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*Transport in Animals

Rhea Sekhon Biology A level Englisch 6 Seiten

Inhalt der Notizen (6)

Seite 1

Transport Systems

Single-celled/small organisms DON'T need transport systems (diffusion = enough excretion + obtaining)

Larger, multicellular organisms NEED transport systems as they have a greater SIZE, smaller SA:VOL ratio, and higher levels of metabolic activity (need to exchange substances FAST - especially endotherms) - also excrete MORE WASTE

Materials transported = O2, enzymes, waste products of metabolism, eg. urea, CO2, hormones

Multicellular organisms have SPECIALISED CIRCULATORY SYSTEMS. Made up of a HEART (pump to create pressure to push blood), BLOOD (fluid to carry substances), and VESSELS (space for the fluid to flow/exchange surfaces)

OPEN CIRCULATORY SYSTEMS = heart-like organ pumps the HAEMOLYMPH FLUID through short vessels, into a large cavity called the HAEMOCOEL. Here, the haemolymph directly BATHES organs + tissues for diffusion. When the heart relaxes, the haemolymph is sucked back via pores called OSTIA. Haemolymph moves around the haemocoel due to BODY MOVEMENTS (but still happens at rest). Movements that move haemolymph from one end of body to another = PERISTALSIS

Disadvantages - slow, reliant on body movements, low blood pressure

CLOSED CIRCULATORY SYSTEMS = blood is fully enclosed within vessels at ALL TIMES. Blood is pumped from heart through a series of successively smaller vessels. Blood returns to heart through a series of progressively larger vessels. Single/double. Blood under high pressure, quicker, doesn't rely on body movements

SINGLE CIRCULATORY SYSTEMS: the blood passes through the two-chambered heart ONCE in every complete circuit of the body (heart to gills, to body, to heart). Advantages = less complex, fish are ectotherms + need less energy than mammals, low blood pressure in capillaries for efficient exchange. Disadvantages = low blood pressure in body, slow blood movement, limited rate of transportation, animals need a lower metabolic rate.

DOUBLE CIRCULATORY SYSTEMS = blood passes through a four-chambered heart TWICE in every complete body circuit. Has PULMONARY SYSTEM and SYSTEMIC SYSTEM (heart to lungs, to heart to body to heart).

Advantages = blood pumped further around body as can increase pressure for systemic circulation, keeps up w/ mammals fast needs. Disadvantages = needs more energy, pressure can't be high in pulmonary circulation, flow of blood in lungs must be SLOW for gas exchange

Seite 2

Blood Vessels (5 types):

Arteries + arterioles = blood AWAY from heart, veins + venules = blood TO heart. Pulmonary artery = only artery w/ deoxygenated blood, pulmonary vein = only vein w/ oxygenated blood.

Components of arteries and veins: ENDOTHELIUM = single layer of smooth epithelial cells to reduce friction w/ flowing blood, ELASTIC FIBRES = stretch + recoil to provide vessel w/ flexibility to maintain blood pressure, SMOOTH MUSCLE (contracts + relaxes to change size of lumen + withstands high blood pressure, COLLAGEN = structural support to maintain shape + volume of vessel + prevent over-stretching.

ARTERIES = carry blood away from heart at HIGH pressures: Narrow lumen to maintain high pressure, endothelium (TUNICA INTIMA) has folds to allow lumen to expand w/ increased blood flow, Smooth muscle + elastic fibres = TUNICA MEDIA - THICK so artery withstands + maintains high pressure. Collagen = TUNICA EXTERNA (strength + durability).

VEINS = carry blood back to the heart at LOW pressures: valves = prevents the backflow of blood, lumen = WIDE as don't need to maintain a high pressure, endothelium similar to arteries, smooth muscle + elastic tissue = THINNER than arteries, collagen = thinner than arteries

CAPILLARIES form capillary beds - carry blood as close to the cells as possible, for efficiency. Capillary = A LUMEN (only 1 cell thick) - erythrocytes travel in a SINGLE PATH, walls are LEAKY for exchange.

ARTERIES + ARTERIOLES = thick elastic + smooth muscle so vessel can expand + recoil w/ heartbeat - PULSE

Arterioles = MORE SMOOTH MUSCLE THAN ELASTIC FIBRES (contraction of smooth muscle constricts the diameter of the arterioles, reducing rate of blood flow - this can be used to DIVERT BLOOD FLOW TO DIFFERENT REGIONS OF THE BODY needing more O2 (they constrict + dilate)

VEINS + VENULES = no pulse, as low blood pressure. Venules = THIN layer of muscle, elastic fibres + collagen

If valves become leaky + allow backflow, this could lead to VARICOSE VEINS (usually in superficial, non-urgent veins)

VALVES + CONTRACTION OF SKELETAL MUSCLE prevents backflow. When skeletal muscles CONTRACT, blood beyond site of contraction is forced TOWARDS the heart, opening the valves (valves behind close to prevent backflow), when skeletal muscles relax, blood pushes back against the valves, forcing them to CLOSE + prevent backflow.

Seite 3

Exchange of fluids at the capillaries

Blood = specialised transport system - fluid in blood vessels + a special type of CONNECTIVE TISSUE. Contains DISSOLVED SUBSTANCES eg. water, proteins, ions, hormones etc. Most = CELLS eg. erythrocytes, leucocytes, thrombocytes

Blood functions = thermoregulation, transport system, defence, maintaining pH of bodily fluids

TISSUE FLUID = similar to blood plasma but doesn't contain any PLASMA PROTEINS and many BLOOD CELLS. Formed by the plasma LEAKING from capillaries. Surrounds cells in tissues + supplies them with oxygen and nutrients.

Tissue fluid forms due to the balance of HYDROSTATIC PRESSURE and ONCOTIC PRESSURE

Half of plasma proteins = albumins (proteins involved in the transport of other substances eg. fatty acids + help regulate ONCOTIC PRESSURE

HYDROSTATIC PRESSURE = the pressure created by a fluid pushing against the container its in

ONCOTIC PRESSURE = the pressure created by the osmotic effects of solutes in a solution (consider similar to water potential). If water moves OUT of an area, ONCOTIC PRESSURE DECREASES + becomes more negative (substances remaining eg, plasma proteins exert osmotic effects.

ODEMA = accumulation of tissue fluid, SERUM = plasma w/ fibrinogen removed, preventing clotting - treats PLASMA LOSS in severe burns

SMALL molecules are pushed OUT into tissue fluid eg. inorganic mineral ions, glucose, urea, amino acids, water. Larger molecules REMAIN IN BLOOD eg, erythrocytes, leucocytes (only some WBC's go through), platelets + proteins.

Tissue Fluid

FORMATION OF TISSUE FLUID AT ARTERIOLE END: blood is at a high hydrostatic pressure, caused by the contraction of the heart. Net hydrostatic pressure out = 4.3 - 1.1 = 3.2 kPa out. Net oncotic pressure = -3.3 - (-1.1) = -2.0kPa IN. Net oncotic pressure is lower than net hydrostatic pressure so fluid is pushed OUT the capillary (ultrafiltration) - forms tissue fluid - surrounds cells for exchange 3.2 - 2.0 = 1.2 kPa out

RETURNING TO CAPILLARY AT VENULE END: hydrostatic pressure is decreased as small molecules were forced out at arteriole end so volume of fluid has decreased. Net is now 0.5kPa out. Plasma proteins remaining exert an OSMOTIC EFFECT. Net oncotic pressure = 2.0 kPa in so fluid moves BACK INTO CAPILLARIES (1.5 kPa in) + fluid brings waste back in. 5-10% tissue fluid doesn't go back

LYMPHATIC SYSTEM = some tissue fluid is drained into the lymphatic system (secondary circulation, immune) - now known as LYMPH. Lymphatic vessels in tissue drain excess fluid into larger vessels (contain valves). LYMPH NODES FILTER BACTERIA FROM LYMPH. Lymphatic vessels return to circulatory system by returning fluid through SUBCLAVIAN VEIN. Its the LYMPHOCYTES produced by lymph nodes that destroy bacteria. Lymph = colourless + contains more lipids than tissue fluid.

Seite 4

Structure of the Heart

Muscular PUMP. The heart squeezes + forces blood at a HIGH PRESSURE. Right side pumps deoxygenated blood to the lungs, left side pumps oxygenated blood around the body.

CORONARY ARTERIES = supplies oxygenated blood w/ nutrients to the actual heart muscle. If constricted, there's restricted blood flow to the heart + can cause angina/myocardial infarction.

SEPTUM = wall of muscle separating the two ventricles, ensuring that oxygenated and deoxygenated blood are kept SEPARATE

The heart is located in between the lungs, in the THORAX. There is a layer of fat around the heart for PROTECTION.

ATRIOVENTRICULAR (AV) VALVES: valves between the atria and ventricles, preventing the backflow of blood back into the atria. Tricuspid = right, Bicuspid = left

SEMILUNAR (SL) VALVES: prevents blood from re-entering the heart, from the arteries - aortic valve, pulmonary valve

TENDINOUS CORD = attached to the valves + prevents them from turning inside-out when the ventricle walls contract.

Heart is mainly made out of CARDIAC MUSCLE, that contracts INVOLUNTARILY (skeletal = voluntary). Called MYOCARDIAL TISSUE. Consists of FIBRES that BRANCH, producing CROSS - BRIDGES (helps spread wave of excitation across the heart + ensures a squeezing action can be produced. Many MITOCHONDRIA between muscle fibres (myofibrils) for contraction energy.

Muscle cells are separated by INTERCALATED DISCS (facilitate synchronised contraction). Cells divided into contractile units (sarcomeres)

Atrial walls = THIN as don't need much pressure to pump blood to ventricles. Right ventricle wall is THICKER than atria (pump to lungs), but THINNER than the left ventricle wall as it pumps blood around the whole body (highest pressure chamber).

Seite 5

The Cardiac Cycle

THE CARDIAC CYCLE = the sequence of events that occur during one full heartbeat. Its the control + coordination of the muscular walls of the heart's 4 chambers' contractions, allowing the heart to fill with blood before pumping. The atria contract together, and the ventricles contract together. 3 stages.

ATRIAL SYTOLE = the atria are both filled with blood from the vena cava and pulmonary vein. The muscles of the atria wall CONTRACT (semi - lunar valves close to prevent backflow). The volume inside the atria decreases, so pressure increases, opening the AV valves + allowing blood to flow into the ventricles. Ventricles fill w/ blood + atrial pressure decreases.

VENTRICULAR SYSTOLE = ventricles filled w/ blood from atria. The ventricles CONTRACT (starting at apex of heart), and this closes the AV valves. Ventricular pressure increases, as the volume decreases, so SL valves OPEN + blood is forced into the aorta + pulmonary artery

DIASTOLE = as the ventricles relax, the pressure inside them decreases, so the SL valves CLOSE. All heart muscles relax as, due to ELASTIC RECOIL, the volume inside the chambers increases. Blood flows into the atria from the veins, due to elastic recoil but pressure remains low. Blood starts to trickle into ventricles as atrial pressure increases but atria DON'T contract.

Pulse = caused by ventricular systole.

'Lub' = sound of AV valves closing, 'Dub' = sound of SL valves closing

The amount of blood pumped around the body = CARDIAC OUTPUT. Depends on stroke volume (volume of blood pumped by left ventricle in a heartbeat) and heart rate (frequency)

Cardiac output = stroke volume x heart rate

Causes of fluctuations of pressure in heart: pumping of ventricles. Pressure changes in the cardiac cycle can be shown on GRAPHS. Fluctuation causes: pumping of heart, decreased pressure from increased cross-sectional area of arteries (blood enters aorta + pulmonary artery in a rapid spurt, but tissues need a more even flow so walls have a lot of elastic tissue that STRETCHES when blood leaves heart - elastic recoil helps maintain pressure further from the heart but it drops as it gets further away + fluctuations less obvious - important to maintain pressure gradient between arteries and arterioles).

Coordination of the Cardiac Cycle

The heart can initiate its OWN MYOGENIC CONTRACTION, without nervous system. MYOCYTES (muscle cells) in the heart have a slight ELECTRICAL CHARGE across their membranes (are polarised). When a contraction occurs, the nodes are DEPOLARISED, stimulating a move of electricity in the heart. This is initiated in the SAN (right atrium wall PACEMAKER). The heart needs coordination as the atria contract more frequently than the ventricles.

The SAN initiates a WAVE OF EXCITATION at regular intervals, which are sent to the AVN for ventricular contraction.

STIMULATING ATRIAL SYSTOLE = the SAN in the wall of the right atrium acts as a pacemaker and sends a WAVE OF EXCITATION through the walls of both atria 55-80 times a minute. The wave travels along the muscle tissue and causes the cardiac muscle to CONTRACT almost simultaneously, causing atrial systole.

STIMULATING VENTRICULAR SYSTOLE = the AVN picks up the wave from the SAN + after a short delay of 0.1 seconds (to allow all the blood to flow into the ventricles + atria to finish contracting), the AVN sends its own wave of excitation down specialised muscle fibres in the septum called the BUNDLE OF HIS, then down the PURKYNE FIBRES (network of more specialised muscle cells) to MYOCYTES in ventricle walls. Wave spreads from apex, UP ventricle walls - causes contraction

In diastole, the muscle cells of the ventricle walls REPOLARIZE

Artificial pacemakers = devices implanted under the collarbone in people with faulty electrical conduction eg. SAN not firing, disruption of impulses between AVN and SAN/ in bundle of His. Pacemaker stimulate atria/ventricles to contract when they need to (impulses down electrodes in heart walls).

ECG (electocardiograms) can diagnose arrhythmias (abnormalities in heart rate) + heart problems. Can do a STRESS TEST.

Bradycardia = slow heart rate, tachycardia = fast heart rate, ectopic heartbeat = extra beats, followed by gaps, atrial fibrilation = atria contract more frequently than ventricles, fibrilation = complete uncoordination of the heartbeat - needs to be defibrilated to survive

Electrical activity of the heart is measured by an ELECTROCARDIOGRAPH (detects changes in polarisation - corresponds to heart contractions) - draws an ECG

ECG trace: P wave (atrial systole), PR interval (time taken for wave to go from SAN to AVN), QRS complex (ventricular systole) ST segment (interval between end of ventricular depolarisation (sytole) and start of repolarisation (diastole). T wave = diastole.

Seite 6

Transporting Oxygen

Transported by reversible binding with HAEMOGLOBIN, in erythrocytes, forming OXYHAEMOGLOBIN. Haemoglobin = globular, quaternary structure protein w/ 4 sub-units. Each subunit = polypeptide chain bound to a non-protein HAEM GROUP. Each haem group contains a Fe2+ ion that can attract and hold ONE OXYGEN MOLECULE (high affinity for oxygen). So, one mole of Hb can hold 4 OXYGEN MOLECULES

Saturation of Hb is measured in %, O2 absorbed into the blood as it passes across the alveoli in the LUNGS. O2 diffuses into blood plasma, then into erythrocytes + becomes associated w/ Hb reversibly - takes O2 out of solution, maintaining a STEEP CONCENTRATION GRADIENT (allows more O2 to enter blood) - then goes to HEART, before travelling around body. At tissues, oxyhaemoglobin dissociates O2.

Ability of Hb to associate w/ + release O2 depends on conc. of O2 in surrounding tissues. (Binds in high conc., dissociates in low conc.)

Concentration of a gas in a mixture of gases can be quantified in terms of PARTIAL PRESSURE (kPa) eg. P(O2). Also can be called OXYGEN TENSION.

THE OXYGEN DISSOCIATION CURVE = 'S' shaped

At low partial pressures of O2, most Hb's only take up 1 O2, or none. Few haem groups bind to O2 as the haem groups are at the CENTRE of Hb and hard to reach.

As p(o2) increases, diffusion gradient into Hb increases. Once Hb has picked up 1 O2, the oxygen affinity INCREASES as the binding of one O2 causes a CONFORMATIONAL SHAPE CHANGE so more O2 can bind with the haem groups more easily (small increase in O2 availability leads to a LARGE increase in saturation) - Graph at steepest of 'S'.

Once a high saturation is reached, some Hb's are 100% saturated so can't take up any more O2. Further rises in partial pressure leads to LESS difference to saturation - graph levels out

Erythrocytes in the foetal bloodstream contain special foetal Hb that has a HIGHER AFFINITY for O2 than adult Hb (dissociation curve more left) as foetal Hb must associate w/ O2 from mother's bloodstream (some O2 already lost before reaching placenta, where partial pressure is low enough to make mother release O2 to foetus.

Transporting Carbon Dioxide

CO2 is released from respiring tissues + transported to lungs for excretion in 3 ways: 1. 5% dissolved in blood plasma, 10-20% combines w/ hameoglobin to form carbaminohaemoglobin, 75-80% transported as HCO3- ions.

P(O2) is LOWER in respiring tissues than in the lungs so O2 diffuses out of the Hb and into respiring tissues (DISSOCIATES). Hb is then affected by CO2 diffusing in to be transported to the lungs (free to take up H+ ions in the formation of hydrogencarbonate ions).

FORMING HCO3- IONS:

Oxyhaemoglobin dissociates

O2 used in respiration diffuses from erythrocytes, through capillary wall and into tissue fluid, then into respiring cells

Respirarion releases co2, which diffuses out of cells, into tissue fluid, then into erythrocytes

The CO2 reacts with H2O, forming CARBONIC ACID (H2CO3-), catalysed by CARBONIC ANHYDRASE

Carbonic acid DISSOCIATES to release H+ and HCO3- ions

H+ ions building up in erythrocytes causes acidity, so H+ ions are taken out of solution by associating with Hb, producing HHb (HAEMOGLOBINIC ACID) - acts as buffer

HCO3- ions diffuse out red blood cells

As HCO3- ions diffuse out into plasma, RBC becomes more +ve so Cl- ions move into the red blood cells, to maintain cell charge (CHLORIDE SHIFT)

THE BOHR SHIFT = the effect that increasing conc. of CO2 has on haemoglobin's oxygen affinity. The formation of H+ ions when forming HCO3- ions LOWERS the pH of blood, so more acidic - AFFECTS TERTIARY STRUCTURE OF HB, so the oxygen affinity of it is LOWERED - increases the RELEASE of O2

So CO2 DECREASES O2 affinity

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A level Biology Notiz am *Transport in Animals, erstellt von Rhea Sekhon am 04/06/2021.
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