Platelet Clumping in vivo

Abstract

Wharton-Jones¹ and Bizzozero² showed that, when an artery was injured, white masses would build up at the site of injury and embolize. Honour and Ross-Russel³ examined this response to injury in considerable detail, in arteries on the surface of the rabbit brain. They showed that the white bodies were composed of closely packed but morphologically discrete platelets, and they were unable to influence the rate of formation of the white bodies or their size by heparin, anti-histamines, or 5-hydroxytryptamine (5-HT) antagonists. The demonstration by Gaarder et al.⁴ that adenosine diphosphato (ADP) was capable of producing clumping of human platelets in vitro, led Mitchell and Sharp⁵ to investigate related substances, together with other substances normally carried by the platelet. They confirmed that ADP clumped citrated human platelets at a concentration of 0.04 (µg/ml, and that adenosine triphosphate (ATP) was much less active, a concentration of 1.5 [µg/ml. being required. They also found that human platelets were clumped by 5-HT, and by noradrenaline at a concentration of 0.06 (µg/ml. Rabbit platelets were clumped by ADP at a concentration of 0.05 (µg/ml., were much more sensitive to ATP than human platelets, 0.22 µg/ml, sufficing to produce clumping, were insensitive to noradrenaline, and showed a variable response to 5-HT.