Abstract
During torpor in a 13-lined ground squirrel heart rate and blood flow decrease, increasing the risk of blood clot formation. In response, cells involved in clotting called platelets are sequestered in the liver, stored in the cold for months, and released back into circulation upon arousal. This is in contrast to non-hibernating mammals, including humans, in which chilled platelets undergo cold storage lesions and phagocytosis, leading to rapid clearance from circulation post-transfusion. Because of this, human platelets must be stored at room temperature, limiting their shelf life to 7 days due to the increased risk of microbial contamination at warmer temperatures. Human and ground squirrel platelets were stored at room temperature or 4 °C before being analyzed for cold storage lesions. Human platelets stored at 4 °C displayed progressive increases in phosphatidylserine surface exposure and caspase activation, while ground squirrel platelets showed minimal change. Following cold storage, sialic acid residues on human platelets were cleaved, leading to increased phagocytosis of human platelets by HepG2 cells. Ground squirrel platelets stored in the cold showed no changes in desialylation and phagocytosis, with Taxol-treated ground squirrel platelets showing the lowest phagocytosis rates between both species and all treatments. These results suggest that ground squirrel platelets may be resistant to cold storage lesions seen in human platelets. Although these experiments were done in vitro, they suggest a mechanism by which ground squirrel platelets are adapted to be stored during hibernation and remain functional following arousal. Other hibernating species may employ similar adaptations to retain functional platelets following torpor.