(a) Explain why animals with high metabolic rate require more complex excretory and circulatory system. (20 marks) (b) Explain…

(a) Why animals with a high metabolic rate need more complex excretory and circulatory systems (20 marks)

Metabolic rate per unit of body mass is highest in small, warm-blooded animals (birds and small mammals), roughly in proportion to mass to the power of 0.75, so a shrew or a sparrow uses far more oxygen per gram than an elephant or a lizard. A high metabolic rate means faster oxygen use and faster production of carbon dioxide, heat, water and nitrogenous and acid wastes. It has two consequences.

Circulatory system: oxygen and nutrients must be delivered, and carbon dioxide and heat removed, quickly. This needs:

• A four-chambered heart in birds and mammals, with complete separation of oxygenated and deoxygenated blood, so that the systemic circuit gets fully oxygenated blood at high pressure and the pulmonary circuit is a low-pressure one. Fish (two chambers) and amphibians and most reptiles (three chambers) mix blood and manage on a low metabolic rate.
• A high heart rate and cardiac output (a mouse about 600 beats a minute, an elephant about 30), and a strong ventricle.
• Dense capillary beds, a high haemoglobin and red-cell content, and efficient regulation of blood flow to active tissues.
• Blood is also the route by which heat reaches the skin for thermoregulation.

Excretory system: the higher intake and breakdown of protein and the higher metabolic rate produce large amounts of urea (or uric acid in birds), acids and metabolic water that must be cleared while conserving water. This needs:

• Large numbers of nephrons, a high renal blood flow (about a fifth to a quarter of the cardiac output) and a high glomerular filtration rate.
• Long loops of Henle and a countercurrent mechanism, which concentrate urine to save water (long-looped juxtamedullary nephrons); in birds, reptilian-type and mammalian-type nephrons and the excretion of uric acid, which saves water.
• Precise regulation of acid-base, water and electrolytes by the kidney under the control of antidiuretic hormone, aldosterone and the renin-angiotensin system.

Thus, the more complex circulatory and excretory systems keep the internal environment constant despite a high rate of turnover.

(b) Three stages of blood coagulation with the role of platelets and fibrinogen (15 marks)

Coagulation is the change of blood from a liquid to a gel, by a cascade of clotting factors, to stop bleeding. In the classical scheme it has three stages.

Stage 1, formation of prothrombin activator: after injury, the extrinsic pathway (tissue factor released from damaged tissue with factor VII) and the intrinsic pathway (contact of blood with collagen, activating factor XII, then XI, IX and VIII) both lead to the activation of factor X. Activated factor X (Xa) combines with factor V, calcium ions and platelet phospholipid (platelet factor 3) to form prothrombin activator.

Stage 2, conversion of prothrombin to thrombin: prothrombin activator, on the platelet surface, splits the plasma protein prothrombin (factor II, made in the liver, with vitamin K) to thrombin.

Stage 3, conversion of fibrinogen to fibrin: thrombin splits soluble fibrinogen (factor I, made in the liver) into fibrin monomers, which polymerise into loose threads. Thrombin also activates factor XIII, which cross-links the threads into a strong, stable mesh that traps red cells and platelets and forms the clot. Thrombin also gives positive feedback by activating factors V and VIII.

Role of platelets: they stick to damaged vessel wall and collagen (with von Willebrand factor) and to each other (aggregation, with ADP and thromboxane A₂) to form the primary platelet plug; they release serotonin (vasoconstriction) and clotting factors; they provide the phospholipid surface for stages 1 and 2; and they cause clot retraction, which pulls the edges of the wound together. Afterwards, plasmin dissolves the clot (fibrinolysis).

(c) Role of chemoreceptors in regulating heartbeat and cardiac output during hypoxia (15 marks)

Peripheral chemoreceptors are the carotid bodies (at the carotid bifurcation) and the aortic bodies (on the aortic arch). Their glomus cells are stimulated by a fall in arterial PO₂ (mainly below about 60 mm Hg), and also by a rise in PCO₂ and H⁺. Their afferents go by the glossopharyngeal (carotid) and vagus (aortic) nerves to the nucleus of the tractus solitarius in the medulla, which acts on the respiratory and the cardiovascular centres. (Central chemoreceptors in the medulla respond mainly to CO₂ and H⁺, not to hypoxia.)

Effects during hypoxia:

• Respiratory: increased rate and depth of breathing (hyperventilation), the main response.
• Cardiovascular: chemoreceptor stimulation activates the sympathetic system and inhibits the vagal cardiac centre through the vasomotor and cardio-inhibitory centres. Sympathetic outflow to blood vessels causes vasoconstriction in the skin, gut and muscle, which raises blood pressure and diverts blood to the brain and heart.
• Heart rate: the direct chemoreceptor effect is a slowing (bradycardia), but the hyperventilation and lung inflation reflexes reverse it, so in the intact animal the net effect is tachycardia and a rise in cardiac output, helped by catecholamines from the adrenal medulla.
• Local effect: hypoxia dilates the coronary and cerebral vessels.

In severe, prolonged hypoxia (PO₂ below about 40 mm Hg) the medullary centres and the myocardium are depressed directly, so heart rate and output fall.