Veins returning blood Veins have large radii and

Veins returning blood Veins have large radii and low resistance. Walls are thin, not elastic Most blood volume is in veins

Veins Valves prevent engorgement and backflow Sympathetic NS constricts veins to increase venous return Skeletal muscles also help return

Baroreceptor reflex Baroreceptors detect fluctuations in blood pressure and send info to medulla Signals go to ANS Baroreceptors

Response to low pressure

Problems with vessels Aneurysm Hemorrhage Why do aneurysms form? Hypertension, inflammation, arteriosclerosis, genetics… How are they treated?

Blood pressure problems Hypertension – Blood pressure over 140/90 Baroreceptors can adjust to higher BP High BP puts stresses on vessels, elasticity (atherosclerosis, strokes) and stresses on heart (heart attacks), kidneys

Blood pressure problems Treatments for hypertension: Low salt diet, reduce stress, increase exercise ACE inhibitors (reduce blood volume) Alpha, beta blockers (reduce sympathetic effects) Calcium blockers (reduce cardiac contractions)

Blood pressure problems Circulatory shock – blood pressure drops too low to serve tissues. From weak heart, blood loss, dilation from allergic response Body compensates w/sympathetic signals, fluid shifts

Components of blood Plasma Blood cells: erythrocytes (RBC) leukocytes (WBC), and platelets Hematocrit is the % of blood occupied by RBC.

What is plasma? Ions: mostly Na+ and Cl-. Gasses, waste, nutrients, hormones Plasma proteins: Albumins establish an osmotic gradient, carry some hormones Globulins (alpha, beta, gamma) transport molecules, serve as antibodies Fibrinogen - blood clotting

RBCs have no nuclei, ribosomes, or organelles Packed with hemoglobin “Doughnut-like” shape

Hemoglobin Heme - contains iron and binds with one molecule of O 2 Globin - 4 protein chains Turns bright red when combined with oxygen CO 2, CO, H+ can also bind

RBCs replenished every second Spleen removes old RBCs, RBCs last about 4 months RBCs are produced in bone marrow from pluripotent stem cells (2 M/sec)

Kidney controls RBC production Kidney is sensitive to anemia and releases erythropoietin

Blood doping Banned in competitive sports: Erythropoietin (EPO) can be synthesized and injected to enhance endurance An athlete’s own blood can be stored and reinjected to boost RBC’s Hematocrit can detect

Causes of anemia? Anemia – O 2 to tissues is low Due to RBC, erythropoiesis, or hemoglobin “Pernicious anemia” – lack of B 12 results in low RBC production Aplastic anemia – bone marrow production

How the body repairs itself Initial response: vascular spasm - reduces blood flow through the vessel platelet plug - Aggregation of platelets. Platelets attach to areas with exposed collagen These processes are stimulated by ADP

Platelets are cell fragments that are functional for 10 days Reduce blood loss (maintain hemostasis) Platelets and a RBC

Positive feedback at injury site Initial stimulus is exposed collagen Repair is contained to site of injury Inhibits platelet aggregation Prostacyclin and nitric oxide Vessel wall 3 ADP Platelets Inhibits platelet aggregation 2 4 Normal endothelium Plug 1 Injury site Prostacyclin and nitric oxide 5 Normal endothelium

How the body repairs itself Stopping blood loss: Fibrinogen (plasma protein) is converted into fibrin (thread-like protein). This conversion is catalyzed by thrombin Fibrin threads trap RBCs, forming a clot

How the body repairs itself Stopping blood loss: Fibrinogen (plasma protein) is converted into fibrin (thread-like protein). This conversion is catalyzed by thrombin Fibrin threads trap RBCs, forming a clot Thrombin is formed from inactive prothrombin in plasma

The clotting cascade. . . ! Clotting cascade is a series of reactions activating enzymes in a series. . . final conversion is fibrinogen into fibrin

Vessel damage Exposed collagen Platelet aggregation PF 3 Hageman factor Cascade is initiated when a platelet plug is present or from exposed collagen. Activation of next thrombin Activation of thrombin Formation of fibrin meshwork Damaged vessel is sealed Clotting cascade

Clots are temporary Fibroblasts form scar tissue for vessel repair. The clot is dissolved slowly by the enzyme plasmin (breaks down fibrin). Plasmin is activated by the clotting cascade Phagocytic WBC remove the products of clot breakdown

Ok, but what is pus? Well, pus comes from infected wounds and consists of phagocytes, dead tissue and bacteria.

White blood cells There are five kinds of WBCs defend against pathogens, cancer and clean up debris

Introduction to the WBCs Granulocytes Eosinophils - attack parasitic worms Basophils - make and store histamine and heparin Neutrophils - phagocytes, 1 st to respond to infection Monocytes - settle in tissue and become macrophages Lymphocytes Neutrophil B and T cells of specific immune response Eosinophil Monocyte Lymphocyte Basophil

Production of WBCs Produced from pluripotent stem cells in bone marrow Lymphocytes made in lymph tissue during adulthood Two-thirds of the leukocytes in the blood are granulocytes, mainly neutrophils

Immune system Body must resist disease in order to function Defends against pathogens, identifies and destroys abnormal cells. The primary pathogens are bacteria and viruses.

Nonspecific immunity vs. Adaptive immunity Nonspecific responses work immediately - 1 st line of defense. Neutrophils, macrophages, inflammation, MAC attack Adaptive immunity specifically targets certain pathogens to which the body has been exposed B and T lymphocytes, antibodies

Nonspecific response: inflammation Redness and warmth Blood flow due to vasodilation Swelling Increased capillary permeability Pain inflamed knee Nociceptors stimulated by fluid pressure

Inflammation : the beginning First response involves cells already in nearby tissue: macrophages and mast cells Macrophages ‘eat’ bacteria Triggered by infection, mast cells secrete histamine, causing vasodilation Fibrin walls off infection Guided by chemotaxins, neutrophils and monocytes go to the area Mast cells in tissue

How do phagocytes know what to eat? Bacteria get labeled for destruction by opsonins Opsonins are made from complement cascade, helper T cells, antibodies Bacteria acquire opsonins, getting labeled for macrophage to engulf it

Phagocytes also send signals They present antigens to helper T-cells to induce a specific response They ‘wear what they eat’

plasma proteins histamine (including opsonins and chemotaxins) Phagocytes: stimulate histamine release, trigger clotting cascade, release pyrogen which causes fever, induce more WBC

Review

What do those plasma proteins do? Some are clotting proteins. . clotting cascade! Some are antibodies! (discussed later) Some are part of the complement system! (discussed now…)

Nonspecific response : Complement system Complement = cascade of plasma proteins Cascade activated by molecules on surface of bacteria or antibodies Complement proteins are opsonins, chemotaxins or form MAC attack MAC

Bacterial wall has holes from membrane attack complex Complement has the potential to be very damaging to host tissues

Nonspecific response: What about viral infections? Infected cells release interferon Cause neighboring cells to produce virusfighting enzymes Attracts natural killer cells Host Nasty virus Interferon

Adaptive immune response Also fights viral and bacterial infections but uses B and T lymphocytes found in lymph Pathogens have particular antigens, which induce a specific response from B and T cells. Only cells with the antigen are attacked.

B cell response B lymphocytes respond to bacteria and toxins An antigen stimulates some specific B cells to become plasma cells and produce antibodies Contact with antigen can occur via macrophages

B cell response How antibodies work antigen bacteria binding site for this specific antigen Labels cell to be killed Once labeled, bacteria killed by: MAC attack Phagocytosis Killer cells

Result of labeling