Mechanisms of thrombosis

  • Noel Clarke
The Graves Lecture, 1968

DOI: 10.1007/BF02958782

Cite this article as:
Clarke, N. I. J. Med. Sc. (1968) 1: 343. doi:10.1007/BF02958782

Summary

Haemostasis or the arrest of bleeding is a fundamental physiological mechanism, which prevents the leakage of blood after vessel injury by platelet clumping, vasoconstriction and fibrin formation. The haemostatic plug is composed primarily of platelets.

The process of thrombosis involves mainly platelet clumping, and thrombi are very similar in composition to the haemostatic plug. There is accumulating evidence that recurrent thrombi forming on the walls of arteries may become absorbed into the wall and degenerate into atheromatous plaques. In this lecture some of the links have been drawn between the disease, atheroma and thrombosis and also between thrombosis and that vital phenomenon, haemostasis.

Since cell injury is one of the earliest events in both haemostasis and thrombosis, we have broken open human cells and separated the intracellular components by differential centrifugation into ‘nuclear’, ’mitochondrial’, ‘microsomal’ and soluble fractions. The homogenates and individual cell fractions have been tested for their effect on platelet aggregation, coagulation and fibrinolysis. The findings indicate that the homogenates and cell particles from these human cells can cause platelet aggregation. It has also been established that the highest coagulative activity is in the ‘microsomal’ fraction and probably associated with the endoplasmic reticulum. These investigations on cell injury may have a relevance to the pathogenesis of shock, surgical trauma, acquired afibrinogenaemia of pregnancy, etc. as well as to the earliest lesions following cell injury at the vascular level.

Copyright information

© Springer 1968

Authors and Affiliations

  • Noel Clarke
    • 1
  1. 1.Department of PathologyUniversity CollegeDublin 2Ireland