Platelet-Endothelial Function in Relation to Environmental Temperature

摘要

Thromboembolic phenomena are commonly observed in frostbite injury to the microvasculature. Large blood vessel endothelium was used to assess any alterations in platelet-endothelial interaction resulting from low environmental temperatures. Media from bovine endothelial cells (37, 24, 4C) did not cause or enhance platelet aggregation. Yet ADP (120 micrometers) stimulated aggregation of all platelet samples. Bovine and porcine endothelial cells were incubated at 37, 24, 4, and 0.5C with homologous platelets suspended in Tyrodes at 37, 24, 4, and 0.5C with homologous platelets suspended in Tyrodes buffer plus albumin, and the rate of ADP-stimulated platelet aggregation was compared with control platelets. Bovine venous endothelial cells (at 37 C) inhibited platelet aggregation more strongly than aortic endothelial cells. This inhibition was blocked by aspirin (7mM) and was independent of environmental temperature. Porcine endothelial cells also inhibited platelet aggregation. This inhibition (maximal at 37 C) was significantly attenuated by temperatures < or = 24 C. A significant loss of inhibition of platelet aggregation could lower the threshold at which parenchymally-derived nucleotides or other substances from damaged cells can cause aggregation. Thus, in porcine endothelial cells > bovine endothelial cells, a possible mechanism for the thromboembolic action of cold is suggested.