The Basics: Haemostasis (Part 1)

Every day that you exist, your vessels take a pounding, and several hundred small breaches (and possibly one or two big ones) open up. This post is about what happens next.

Immediately after vessel injury, there is a brief period of intense vasoconstriction that serves to minimise blood loss in the short term. You can think of this move as buying time until the proper repairmen arrive.

There are two sets of repair teams that work simultaneously, and the first of these is the platelet team. Platelets are small fragments that have been broken off cells called megakaryocytes while they were still in the bone marrow, and there are normally an amazing 150-450 billion platelets in each litre of blood rushing around your body. They are triggered into binding to an injured vessel when they encounter either collagen or von Willebrand factor (vWF). Collagen is normally present in the subendothelial matrix beneath the endothelium, and is therefore not exposed to flowing blood under normal conditions. However, a breach of the endothelial barrier allows blood (and therefore platelets) to come into contact with the collagen. Greatly supplementing this interaction is the protein called 'von Willebrand factor' which also normally circulates in the blood stream and grabs on to any exposed collagen. Platelets bind, with a specific receptor in each case, to either collagen or vWF.

The adhesion to collagen activates the platelets, or alternatively they may be activated by thrombin (the latter coming from the second of our teams - more on this in a short while). These activated platelets release their granules, which can be either alpha granules or dense granules. Alpha granules contain a variety of proteins that promote haemostasis (like vWF and several of the coagulation factors) whereas the dense granules contain ADP, calcium and serotonin, which also promote haemostasis in complicated ways.

An activated platelet can also recruit more platelets into this developing platelet plug. Some of the mediators listed above, like ADP and serotonin, do this. Also fibrin (produced, like thrombin, by the second team) can act as a bridge between platelets, which express a specific receptor for it. In this way, the platelet plug is stabilised.

Now let's we're ready to turn to the second of our teams in the next post - the coagulation factor team.