Red blood cells (formally called erythrocytes) are the next most plentiful component, constituting about 44 percent of the total volume of the blood. Red blood cells are exquisitely designed to do one job: deliver oxygen. They are very small but superabundant. A teaspoon of human blood contains about twenty-five billion red blood cells, and each one of those twenty-five billion contains 250,000 molecules of hemoglobin, the protein to which oxygen willingly clings. Red blood cells are biconcave in shape—that is, disk shaped but pinched in the middle on both sides—which gives them the largest possible surface area. To make themselves maximally efficient, they have jettisoned virtually all the components of a conventional cell—DNA, RNA, mitochondria, Golgi apparatus, enzymes of every description. A full red blood cell is almost entirely hemoglobin. It is essentially a shipping container. A notable paradox of red blood cells is that although they carry oxygen to all the other cells of the body, they don’t use oxygen themselves. They use glucose for their own energy needs.
Hemoglobin has one strange and dangerous quirk: it vastly prefers carbon monoxide to oxygen. If carbon monoxide is present, hemoglobin will pack it in, like passengers on a rush-hour train, and leave the oxygen on the platform. That’s why it kills people. (About 430 of them a year in the United States unintentionally, and a similar number by suicide.)
Each red corpuscle survives for about four months, which is pretty good going considering what a jostling and busy existence it leads. Each will be shot around your body about 150,000 times, logging a hundred miles or so of travel before it is too battered to go on. Then these corpuscles are collected by scavenger cells and sent to the spleen for disposal. You discard about a hundred billion red blood cells every day. They are a big component of what makes your stools brown. (Bilirubin, a by-product of the same process, is responsible for the golden glow of urine as well as the yellow blush of fading bruises.)
* * *
—
White blood cells (or leukocytes) are vital for fighting off infections. In fact, they are so important that we will treat them separately in chapter 12, on the immune system. For the moment, it is enough to know that they are much less numerous than their red siblings. You have seven hundred times as many red blood cells as white ones, which constitute less than 1 percent of the total.*3
Platelets (or thrombocytes), the final part of the blood quartet, also account for less than 1 percent of blood’s volume. Platelets were for a long time a mystery to anatomists. They were first seen under a microscope in 1841 by a British anatomist named George Gulliver, but they weren’t named or properly understood until 1910 when James Homer Wright, chief pathologist at the Massachusetts General Hospital in Boston, deduced their central role in clotting. Clotting is a tricky business. The blood must be perpetually on alert to clot at a moment’s notice, but equally mustn’t clot unnecessarily. As soon as a bleed starts, millions of platelets begin to cluster around the wound and are joined by similarly vast numbers of proteins, which deposit a material called fibrin. This agglomerates with the platelets to make a plug. To try to avoid errors, no fewer than twelve fail-safe mechanisms are built into the process. Clotting doesn’t work in the principal arteries, because the flow of blood is too fierce; any clot would be swept away, which is why major bleeds must be stopped with the pressure of a tourniquet. In severe bleeding, the body does all it can to keep blood flowing to the vital organs and diverts it away from secondary outposts like muscles and surface tissues. That’s why patients who are bleeding heavily turn a cadaverous white and are cold to the touch. Platelets live for only about a week, so must be constantly replenished. In the last decade or so, scientists have realized that platelets do more than just manage the clotting process. They also play important roles in immune response and in tissue regeneration.
* * *
—
For the longest time, almost nothing was known about the purpose of blood beyond that it was somehow vital to life. The prevailing theory, dating since the time of the venerable but frequently mistaken Greek physician Galen (ca. 129—ca. 210), was that blood was manufactured continuously in the liver and used up by the body as fast as it was made. As you will doubtless recall from your school days, the English physician William Harvey (1578–1657) realized that blood is not endlessly consumed, but rather circulates in a closed system. In a landmark work called Exercitatio anatomica de motu cordis et sanguinis in animalibus (On the Motion of the Heart and Blood in Animals), Harvey outlined all the details of how the heart and circulatory system work, in more or less the terms we understand today. When I was a schoolboy, this was always presented as one of those eureka moments that changed the world. In fact, in Harvey’s day the theory was almost universally ridiculed and rejected. Nearly all Harvey’s peers thought him “crack-brained,” in the words of the diarist John Aubrey. Harvey was abandoned by most of his clients and died a bitter man.
Harvey didn’t understand respiration, so couldn’t explain what purpose blood served or why it circulated—two pretty glaring deficiencies, as his critics were quick to point out. Galenists additionally believed that the body contains two separate arterial systems—one in which the blood is bright red and another in which it is much duller. We now know that blood traveling from the lungs is full of oxygen and therefore shiny crimson, while blood returning to the lungs is depleted of oxygen and thus rather duller. Harvey couldn’t explain how blood circulating in a closed system could be of two colors, which became yet another reason to scorn his theories.
The secret of respiration was deduced not long after Harvey’s death by another Englishman, Richard Lower, who realized that blood dulls in color on its way back to the heart because it has given up its oxygen, or nitrous spirit, as he called it. (Oxygen wouldn’t be discovered until the following century.) That, Lower reasoned, was why blood circulated, to continuously pick up and discharge nitrous oxide, which was quite a big insight and one that should have made him famous. In fact, Lower is remembered more now for another aspect of blood. In the 1660s, Lower was one of several eminent scientists who became interested in the possibility of saving lives through blood transfusions, and he became involved in a series of often gruesome experiments. In November 1667 before an audience of “considerable and intelligent persons” at the Royal Society in London, and without having any idea at all what the consequences might be, Lower transfused about half a pint of blood from a live sheep into the arm of an amiable volunteer named Arthur Coga. Then Lower and Coga and all the distinguished onlookers sat keenly for many minutes waiting to see what would happen. Happily, nothing did. One of those present reported that Coga afterward was “well and merry, and drank a glass or two of canary, and took a pipe of tobacco.”
Two weeks later, the experiment was repeated, again without ill effect, which is really surprising. Normally, when foreign substances are introduced in volume into the bloodstream, the recipient goes into shock, so why Coga escaped a miserable experience is puzzling. Unfortunately, the results emboldened other scientists across Europe to conduct transfusion tests of their own, and these took on an increasingly inventive, not to say surreal, cast. Volunteers were transfused with milk, wine, beer, and even mercury, as well as the blood of every species of domesticated creature. The results all too often were distressingly agonized, embarrassingly public deaths. Very quickly transfusion experiments were banned or fell into abeyance, and for about a century and a half they remained out of favor.