Reversible Suppression of Hemostasis in Hibernation and Hypothermia
|PhD ceremony:||dr. E.L. de Vrij|
|When:||February 27, 2019|
|Supervisor:||prof. dr. R.H. (Rob) Henning|
|Co-supervisor:||dr. H.R. (Hjalmar) Bouma|
|Where:||Academy building RUG|
|Faculty:||Medical Sciences / UMCG|
Many mammal species survive winter by hibernating, saving energy by reducing metabolism and body temperature during periods called torpor. During hibernation or torpor the animals are expected to suffer from thrombosis (blood clots) and subsequent organ damage due to prolonged immobility, reduced heart rate and blood flow and increased blood viscosity. Despite these risk factors for thrombosis, hibernators wake up healthy. This PhD research studied why hibernators do not suffer from thrombosis and whether their anti-thrombotic mechanisms can be applied to non-hibernating mammals.We studied hibernating hamsters in climate controlled chambers and analyzed factors involved in thrombosis. We found that during torpor the hamsters reduce circulating platelet count with more than 90% in a body temperature dependent fashion, and reduce plasma level of several coagulation factors with approximately 70%. Clotting times (PT and APTT) prolong up to 10 times. All these changes point to a great suppression of hemostasis (blood clotting) in torpor. During arousal, when metabolism and body temperature increase, all these changes are reversed to normal summer level. We found that decreasing body temperature induces the drop in platelet count, which can be mimicked in non-hibernating mammals such as mouse and rat during hypothermia and found platelets in torpor/hypothermia to be stored in liver and released from liver during arousal/rewarming both in hibernators and non-hibernators. Despite great changes in temperature, platelets were not activated/clotting. Eventually patients may benefit from a hibernation-strategy too to prevent thrombosis or cold activation of platelet transfusions.