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UCONN / Physiology / PNB 2265 / cardioacceleratory center

cardioacceleratory center

cardioacceleratory center


School: University of Connecticut
Department: Physiology
Course: Human Physiology and Anatomy
Professor: Kristen kimball
Term: Spring 2016
Cost: 25
Name: Anatomy Week 5
Description: Lectures 12, 13, 14
Uploaded: 02/21/2017
11 Pages 132 Views 0 Unlocks

How are Phagocytes Mobilized?

What are the "chemical alarms" that, when released into the extracellular fluid, mediate the events of inflammation?

o What organelles are present?

Part 2: Blood Pressure Regulation The Blood Pressure Roadmap ∙ Regulation of Mean Arterial Pressure ∙ MAP = CO * TPR o CO = SV * HR  SV = EDV – ESV o Major regulatory control of TPR = arteriolar radius o Due to conductive AND contractile myocytes ∙ Two basic types of control o Short term FAST controls  Nervous ∙ Autonomic  Hormonal o Long term SLOW controls  Kidney ∙ MAP: mean arterial pressure (BP) ∙ TPR: total peripheral resistance ∙ CO: cardiac output ∙ SV: stroke volume ∙ HR: heart rate ∙ EDV: end diastolic volume ∙ ESV: end systolic volume Cardiovascular Control Center ∙ Located in Medulla ∙ Cardioacceleratory Center (Stimulatory)o Cardiac Nerve o Controls Sympathetic Innervation  Conductive and contractile myocytes o Increases MAP ∙ Cardioinhibitory Center (Inhibitory) o Vagus o Controls Parasympathetic Innervation  Only conductive o Decreases MAP ∙ If you activate sympathetic nervous system, you can influence strength and  speed of cardiac contraction and adrenergic receptors on arteriole o Majority of peripheral blood vessels have adrenergic o Constrict blood vessels and increase TPR and cardiac output o Increase MAP ∙ Parasympathetic does not innervate arterioles o Still decreases MAP by reducing frequency of AP in conductive cardiac  myocytes  Reduce cardiac output Sensing Changes in MAP: Baroreceptor Reflex ∙ Arterial baroreceptors are mechanoreceptors located in: o Carotid sinuses o Aortic Arch o Glosso-pharyngeal nerve (IX) ∙ Baroreceptors sense change in pressure by sensing blood flow in vessels o Send afferent signals to change cardiac control centers o Increased pressure activates baroreceptors to activate inhibition center  and inactivate activation center o Decreased BP because change TPR and CO Effect of MAP on Firing Rate ∙ Increasing arterial pressure increases carotid sinus firing rate ∙ Maximal baroreceptor sensitivity occurs near normal MAP ∙ MAP increases, frequency of APs increases too ∙ Sigmoidal: change in AP frequency is most sensitive around normal MAP o Maintaining homeostasis o Small change can have big response Chemoreceptor Reflex: Fast Nervous Control ∙ Sensory neurons located in o Aortic bodies o Carotid bodies ∙ Sensitive to O2; CO2 ∙ Decreased O2, Increased CO2 and Decreased pH: o Stimulate chemoreceptors à o Stimulate excitatory cardiovascular control centers, to cause  Peripheral vasoconstriction  Increased CO, and thus  Increased MAP Hormonal Control: Fast ∙ Adrenal medullao NE (vasoconstrictive) o * EPINEPHRINE o Fight or flight response activates sympathetic nervous system response  Alpha adrenergic receptors  Vasoconstriction  Increase cardiac output and TPR ∙ Effects of EPI o Peripheral vasoconstriction (Increase TPR) o Increase CO by Decreasing ESV ∙ HOW? Increase HR and increase strength of cardiac contraction. Does what to  ESV? Latter DECREASES ESV, which INCREASES SV, increases CO ∙ Atrial Natriuretic Peptide o ↑ MAP, volume (in atria) à ANP à vasodilation àdecreased MAP ∙ ADH (Antidiuretic Hormone; Vasopressin) o ↓ blood volume (and MAP); or ↑ osmolarity; or circulating AII à ↑ ADH à water conservation à ↑ MAP o Controls plasma volume  High PV high BP o ONLY plasma volume ∙ Renin/Angiotensin (AII) /Aldosterone System (RAAS) o Covered in detail with Renal Physiology o AII à peripheral vasoconstriction o Note: With RAAS, we are making a transition from “Fast” hormonal control to “Slow” control o Kidney o Plasma levels AND vasoconstriction Changes in Posture: Orthostatic Hypotension ∙ Stand up to fast Hemorrhage & Compensation ∙ Excessive plasma loss ∙ Regulates cardiac output ∙ Trauma, can’t compensate ∙ Increase stroke volume and contractility, vasoconstrict ∙ Elevates MAP back to homeostatic set point Cardiovascular Effects of Hemorrhage ∙ Large change in volume encourages long loop involves structures in kidney Exam II Defense Mechanisms of the Body I: Non-Specific (Innate Immune Defenses) Non-specific (innate immune) v. specific (adaptive immune) defense mechanisms ∙ Analogy (courtesy of Dr. Moiseff): Bank walls (keep robbers out) vs. surveillance  camera (to identify specific bank robber)  Role of Immune (Specific Responses) ∙ Defend/Protect against infection by microbes: viruses, bacteria, fungi, other  parasites ∙ Immune surveillance ∙ Elimination of damaged cells∙ "Negative" aspect: Allergies/hypersensitivity, autoimmune diseases, organ  transplant reactions.  Overview of Lymphatic System ∙ Lymph ∙ Lymphatic vessels o Capillaries are blind-ended, located at vascular capillary beds c) Lymphoid  tissues / lymphoid organs  ∙ Primary: Bone marrow and Thymus ∙ Secondary: lymph nodes, spleen, peyer’s patches, tonsils ∙ Functions o Body fluid homeostasis o Immune system ∙ Filters out more fluid than you reabsorb in your capillary bed and the lymphatic  system picks it up (lymph) Lymphoid organs (all have a fibrous connective tissue capsule) ∙ Primary lymphoid organs = bone marrow and thymus (“lymphoid tissue”)  o Bone marrow  Site of maturation for B lymphocytes; production of all leukocytes  Makes lymphocytes  o Thymus  Site of maturation for T lymphocytes ∙ Can recognize specific antigens using receptors ∙ Can see or identify  Lymph nodes Lymphoid Organs: Lymph Nodes ∙ Capsule of fibrous tissue; partitions (differentiated from nodules) o Fibrous capsule encloses organs o Lymph nodes have this capsule, so they are organs ∙ Vessels o Including afferent and efferent lymphatic vessels ∙ Macrophages o Cellular clean up ∙ 99% antigens removed; processed ∙ Filters ∙ Dendritic cells o Found in certain tissues; if activated migrate to lymph nodes to present  antigen o Spleen: lymphoid tissue Lymphatic nodules ∙ Lymphocytes densely packed in loose connective tissue ∙ No capsule ∙ Found in connective tissue under epithelium of respiratory, digestive, urinary  tracts o All different ports of entry ∙ Examples: Tonsils, Peyer’s patches o Peyer’s patches in small intestine; nodules in appendix Lymphnoid Organs: Spleen∙ Remove RBCs ∙ Store Fe ∙ May initiate immune response Note – you may encounter these terms ∙ GALT o Gut-associated lymphatic tissue o Also called “MALT” or mucosa-associated lymphatic tissue Recall ∙ Derivation of different blood cells from hemocytoblasts ∙ Myeloid stem cells o All cell types except lymphocytes ∙ Lymphoid stem cells Cells Mediating Immune Responses  ∙ Leukocytes – All from the bone marrow  o Neutrophils: Inflammation; phagocytosis  o Basophils: Produce histamine, heparin  o Eosinophils: worms  o Monocytes: Become macrophages  o Lymphocytes – Specific Immune responses  All (except NK cells) participate in specific immune responses  B cells – specific immune; antibody-mediated   T cells – specific immune; cell-mediated ∙ Cytotoxic ∙ Helper ∙ Suppressor   NK (Natural Killer) cells ∙ A type of lymphocyte but non-specific ∙ Respond to a variety of abnormal antigens – not specific like  T’s and B’s Other Cells Derived from White Blood Cells ∙ Macrophages: phagocytosis o Large phagocytes o May leave circulatory systemother tissues  Kupffer cells in liver o Need to combat things that come into your immune system ∙ Mast cells: histamine ∙ Plasma cells o Effector B cells that produce antibodies o Removes recognition of antigen, exact copy of the receptor found on the  original cell  Derived from B cell that recognizes o What organelles are present? Why?  Nucleus  Extensive endoplasmic reticulum ∙ Making protein, transcription, translation Dendritic Cells ∙ Highly motile∙ Not macrophages o Able to phagocytose ∙ Found in almost all tissues o Especially “ports of entry” where external and internal environment meet Other Defense Mechanisms  ∙ Detoxification o Usually by liver o Microsomal enzyme system  Located in smooth ER of hepatic cells o By metabolic conversion of foreign chemicals (such as EtOh and other  drugs) ∙ Stress Syndrome  o Stress causes sympathetic nervous signals to adrenal medullae o Adrenal medullae release catecholamines into bloodstream o Fight or flight reaction causes reactions in multiple parts of the body Non-Specific Defense Responses Non-Specific Defense ∙ No specific recognition of identity of foreign cell/matter o These responses protect against foreign matter without having to  specifically recognize its identity ∙ Some response regardless of stimulus o You get the same response regardless of invading pathogen ∙ Prevention first o Easier than curing Non Specific (Innate Immune) Defenses: Look at ∙ First line of defense o Physical and chemical barriers ∙ Inflammation ∙ Role of phagocytes ∙ Complement system ∙ Immunological surveillance ∙ Antimicrobial proteins (interferons) ∙ Fever Non-Specific Defense Responses Non-Specific Defense ∙ No specific recognition of identity of foreign cell/matter o These responses protect against foreign matter without having to  specifically recognize its identity ∙ Some response regardless of stimulus o You get the same response regardless of invading pathogen ∙ Prevention first o Easier than curing Non Specific (Innate Immune) Defenses: Look at ∙ First line of defense o Physical and chemical barriers∙ Inflammation ∙ Role of phagocytes ∙ Complement system ∙ Immunological surveillance ∙ Antimicrobial proteins (interferons) ∙ Fever "First Line of Defense" ∙ External Anatomic and Chemical Barriers o Skin and mucous membranes ∙ Unbroken epidermis is a formidable physical barrier to most microorganisms that swarm on the skin o Keratin is also resistant to most weak acids and bases, and to bacterial  enzymes and toxins o Similar physical/mechanical barriers are provided by intact mucosae within the body o Note that the mucosae, by virtue of lining the body cavities that open to  the exterior, are themselves exposed to the external environment. ∙ A variety of protective chemicals are produced by these epithelial membranes o Acidity of skin secretions  Inhibits bacterial growth o Stomach mucosa secretes HCl and proteolytic enzymes o Saliva contains lysozyme  Destroys bacteria o Sticky mucus  Traps microorganisms that enter the digestive and respiratory  passageways ∙ Other factors include ciliated mucosa of respiratory system, hairs, "friendly"  micoorganisms, etc o E.g.: macrophages in alveoli; Kupffer cells in liver. Subcutaneous tissue  contains macrophages and mast cells ∙ If this physical barrier is somehow breached, for example by a cut, other non specific mechanisms come into play, including the inflammation response (next) The Inflammation Response ∙ May be set off by o Physical trauma o Intense heat o Irritating chemicals o Infection by pathogens ∙ Inflammation walls off infection to prevent spread ∙ In summary, the events that occur during the inflammation response serve to  "wall off" an infection, preventing the spread of damaging agents to nearby  organs; dispose of cell debris and pathogens; and set the stage for repair  processes. This nonspecific defense may be set off by physical trauma, intense  heat, and irritating chemicals as well as by infection by microorganisms ∙ Sequence of events: Refer to class diagram.  What are the "chemical alarms" that, when released into the extracellular fluid,  mediate the events of inflammation? They include: ∙ Histamineso Released from mast cells, promote vasodilation and increased capillary  permeability ∙ Kinins o e.g. bradykinin o Cleaved from plasma protein kininogen o Similar effects to histamine plus induce chemotaxis of leukocytes and  stimulate neutrophils to release lysosomal enzymes   (Enhancing generation of more kinins) o Induce pain o Vasodilation, capillary permeability, chemotaxis ∙ Prostaglandins o Eicosanoids (derived from arachidonic acid) o Sensitize blood vessels to effects of other inflammatory mediators o Induce pain ∙ Complement o Antimicrobial protein that lyses microorganisms o Enhances phagocytosis by opsonization o Intensifies inflammatory response (See "antimicrobial proteins" below.)  ∙ Other cytokines (“cell chemicals”) which act as mediators/signals for  inflammation o May also play roles in specific defense mechanisms:  o Factors released by injured cells  Causes release of neutrophils form bone marrow o Opsonins  Stimulate phagocytosis  How are Phagocytes Mobilized? ∙ Neutrophils enter blood from bone marrow o Travel to damaged area ∙ “Margination” (pavementing) o Neutrophils adhere to vessel wall ∙ Diapedesis o Neutrophil moves through capillary wall, which is more permeable during  inflammation response, and moves into tissue space ∙ Positive chemotaxis o Neutrophils move (by ameboid movement) toward site of inflammatory  response, following the “chemical trail” of inflammatory chemicals  diffusing away from the inflamed site Process of phagocytosis – Fig. 18.4V  ∙ Intracellular desctruction of microbe Complement System ∙ Group of at least 20 different plasma proteins that normally circulate in the  blood in an inactive state ∙ Major mechanism for destroying foreign substances in the body o >20 plasma proteins o Activated via cascade o Two pathways for activation: classical ad alternative ∙ Proteins are designated C1 - C9, and factors B, D, and P (properdin).  ∙ Once activatedo A cascade occurs in which chemical mediators are unleashed to amplify  virtually all aspects of the inflammatory process o Other complement proteins kill bacteria and other cell types by lysis  Directly lyse target cells vis membrane attack complex o Oponization  Enhance phagocytosis (through chemotaxis) Complement can be activated by either of two pathways:  ∙ Classical pathway o Antigen-antibody complex initiates compliment fixation o C1 binds constant (Fc) region of antibody  The classical pathway, which depends on binding of antibodies to  invading organisms and the subsequent binding of C1 to the  antigen-antibody complex (a step called complement fixation) ∙ Activated by C1 ∙ Alternative pathway o Polysaccharides on cell surfaces of certain fungi and bacteria o Secrete factors B, D, etc. o The alternate complement pathway is commonly triggered by an  interaction between factors B, D, and P and polysaccharide molecules  present on the surface of certain microorganisms (bacteria and fungi).  ∙ C3 hydrolysis o Each pathway involves a cascade in which complement proteins are  activated in an orderly fashion, each causing catalysis of next step  Both pathways ultimately converge on C3, cleaving it into two  fragments (C3a and C3b), and initiating a common terminal pathway that causes cell lysis, promotes phagocytosis, and enhances  inflammation ∙ C3b (AKA “activated C3”) binds the target cell's surface, which has 2 effects:  o Triggers insertion of MAC (membrane attack complex)  Forms hole in membrane; and by coating the  surface of the microorganism, C3b molecules  attract macrophages and neutrophils to adhere to  and phagocytize the particle  Process = opsonization Function ∙ Increase/enhance inflammatory response; ∙ Kill bacteria and other cell types. ∙ Mechanism by which “tagged” (antibody-bound) antigens are targeted for  destruction o Involves the specific immune system Antimicrobial Proteins  ∙ Protein family with antiviral effects o Host (not virus) specific o Interfere with viral replication, stimulate NK cells, and stimulate  macrophages ∙ Interferon: Family of related small proteins with antiviral effects o Not virus-specific, but are host-specifico Once secreted by virus-infected cells, they diffuse to nearby cells and  stimulate the synthesis of other proteins which inhibit or “interfere" with  viral replication in those cells o They are produced by a variety of different body cells. Interferons activate  other cells to prevent viral entry  Inhibit viral replication, and stimulate NK cells and macrophages ∙ Type I Interferons o Produced by most cell types; stimulate cells to produce antiviral proteins;  include   Alpha interferons  ∙ Produced by leukocytes; produce antiviral proteins ∙ Type II Interferons include  o Gamma interferons  Produced by Helper T cells  Help activate Tc and B cells during specific immune response  Toll-Like Receptors (TLRs) ∙ Many pathogens share molecular features known as PAMPs (pathogen  associated molecular patterns) ∙ Certain immune cells, including macrophages and dendritic cells, express toll like receptors that recognize and bind to PAMPs ∙ These cells now secrete inflammatory mediators o Enhance innate response o May also be involved in adaptive immune response to pathogen ∙ Receptors on certain immune cells (macrophages and dendritic cells included)  that recognize and bind to highly conserved (through evolution) molecular  features associated with pathogens (PAMPs or pathogen-associated molecular  patterns.)  ∙ This recognition is not SPECIFIC to a single pathogen/epitope (such as we see  with the specific immune system’s antibodies) but rather a more general  recognition of “pathogen.”  ∙ In response to PAMP-TLR binding, innate responses such as inflammation may be enhanced, or an adaptive (specific) immune response initiated, as we will see  when we cover “antigen presentation.”  ∙ Immunological surveillance o Natural killer cells  Bind directly and non-specifically to virus infected cells and cancer  cells to kill them  Respond to a variety of antigens, including tumor specific antigens  ∙ Fever o Resetting of hypothalamic thermostat  Pyrogens o Adaptive value  Interferes with bacterial replication  Increased MR speeds up defensive reactions and repair o Hypothalamic thermostat reset in response to chemicals called pyrogens  (e.g., interleukin-1) secreted by macrophages exposed to bacteria and  other foreign substances in body)o Moderate fever is probably adaptive as it causes the following:   Liver and spleen sequester the iron and zinc needed by bacteria  Increases metabolic rate of tissues, speeding up defensive reactions  and repair processes  For each 1°C increase in temp., metabolic rate increases 10%

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