Abstract
1. Heparin, dicumarol, Tromexan and phenylindanedione did not prevent, but actually enhanced, the formation of platelet plugs at the site of hemorrhages produced at the tip of a stimulating microelectrode in contact with the walls of small blood vessels in the hamster cheek pouch. Furthermore, these anticoagulants per se produced an increased adhesiveness of platelets and leukocytes to the endothelium of small venules. In particular, heparin produced platelet embolism immediately after administration. The circulating emboli varied in size from that of leukocytes to cylindrical masses which filled the lumina of vessels measuring up to 75 µ in diameter. Platelet embolism was not found during the first five days of administration of dicumarol, but appeared subsequently.
2. The significance of increased platelet agglutinability during the hypocoagulable state induced by anticoagulants and the need for a critical distinction between agglutinability of the formed elements and coagulation involving fibrin are discussed.
3. An increase in the fragility of the walls of venules followed the administration of heparin, dicumarol, Tromexan and phenylindanedione. A brief series of relatively weak faradic shocks from a micro-electrode produced a hemorrhage. Shocks of much greater strength applied to venules of normal untreated hamsters produced no visible effect. This method is proposed as a new semiquantitative procedure for investigation of vascular fragility in accessible membrane preparations. It may possibly distinguish between fragility in the sense of rhexis or breaking of the wall and petechial formation such as that produced by the application of negative pressure and perhaps erroneously referred to in the literature as "fragility."
4. Petechial hemorrhages appeared at the points of junction of the postcapillary venules after anticoagulant administration, but not on the capillaries. Spontaneous ruptures were not found in capillaries. No evidence was found for an increase in capillary fragility. Consequently, the term "vascular fragility" is proposed to replace "capillary" fragility.
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