformed to zirconia fibers which had relatively high strength and good flexibility, with length of more than 10 cm and diameters of 5-10 mm.

Supersensitivity to isoproterenol (ISO) induced activation of cardiac phosphorylase in diabetic rat heart has been previously demonstrated and was also reproduced in this study. To explore further the nature of this supersensitivity, we examined the activity of phosphorylase kinase and the level of cyclic AMP (cAMP) in this tissue. We observed a significantly enhanced activation of phosphorylase kinase but no increase in cAMP levels in response to ISO stimulation in diabetic rat heart, suggesting that the supersensitivity of phosphorylase activation in diabetic heart may result from an enhanced activation of phosphorylase kinase that does not involve the cAMP pathway. On the other hand, perfusion of diabetic rat heart with verapamil (5 x 10(-8) M) prior to ISO stimulation abolished the enhanced cardiac phosphorylase activation, suggesting a role for calcium in the supersensitivity of phosphorylase activation. Furthermore, treatment of the diabetic rats with an insulin-like compound, vanadyl sulphate, completely abolished the enhanced cardiac phosphorylase activation and restored the increase in ISO-induced cAMP elevation in diabetic heart. The present study has provided further information on the changes of phosphorylase activation in the diabetic rat heart and demonstrated beneficial effects of vanadyl sulphate on the pathway leading to phosphorylase activation in diabetic rat heart.

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