Hilgard P
J Clin Pathol. 1973 Aug;26(8):616-9. doi: 10.1136/jcp.26.8.616.
Experimental hypercalcaemia was induced in rats by (1) transplantation of the solid Walker 256 tumour, and (2) intraperitoneal injections of calcium gluconate. Whole blood clotting was studied by means of thromboelastography and whole blood clotting times in polystyrene and glass test tubes. At serum calcium levels between 10.3 and 11.5 m-equiv/l a slight delay in clot formation was found which was reversible by the addition of EDTA to whole blood. Acute, calcium-gluconate-induced hypercalcaemia, however, leads to a significant shortening of the clotting time in the polystyrene tube and to a lesser degree in the glass tube. Maximal factor XII activation in vitro with ellagic acid levels the difference of clotting times again. From these experiments it is concluded that acute hypercalcaemia induces a hypercoagulable state, possibly by partial contact activation, and thus may favour thrombus formation in vivo.
(1)移植实体Walker 256肿瘤;(2)腹腔注射葡萄糖酸钙。采用血栓弹力图以及在聚苯乙烯和玻璃试管中测定全血凝固时间来研究全血凝固情况。当血清钙水平在10.3至11.5毫当量/升之间时,发现凝血形成稍有延迟,向全血中添加乙二胺四乙酸(EDTA)可使其逆转。然而,急性葡萄糖酸钙诱导的高钙血症会导致聚苯乙烯试管中的凝血时间显著缩短,在玻璃试管中的缩短程度较小。用鞣花酸在体外最大程度激活因子XII可再次消除凝血时间的差异。从这些实验得出结论,急性高钙血症可能通过部分接触激活诱导高凝状态,因此可能有利于体内血栓形成。