Thursday, February 23, 2006

Spleen 2

What is unusual about the spleen is its blood supply. Normally arteries branch into smaller arterioles which branch into leaky thin-walled capillaries. From the capillaries fluid and white cells leak, but red cells remain contained and are collected into venules that coalesce into veins which return the blood to the heart. Fluid and lymphocytes that have left the capillaries are collected by lymphatics which return to the heart via the thoracic duct and the way stations situated on the lymphatics and known as lymph nodes.

In the spleen things are different. First there is a mechanism known as plasma skimming. Small arterioles known as penicillate arteries skim off the plasma and lymphocytes sideways, leaving the splenic arteries with red cells, platelets and much less plasma. The hematocrit rises from 40% to 80%. The arterioles drain not into capillaries but into sinusoids known as the Cords of Bilroth. Theodor Bilroth (1826-1894) is the father of abdominal surgery. His operations for stomach ulcers (Bilroth I and Bilroth II have only recently gone out of fashion). He was a great friend of Johannes Brahms and might have been a musician had it not been for his success in medicine.

These Bilroth Cords are lined with macrophages, and red cells delayed within them tend to get eaten. Escape from the Cords is through very narrow apertures only 1-2 microns in diameter. A red cell is 7 microns in diameter, but extremely flexible. Its shape as a biconcave disc means that it is able to squeeze through the opening. As a red cell ages it gets less flexible (like us all) and gets delayed. Red cells from some hereditary hemolytic anemias are less distensible - for example hereditary spherocytosis or pyropoikilocytosis - and tend to get trapped and eaten.

The macrophages that line the Cords have receptors for immunoglobulin. One of these receptors, FCR1 (or CD64) binds very avidly to immunoglobulin, but all the normal immunoglobulin in plasma tends to shield cells that are covered with antibody from binding to them. In the spleen the high hematocrit means that there is less plasma protecting antibody- coated red cells, and the macrophages start nipping off pieces of antibody-coated red cell membrane. Left with the same content but a smaller membrane, the red cell assumes the shape that contains the largest volume for the smallest surface area; in other words a sphere. Spheres cannot escape from the Cords of Bilroth.

Thus it is that taking out a spleen cures the hemolysis of hereditary spherocytosis and autoimmune hemolytic anemia.

When a spleen enlarges a much greater proportion of the red cells in the body are within it at any time. A normal spleen contains perhaps 100 mls of blood, a very large spleen ten times that amount. Platelets fare even worse; a very large spleen can contain 90% of the platelets in the body. There is no discernable pool of neutrophils in the spleen, however.


Andy said...

Prof. Hamblin,

What is the purpose of the spleen in a healthy organism?

Which brings up the second question: isn't there a disadvantage in losing our spleens to splenectomy?


Anonymous said...


A very interesting lesson in spleen-ology.

I suppose in the healthy individual, the older red blood cells are removed in the spleen, so that would be one purpose.

The spleen is also involved in some immune functions, I am given to understand. I believe those who have had their spleen removed are more susceptible to blood poisoning, to use a layman's term.

Marc said...

Well I have had to read this post several times, and I'm still not sure I quite understand it completely.

In trying to relate this post to your first post about spleens, referencing the short and long routes, I understand the short route is through the arterioles and the long route is through the splenic arteries?

And in a diseased spleen less blood gets skimmed into the arterioles, were the red cells tend to get eaten, leaving the remaining, which did not get skimmed, lost in the spleen? Is that a relatively accurate laymans interpretation? or am I way off base?

As far as the macrophages binding to the immunoglobulin, I just can't seem to get handle on that.

When you say, "In the spleen the high hematocrit means that there is less plasma protecting antibody- coated red cells", do you mean there is less immunoglobulin? So then the red blood cells get nipped away at by the macrophages, and get trapped?

I'm not sure how important it is for me to really understand all this, but when you have an enlarged spleen, it does become slightly more pertinent.

Terry Hamblin said...


Think of the spleen as a large filter on the blood stream. The quick way through is to by-pass the filter- that only takes a few seconds, but if you go through the filter it takes about an hour.

The plasma skimming is to divert most of the plasma and the white cells into the white pulp. This leaves the reamaining red cells going through the filter at a higher concentration. Should any of the red cells be coated with immunoglobulin they are succeptible to the immunoglobulin receptors on the macrophages. Normally these receptors are occupied by normal immunoglobuin from the plasma, but in the spleen most of the plasma has been skimmed off so the receptors can bind to the immunoglobulin on the red cells. There are macrophages elsewhere than the spleen - the liver and lungs for instance, but these cannot bind the red cells because their receptors are occupied by plasma immunoglobulin.

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