The primary hemostatic response involving the platelet-blood vessel wall reaction in mammals resembles, to a significant extent, the basic cellular defense mechanisms of more primitive forms such as invertebrates. Mammalian primary hemostasis appears to have retained a phylogenetic vestige of primitive leukocyte behavior (Salt, 1970). In this evolutionary sense, the platelet might be thought of as a special form of leukocyte. Human platelets contain intracellular granules similar to the classic lysosomes of polymorphonuclear leukocytes (Marcus et al., 1966) and contribute to the inflammatory response accompanying tissue injury by releasing constituents which may alter blood vessel reactivity. Platelets have long been known to contain vasoactive amines which are released upon aggregation. Platelets interact with many types of particulate matter including bacteria and viruses and immune complexes which lead to the release of intracellular constituents, including serotonin (Mustard and Packham, 1970), prostaglandins (Smith and Wallis, 1971), cationic proteins (Packham et al., 1966), and various proteolytic enzymes such as cathepsin A (Nachman and Ferris, 1968), elastase (Robert et al., 1970), and collagenase (Chesney et al., 1974).