Primary hemostasis

Objective: To review the current understanding of the mechanisms responsible for primary hemostasis and to give an overview of primary hemostatic syndromes in small animal patients. Current and future therapeutic options for dysfunction of primary hemostasis are discussed. Data sources: A thorough search of the human and veterinary literature using the keywords platelets, primary hemostasis, von Willebrand factor (vWF), von Willebrand disease, aspirin, thromboxane, and aggregation, were performed. Databases searched included OVID Medline, Pubmed, and CAB abstracts. Conclusions: Primary hemostasis occurs when platelets adhere to an injured or disrupted endothelial surface. Adherence is followed by activation, or the release of platelet granule contents. The agonists released from platelet granules recruit additional platelets and induce their activation and aggregation. Adhesion, activation, and aggregation are mediated by different receptors and ligands depending on the local blood flow conditions. vWF and adenosine diphosphate are the primary mediators of adhesion, activation, and aggregation under high shear conditions. During low shear conditions collagen, fibronectin, and laminin mediate adhesion, thromboxane A₂ promotes activation, while aggregation is mediated by glycoprotein Ib-IX-V (GP Ib-IX-V) and fibrinogen. Knowledge of the receptor interactions during different blood flow conditions is crucial to the understanding of the various inhibitors of primary hemostasis available to clinicians.