If you have normal blood and suffer a cut, tiny cells known as thrombocytes, or platelets, come to your rescue. These disclike cells, the smallest in the blood stream, clump together within seconds to seal off the wound. But first they need something, such as the feel or a damaged blood-vessel wall, to jolt them into action.
The first platelets to detect a hole in the blood-vessel wall become sticky, so that they can fasten on the sides of the gap. As they do so, they change shape, becoming spiky globes that help them lock together. Signals go out to other platelets to help fill the breach. Every drop of blood usually holds about fifteen million platelets, so extra help is never far off. If the wound is not serious, this emergency force soon has everything under control. Normality returns almost without your knowing that it has been interrupted.
A final stage in the closing off of a wound is coagulation, the hardening of blood to form a tight seal. In a complex series of sates, know as the coagulation cascade, the blood produces a strongly protein called fibrin, the main component of all blood clots. Inactive molecules in the plasma suddenly become active, one triggering another in a remarkable chain reaction. Within seconds, one active molecules may convert some 30,000 others.
Deficiencies in the blood may cause it to flow sluggishly or to clot unnecessarily. Other defects, such as a shortage of platelets, may stop it from clotting, causing haemophilia. Doctors test the blood’s ability to clot by pricking the skin, usually of the ear or forearm, and seeing how long it takes for the bleeding to stop. Three to eight minutes is the average. There is always body wonders.