Transmission, scanning and analytical electron microscopy, ultrastructural cytochemistry, biochemistry, immunochemistry and physiology will be combined in our continuing effort to identify specific lesions responsible for the rapid deterioration of blood platelets during storage in vitro. Efforts during the first three years of support from this grant have suggested that loss of ability to regulate calcium flux is a major factor responsible for the severe cellular damage. Experiments designed to circumvent this injury have resulted in preservation of platelet morphology, biochemistry and function for 15 to 21 days, at least 4-5 times the period reported by others. Experiments during the next three years will further clarify the structural and biochemical nature of the storage lesion, improve the conditions which have resulted in a dramatic improvement of platelet functional survival, and seek new ways to increase the preservation time in vitro to 4-6 weeks.