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Blood is a connective tissue with a fluid matrix. The components become apparent when a blood sample is spun in a centrifuge. Plasma is the clear extracellular matrix; it accounts for 55% of blood. The main component of plasma is water; it also contains proteins (albumin), nutrients, electrolytes, hormones, and gases. Plasma proteins play roles in blood clotting, the immune system, and the regulation of fluid volume. Plasma without clotting proteins is called serum. Formed elements include erythrocytes (red blood cells, or RBCs), leukocytes (white blood cells, or WBCs), and platelets); they make up 45% of blood. RBCs are the heaviest of the formed elements and sink to the bottom of the sample. This percentage of RBCs in a sample of blood is called the hematocrit. WBCs and platelets form a narrow buff-colored band just underneath the plasma. Called the buffy coat, these cells constitute 1% or less of the blood volume. The combination of plasma and blood cells determines the viscosity (“stickiness”) of blood.
Red bone marrow is found in the ends of long bones and in flat irregular bones such as the sternum, cranial bones, vertebrae, and pelvis. Lymphatic tissue is found in the spleen, lymph nodes, and thymus gland.
An RBC’s disklike shape provides a large surface area through which oxygen and carbon dioxide can diffuse. RBCs lose almost all of their organelles during development; because they lack a nucleus and DNA, they cannot replicate. The cytoskeleton of the RBC contains stretchable fibers that make it flexible, allowing it to fold and stretch as it squeezes through tiny capillaries and then spring back into shape.
More than a third of the interior of a red blood cell (RBC) is filled with hemoglobin—a red pigment that gives blood its color. Hemoglobin consists of four ribbon-like protein chains called globins; bound to each globin is an iron-containing molecule called heme. Each heme molecule can combine with one molecule of oxygen; therefore, one hemoglobin molecule can unite with four molecules of oxygen to form oxyhemoglobin. (Hemoglobin also carries CO2, but instead of binding with heme, CO2 binds with globin.) How much oxygen the blood can carry depends on the quantity of RBCs and hemoglobin it contains.
RBCs circulate for about 120 days; they then die, break up, and are consumed by phagocytic cells in the spleen and liver. The body constantly produces RBCs to maintain homeostasis: a process called erythropoiesis. The process is maintained through a negative feedback loop: Oxygen levels decline as damaged RBCs are removed from circulation. Kidneys detect decreasing oxygen levels and secrete hormone EPO. EPO stimulates red bone marrow to create new erythrocytes. Immature erythrocytes (called reticulocytes) are released into circulation. After 1 to 2 days, reticulocyte becomes mature erythrocyte. Increased number of RBCs causes oxygen levels to increase; less EPO is produced and RBC production declines.
Macrophages in the liver and spleen ingest and destroy old red blood cells (RBCs). In the process, hemoglobin is broken into its two components: globin and heme. Globin is broken down into amino acids, which are used for energy or to create new proteins. Heme is broken down into iron and bilirubin: iron is used to create new hemoglobin, and bilirubin is excreted into intestines as part of bile. When the destruction of RBCs becomes excessive (hemolysis), the body can’t assimilate the increased amounts of bilirubin. The excess bilirubin enters the tissues, causing the skin and sclera to take on a yellowish hue (jaundice).
Leukocytes are the fewest of the formed elements. The body contains five types of white blood cells (WBCs)—all different in size, appearance, abundance, and function. All leukocytes contain a nucleus. Leukocytes contain other internal structures that look like granules when stained and examined under a microscope. Granulocytes have obvious granules; agranulocytes have few or no granules. Granulocytes contain a single multilobular nucleus. The three types of granulocytes are neutrophils, eosinophils, and basophils. Agranulocytes include lymphocytes and monocytes. Note: A chart in the textbook details the characteristics, functions, and life cycles of the various WBCs.
Platelets (also called thrombocytes) are the second most abundant of the formed elements; they play a key role in stopping bleeding (hemostasis). Platelets are fragments of larger bone marrow cells (called megakaryocytes). The edges of the megakaryocyte break off to form cell fragments called platelets. Platelets live only about 7 days.
When a blood vessel is cut, the body must react quickly to stop the flow of blood. It does so through the following sequence of events: vascular spasm, the formation of a platelet plug, and the formation of a blood clot. As soon as a blood vessel is injured, smooth muscle fibers in the wall of the vessel spasm, which slows flow of blood.
The break in the blood vessel exposes collagen fibers, creating a rough spot on the vessel’s normally slick interior. This rough spot triggers transforms passing platelets into sticky platelets. Sticky platelets stick to the vessel wall and to each other, forming a platelet plug. The platelets facilitate clumping by secreting several chemicals: Some cause the vessel to constrict further, whereas others attract more platelets. The platelet plug forms a temporary seal in the vessel wall. A more stable solution requires the formation of a clot.
Blood clotting (coagulation) involves a complex series of chemical reactions using proteins called clotting factors. The first several reactions vary, depending on whether the process has been stimulated by factors inside or outside the blood. When the damaged blood vessel and surrounding tissues (areas outside or extrinsic to the blood) release clotting factors, a cascade of events called the extrinsic pathway begins. When the clotting factors are activated within the blood (such as by the platelets as they adhere to the collagen in the damaged vessel wall), a cascade of events called the intrinsic pathway begins. The extrinsic pathway activates factor X through a single reaction; the intrinsic pathway requires four different reactions to activate factor X. Once factor X is activated, the formation of a blood clot follows a common pathway.
Common pathway begins with production of an enzyme called prothrombin activator. Prothrombin activator acts on a globulin called prothrombin (factor II), converting it to the enzyme thrombin. Thrombin transforms the soluble plasma protein fibrinogen into fine threads of insoluble fibrin. Sticky fibrin threads form a web at the site of the injury. Red blood cells and platelets flowing through the web become ensnared, creating a clot of fibrin, blood cells, and platelets. A blood clot can effectively seal breaks in a smaller vessel; blood clotting alone may not stop a hemorrhage from a large blood vessel.
Soon after the blood clot forms, platelets trapped within the fibrin web contract, pulling the edges of the damaged vessel closer together. After the vessel has healed, a chain of reactions converts an inactive plasma protein (plasminogen) into plasmin. Plasmin dissolves the fibrin meshwork and the clot breaks up. This process is called fibrinolysis.
It is important to prevent formation of unwanted clots. A smooth endothelium prevents platelets from sticking. Normal circulation dilutes thrombin (which is normally present in small amounts); when blood pools in legs (such as during prolonged sitting or lying down), thrombin can accumulate and lead to clot formation. Basophils and mast cells secrete heparin, which blocks action of thrombin. An unwanted blood clot inside of a vessel is called a thrombus. If a piece of the clot breaks off and circulates through the bloodstream, it is called an embolus.
The surface of each red blood cell carries a protein called an antigen (also called agglutinogen). There are two antigens: A and B. People with type A blood have the A antigen on their RBCs. People with type B blood have the B antigen. People with type AB blood have both A and B antigens. People with type O blood have neither antigen.
Whereas the blood cell carries antigens, the blood plasma carries antibodies (called agglutinins) against the antigens of the other blood types. Type A blood has anti-B antibodies. Type B blood has anti-A antibodies. Type AB blood has no antibodies. Type O blood has both anti-A and anti-B antibodies.
Transfusions are successful as long as the recipient’s plasma does not contain antibodies against the ABO type being transfused. If such antibodies are present, they will attack the donor’s RBCs, causing a transfusion reaction. The clumping of RBCs blocks blood vessels, cutting off the flow of oxygen. The RBCs also burst (hemolysis) and release their hemoglobin into the bloodstream. The free hemoglobin could block tubules in the kidneys, leading to renal failure and possibly death.
Blood is also classified as Rh positive or Rh negative. Rh-positive blood contains the Rh antigen; Rh-negative blood lacks this specific antigen. Blood does not normally contain anti-Rh antibodies. Someone with Rh-negative blood develops anti-Rh antibodies after being exposed to Rh-positive blood (either through a transfusion or when an Rh-negative mother becomes pregnant with an Rh-positive fetus). If someone with Rh-negative blood receives a transfusion of Rh-positive blood, the person’s body interprets the Rh antigen as something foreign. To protect itself, it develops anti-Rh antibodies. If the person receives a subsequent transfusion of Rh-positive blood, the anti-Rh antibodies formed during the first transfusion will attack the Rh antigen in the donor blood, causing agglutination.
A similar condition may result when a woman with Rh-negative blood and a man with Rh-positive blood conceive a baby who is Rh-positive. Because maternal and fetal blood does not mix, the first pregnancy with an Rh-positive fetus will proceed normally. During delivery (or miscarriage), the fetus’s blood often mixes with that of the mother, thus introducing Rh antigens into the mother’s bloodstream.
3. The mother’s body responds by forming anti-Rh antibodies against this foreign substance. 4. In a subsequent pregnancy with another Rh-positive baby, the anti-Rh antibodies can pass through the placenta even if the red blood cells (RBCs) can’t. They attack the fetal RBCs, causing agglutination and hemolysis. The infant develops a severe anemia called erythroblastosis fetalis.