Remarkably, American black bears (Ursus Americanus) are capable of varying their heart rates to coincide with their breathing, creating pauses of 30 seconds or more, yet they do not appear to suffer from embolic events. We evaluated some features of the clotting cascade of black bears, providing novel insights on the underlying mechanisms they evoke for embolic protection during hibernation.
We measured activated clotting times, prothrombin times, and activated partial thromboplastin times during early-denning (December), late-denning (March), and summer (August). Activated clotting times during early hibernation were ∼3 times longer than those observed among non-hibernating animals. Clotting times declined later in hibernation, when bears were within ∼1 month of emerging from dens. Prothrombin times were similar for each seasonal time point, whereas activated partial thromboplastin times were highest during early-denning and decreased during late-denning and summer. We also examined D-dimer concentrations to assess whether the bears were likely to have experienced embolic events. None of the non-parturient bears exceeded a D-dimer concentration of 250 ng/mL (considered the clinical threshold for embolism in mammals).
Our findings suggest there is unique expression of the clotting cascade in American black bears during hibernation, in which extrinsic pathways are maintained but intrinsic pathways are suppressed. This was evaluated by a significant difference between the activated clotting times and activated partial thromboplastin times during the denning and non-denning periods. These changes are likely adaptive, to avoid clotting events during states of immobilization and/or periods of asystole. Yet, an intact extrinsic pathway allows for healing of external injuries and/or foreign body responses.
- Received April 7, 2016.
- Accepted November 17, 2016.
- © 2016. Published by The Company of Biologists Ltd