AGGREGATION OF KILLER WHALE PLATELETS

The aggregation of blood platelets is a crucial step in normal hemosta sis for all mammals. Circulating platelets are sensitive to a large va riety of physiologic and non-physiologic stimulants, some of which are formed or exposed in conjunction with vascular damage or endothelial cell denudation. In addition, drastic pressure changes activate human platelets. Killer whale platelet function, on the other hand, is very intriguing since these animals do not seem to experience untoward plat elet reactions during or after diving to great depths, nor do they exp erience abnormal bleeding associated with sub optimal platelet functio n. We examined this concept and determined that killer whale platelets , in response to ADP, PAF, and arachidonic acid, appeared to aggregate normally during the first 2-5 minutes after addition of the agonist, but had completely disaggregated at 10 minutes. Collagen- and A23187-i nduced aggregation appeared normal and complete within 10 minutes, whi le there was no response to epinephrine or ristocetin. Thromboxane pro duction by killer whale platelets appears to be quantitatively similar to that produced by human platelets in response to ADP and PAF and ex ceeded that produced by human platelets when collagen was used as the agonist. In summary, this study reports a reduced platelet aggregation reaction in killer whales in response to several platelet agonists wh ich does not appear to be related to the generation of thromboxane. Th is phenomenon may serve a protective role in these mammals by preventi ng thrombosis during diving and resurfacing.