Pretty much everyone has seen blood; it's that bright red stuff that comes through the skin when you cut yourself. However, it also has a very important role - in fact, you could say it's one fo the most important substances in the body. Without it, you simply couldn't survive.
All cells need energy to do the things they do - nerve cells require energy to send signals to each other, muscle cells need energy in order to contract. They get this energy through metabolism which produces energy in the form of ATP. This involves a series of reactions, which need to occur in every cell. Therefore, the ingredients or reactants need to be delivered to the cells, and the by-products (the things which are produced that we don't want) need to be taken away.
Blood is made up of red blood cells, white blood cells, platelets and plasma. Plasma, being the fluid in which everything else is dissolved, makes up the greatest proportion of blood.
So blood is mainly about transport: taking things to where they're needed, and taking waste away. It does this in a very clever way, and it is made up of various different things to enable it to perform its function.
The following gives some more specific details, and explains how blood is brilliantly designed to serve its purpose.
Making up most of the blood cells are red blood cells (RBCs) or erythrocytes. They play the functional role in oxygen delivery to cells, which means that when it comes to delivering oxygen, red blood cells are very important. They are much like other cells in that they are wrapped in a plasma membrane, but they are unusual because they don't contain much else - there are no nuclei, for example. This is because all they really need to do is bind to oxygen, and they are therefore made up of a special protein called haemoglobin. Each molecule of haemoglobin (Hb) can bind to four molecules of oxygen if there is enough kicking about, which makes it a very effective carrier of oxygen.
A key feature of red blood cells has to be their shape. Since they're basically parcels of haemoglobin, there is no risk of squashing some other important part of the cell, and the erythrocytes can therefore bend and squeeze themselves through the small tubes which they have to go through. However, most importantly they are shaped for efficient absorption of oxygen. They only have a few seconds in the lungs, and have to quickly get rid of carbon dioxide and get some oxygen; so they have to have a large surface area to be able to make the exchange quickly.
This is achieved with the bi-concave disc shape - a circular disc, a bit like a donut but without the hole cut out properly. Looking from the top, it's a circle with a dip in the middle. This dip occurs on both sides. Because of all the curved sides, oxygen can diffuse very easily into the cell - there is plenty of space around the cell to do so; and the haemoglobin snaps up the oxygen the moment it appears.
Blood cells are actually very small. While platelets are smaller than red blood cells, the simplicity of erythrocytes does allow them a small size. Without a nucleus or any other organelle, the cell is able to remain very small and float through small vessels, delivering its precious load of oxygen.
Red blood cells also act as a buffer for blood - that is, they make sure the pH of blood remains constant. If there are more hydrogen ions in solution, it could make blood more acidic, which will change the way that reactions occur and could be a serious problem; in this situation, hydrogen ions can attach to the haemoglobin of erythrocytes, bringing the number in solution back to normal. Similarly, if there are too many, haemoglobin in red blood cells usually has a few spare to donate into the blood stream.
It's important to know the difference between arterial blood and venous blood because they have different properties. Arterial blood is the blood which is coming away from the heart - it is represented as bright red, because the blood is oxygenated. Venous blood travels towards the heart, and is blue because it is deoxygenated.
The protein haemoglobin in blood cells contains something called a haem group. This contains a ferrous ion (Fe2+) which gives the protein a bright red colour when it is bonded to oxygen. The combination of oxygen and haemoglobin is called oxyhaemoglobin, and in the blood vessels of the lungs, when the two combine, blood is said to be oxygenated.
So at the lungs, blood gains oxygen to become bright red, and looses the waste carbon dioxide it picked up in the body. Well, when it goes back to the various parts of the body it needs to supply, the cells of the body pick up the oxygen which the blood is delivering, and pass some waste carbon dioxide to the blood. When the blood looses its oxygen, it looses its bright red colour, and becomes a dull red which is seen as blue through the skin; blood is said to be deoxygenated.
Generally speaking, blood returning to the heart is coming from the body, and will therefore be deoxygenated; and blood leaving the heart has recently been through the lungs, and will therefore be oxygenated. Generally, then, arterial blood is oxygenated and venous blood is deoxygenated.
Unfortunately, for complication's sake, blood returning to the heart from the lungs is still venous blood, but it is coming from the lungs and is therefore oxygenated. Blood going from the heart to the lungs is arterial blood because it is moving away from the heart, but it is deoxygenated because it hasn't reached the lungs yet. This is an important distinction - an exception to an otherwise very helpful rule.
Blood cells, when mature, are essentially very simple.
However, to be packed full of haemoglobin, the cell must first produce it. Young blood cells contain a nucleus, endoplasmic reticulum, mitochondria....
First, the kidney secretes something called erythropoietin when it thinks we're short of red blood cells. The bone marrow is happily producting pluripotent cells which can turn into any sort of blood cell; some of these head down a specific path which will turn them into erythrocytes, and erythropoietin encourages this.
- Erythroid Cell - the cell produced in the bone marrow
- Normoblast - with most of the haemoglobin produced, the nucleus and number of organelles are small.
- Reticulocyte - now rid of the nucleus, the remaining RNA finished haemoglobin production
- Erythrocyte - the finished product!
Red blood cells don't last long - only 120 days, though in comparison to other blood cells that's actually quite long. This means that every three months you will have completely renewed your blood supply, assuming your body is functioning normally.
Considering how important blood cells are, you'd probably be surprised to learn that we loose many millions of them every second! The spleen removes cells that have been produced incorrectly - that are the wrong shape - that have been damaged, or that have simply got to the end of their lives and are ready to finish their job. This means the producing more red blood cells is a constant task - and the kidneys, while performing the take of cleaning the blood, have a huge responsibility in making sure erythropoietin is produced.
Although a lot smaller than red blood cells - indeed, the smallest cellular component of blood, at around 2-3 micrometres - platelets have a very important function within human blood. Although represented on this site by the image on the right, platelets tend to float around as disc shapes, at a concentration of about 2-4 ? 109 per litre of blood.
Unlike red blood cells, they do have organelles - many mitochondria to provide the energy for the processes which occur, and dense granules and alpha granules which contain the chemicals which platelets use to help them perform their function. Like red blood cells, however, they don't have a nucleus. This means that they don't last very long - in fact, platelets only last 8-10 days.
Ultimately the thing which everyone knows platelets for is blood clotting. In actual fact, their function isn't so much blood clotting as much as coping with cuts - which isn't quite the same. True, it's important for blood to clot, but it's also important to make sure the blood doesn't keep leaking. Using special receptors known as glycoprotein receptors, the platelets form bonds with each other and then plug up whichever hole is allowing blood to leak. This, combined with the blood clotting, enables efficient escape from blood loss. Brilliant, hey?!
It's not really a simple answer. Let's take the two main things which happen - a platelet plug forms, plugging up the hole which has been formed as much as possible; and the clotting cascade forms a clot which prevents any further blood loss.
So something sharp pierces the skin. Platelets will be attracted to the exposed collagen and will start to form a plug by connections of their glycoprotein receptors. A substance called von Willebrand's Factor (vWF) bridges the gap between the platelets and the collagen, but receptors also link the platelets straight to it. Platelets are stuck together with fibrinogen linking their glycoprotein receptors.
Importantly, platelets are also activated by the exposed collagen. Along with neutrophils and monocytes (some white blood cells), they release chemicals to try and help the situation - ADP, which helps with the platelets collecting together to form a plug; PAF or Platelet activating factor which activates platelets to release more chemicals; and 5-HT (or 'Serotonin') and TXA2 (or Thromboxane A2), which cause blood vessels to tighten up (or 'vasoconstrict').
The cells lining the blood vessels, known as endothelial cells, also release chemicals to regulate the process. They produce nitric oxide (or NO) and Prostacyclin (or PGI2), which inhibit the effects of ADP, PAF, 5-HT and TXA2. Importantly, TXA2 and PGI2 are both produced from something called arachidonic acid using an enzyme called cyclooxygenase or COX. If you block this enzyme, then this will stop production of both TXA2 and PGI2. However, the nucleus can produce more of the enzyme because enzymes are proteins. Platelets don't have a nucleus, but endothelial cells do; so if you block COX, then platelets can't produce any more TXA2, but endothelial cells can produce some more COX, and then produce some more PGI2. This is how aspirin works: it blocks COX, and therefore helps to prevent clots.
The clotting cascade is a series of reactions, where the product of one reaction makes the next reaction go quicker. So, when something pierces the skin and exposes collagen, the collagen encourages factor XII to turn into the activated form - factor XIIa. This in turn encourages factor XI to turn into factor XIa, which encourages IX to turn into IXa. The wound will also lead to release of something called thromboplastin or 'tissue factor', which encourages activation of factor VII, which is a factor that also activates factor IX.
As the cascade gain momentum, each level increases in effect - for example, if one copy of factor XI is activated, that activated factor can in turn activate many more copies of factor IX. Each time, more and more factors are activated, until thrombin causes fibrinogen to turn into fibrin. Fibrin is something called a monomer, and it can react with itself to form great long strands of fibrin. Fibrinogen is the inactive form; but when you get lots of fibrin kicking around, it reacts with itself to form the stable clot.
Interestingly, thrombin also encourages plasminogen to form plasmin. Plasmin is something which encourages fibrin to turn back into fibrinogen. This may sound complicated, but it basically encourages the reverse reaction. This stops the clot getting out of control - it is a regulatory feature. If there were too much thrombin, then too much fibrinogen would turn into fibrin, but due to the presence of plasmin, it stays at a 'safe' level.
Of course, in the case of conditions like deep vein thrombosis, a clot has formed in an inappropriate time, and the regulatory measures have been insufficient. All of the factors are present in the blood (in a healthy person), but are not activated; however, if the blood is not moving much - is in 'stasis' - then something could trigger a clot to form, leading to this condition of deep vein thrombosis. The reason it is fatal is because the clot gets caught somewhere like the lungs, where the blood vessels get very small, and here it is fatal.