AUSTRALIAN SNAKE VENOMS AND THEIR EFFECT UPON HUMAN PLATELETS

The in vitro effect of Australian snake venoms on human citrated plasma has been documented and the majority induce coagulation, in keeping with the common clinical presentation of D.I.C. following envenomation. The effect of these venoms upon platelets in vitro has hitherto not been studied extensively and clinical evidence is conflicting, some cases with thrombocyto-paenia have been reported. Twenty Australian venoms were tested, 19 elapids and one hydrophiid (Enhydrina schistosa). Four crotalid snake venoms from the Americas and S.E. Asia were also tested. All of the venoms (1 mg/ml) were investigated for t^eir ability to aggregate both fresh washed platelets (200 × 10⁹/l) resuspended in modified Ardlie’s buffer pH 7.35 and formaldehyde fixed platelets (200 × 10⁹/l) in phosphate buffered saline pH 7.35 using a dual channel Chronolog aggregometer. Samples were taken for electron microscopy (EM).

All elapid venoms induced aggregation in fresh platelets, some only minimally and often after a long lag phase. EM studies revealed only clumping without degranulation of the platelets. This was in marked contrast to the crotalid venoms where rapid aggregation and gross degranulation occurred. The hydrophiid venom failed to induce aggregation of the fresh platelets, however upon addition of normal plasma gross aggregation and degranulation was demonstrated. Aggregation of fixed platelets was negligible in the presence of the majority of elapid and the hydrophiid venoms. The crotalid venoms however did induce aggregation, although to a lesser extent than with the fresh platelets.

The elapid venoms, along with the others studied, required metabolically active platelets to exert their maximal effect. Crotalid and hydrophiid venoms were more active against platelets than the elapid venoms. The hydrophiid venom’s action on platelets was unique in that a plasma co-factor appeared to be required and this is the subject of further investigations.