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Vertebrate Closed Circulatory Systems

Vertebrate Closed Circulatory Systems. Closed circulatory systems Cardiac anatomy & its O 2 supply The myogenic heart & the cardiac cycle Blood pressure Anatomical variations Other ‘hearts’. Hearts. Cardiac cycle – pumping action of the heart Two phases Systole – contraction

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Vertebrate Closed Circulatory Systems

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  1. Vertebrate Closed Circulatory Systems • Closed circulatory systems • Cardiac anatomy & its O2 supply • The myogenic heart & the cardiac cycle • Blood pressure • Anatomical variations • Other ‘hearts’

  2. Hearts Cardiac cycle – pumping action of the heart Two phases • Systole – contraction • Blood is forced out into the circulation • Diastole – relaxation • Blood enters the heart

  3. Closed vertebrate circulatory system • Multi-chambered heart • Capillaries connect arterial & venous systems • Respiratory pigments present in red blood cells Tunica media = vascular smooth muscle + elastin fibres Lower BP,thinner walled

  4. Anatomy of the chambered heart bulbus/conus arteriosus Venousbloodpressure • All vertebrates • Similar developmental pathway • Myogenic contractions • Similar intrinsic properties Arterialbloodpressure • Fish: The simplest/earliest design • Four cardiac chambers • All contain muscle (cardiac & smooth) • Surrounded by a pericardial sac • Atrium & ventricle propel blood • Venous BP  atrial contraction  ventricular contraction • Variations • Hagfishes: incomplete pericardial sac • Sharks & Rays: pericardial sac is stiff; conus arteriosus has cardiac muscle • Primitive Fishes: conus is reduced & bulbus also present • Teleosts: bulbus arteriosus (VSM & elastin fibres)

  5. Closed vertebrate circulatory system • Advantages • Blood pressure can be regulated, even venous blood pressure • High blood pressure, high flow rate & faster circulation time • Exquisite control of blood flow distribution at arterioles (VSM) • High capillary density reduces blood velocity & the diffusion distance to cells • Disadvantages • High resistance to flow b/c of small diameter arterioles (R = r4) • High resistance  high blood pressure  thicker-walled hearts & higher cardiac O2 needs

  6. Myocardial cells • Striated cells • Electrically connected (desmosomes) • ‘Unstable’ membrane potential Adult mammalian cardiomyocyte Adult fish cardiomyocyte Fish cardiac myocytes also have a reduced sarcoplasmic reticulum (SR), & lack an extensive t-tubular system Consequence: Ca2+ handling during excitation-contraction varies

  7. Myocardium Two types • Compact– tightly packed cells arranged in a regular pattern • Spongy – meshwork of loosely connected cells Relative proportions vary among species • Mammals: mostly compact • Fish and amphibians: mostly spongy • Arranged into trabeculae that extend into the heart chambers

  8. Cardiac muscle O2 supply • A working muscle requires ATP • ATP requirement proportional to cardiac power output • Spongy • Venous blood supply • Simplest, but intricate design • Last organ supplied with O2 • Compact • Coronary blood supply • Compact design • First organ supplied with O2 • Phylogeny & Ontogeny • Hagfishes & Lampreys: spongy • Sharks & Rays: spongy plus variable compact (athletic ability) • Teleosts: most spongy; some have variable compact (athletic/hypoxia) • Amphibians & reptiles: spongy; some have compact (athletic/hypoxia) • Neonatal birds & mammals: spongy • Adult birds & mammals: 99% compact

  9. Cardiac muscle blood & O2 supply Variable compact/spongy Most fish = Trabeculae = venous Mammals = compact = coronary Octopus coronaries

  10. Initiation of cardiac contraction Neurogenic pacemakers: rhythm generated in neurons (some invertebrates) Myogenic pacemakers: rhythm generated in myocytes (vertebrates and some invertebrates) Artificial pacemakers: rhythm generated by device

  11. Control of Contraction • Vertebrate hearts are myogenic – cardiomyocytes produce spontaneous rhythmic depolarizations • Cardiomyocytes are electrically coupled via gap junctions to insure coordinated contractions • Pacemaker – cells with the fastest intrinsic rhythm • Fish: located in the sinus venosus • Other vertebrates: sinoatrial (SA) node in the right atrium

  12. Myogenic contractions • All cardiomyocytes can contract without an external stimulus • Resting membrane potential is ‘unstable’ = Pacemaker potential • Specialised cells (pacemaker) set intrinsic heart rate • Relative timing & speeds of opening of specific ion channels • Increasing heart rate • Norepinephrine is released from sympathetic neurons and epinephrine is released from the adrenal medulla • More Na+ and Ca2+ channels open • Rate of depolarization and action potentials increase • Decreasing heart rate • Acetylcholine is released from parasympathetic neurons • More K+ channels open • Pacemaker cells hyperpolarize • Time for depolarization takes longer

  13. Increasing Heart Rate

  14. Decreasing Heart Rate

  15. Modulation of heart rate

  16. Depolarization travels through heart in two ways

  17. 1. Directly between cardiomyocytes • Cardiomyocytes are electrically connected via gap junctions • Electrical signals can pass directly from cell to cell

  18. 2. Specialized conducting pathways • Modified cardiomyocytes that lack contractile proteins • Specialized for electrical impulse conduction

  19. Syncitial & sequential cardiac contractions • All cardiomyocytes of a chamber contract together • Electrically coupled cells (desmosomes) • Specialized conduction fibres • Cardiac chambers contract sequentially, after blood has moved • Delays in electrical conduction between chambers (EKG) • Sums all the electrical activity of syncytial contractions & relaxations • P wave: atrial depolarization • QRS complex: ventricular depolarization • T wave: ventricular repolarization

  20. Impulse conduction – step 1

  21. Impulse conduction – step 2a

  22. Impulse conduction – step 2b

  23. Impulse conduction – step 3

  24. Impulse conduction – step 4

  25. Conducting Pathways

  26. EKG

  27. Myogenic contractions • All cardiomyocytes can contract without an external stimulus • But • Different myocardial cells activate different ion channels • Plateau phase – extended depolarization that corresponds to the • refractory period and last as long as the muscle contraction • Prevents tetanus Absence of funny channels Fast Na+ channel Slow L-type Ca2+ channel

  28. Excitation-contraction coupling

  29. Cardiac action potentials

  30. Cardiac pumping cycle • ATP  muscle contraction  blood pressure  blood flow • Isometric contraction  blood pressure (wall tension) until valves open • Isotonic contraction  blood flow (cardiac output) after valves open • Muscle thickness determines pressure

  31. Vertebrate Hearts • Vertebrate hearts have 3 main layers • Pericardium • Myocardium • Endocardium Myocardium

  32. Vertebrate Hearts Have complex walls with four main parts • Pericardium – sac of connective that surround the heart • Two layers: parietal (outer) and visceral (inner) pericardium • Filled with a lubricating fluid • Epicardium – outer layer of heart made of connective tissue • Continuous with visceral pericardium • Contain nerves that regulate the heart • Contain coronary arteries • Myocardium – the middle layer of heart muscle • Endocardium – innermost layer of connective tissue covered by epithelial cells (called endothelium)

  33. Vertebrate hearts - Myocardium • Muscle layer • Composed of cardiomyocytes • Specialized type of muscle cell

  34. Oxygen supply to heart • Myocardium extremely oxidative; has high O2 demand • Coronary arteries supply oxygen to compact myocardium • Spongy myocardium obtains oxygen from blood flowing through the heart

  35. Mammalian cardiac anatomy Two atria Two ventricles

  36. Mammalian cardiac cycle • Step 1: Late diastole, chambers relaxed, passive filling • Step 2: Atrial systole, EDV • Step 3: Isovolumic ventricular contraction • Step 4: Ventricular Ejection • Step 5: Early diastole, semilunar valves close

  37. Electrical and Mechanical Events in the Cardiac Cycle • Heart sounds: opening and closing of valves Figure 9.26

  38. Heart Pressures • The two ventricles contract simultaneously, but the left ventricle contracts more forcefully and develops higher pressure • Resistance in the pulmonary circuit is low due to high capillary density in parallel • Less pressure is needed to pump blood through this circuit • The low pressure also protects the delicate blood vessels of the lungs

  39. Heart Pressures

  40. Heart Pressures

  41. Cardiac Output • Cardiac output (CO) – amount of blood the heart pumps per unit time • Stroke volume (SV) – amount of blood the heart pumps with each beat • Heart rate (HR): rate of contraction • CO = HR X SV • Bradycardia – decrease in HR • Tachycardia – increase in HR

  42. Modulating cardiac output • By changing heart rate • By changing stroke volume Concept check: How would you modulate heart rate? Slow heart rate = bradycardia Fast heart rate = tachycardia Stroke volume is regulated in two ways: • Extrinsically (by nervous system and hormones) • Intrinsically (via local mechanisms)

  43. Modulation of cardiac output

  44. Control of cardiac output: Intrinsic control mechanisms • The importance of cardiac output (Q) • Heart ratePacemaker rate: temperature; body size • Cardiac stroke volume Species variability Effects of filling (venous) pressure

  45. The importance of cardiac output (Q) Flow (output) of blood per unit time from the heart (ml/min/kg) Cardiac power output (= ATP need = O2 need) Power output = Q x [blood pressure developed] Right vs left Atrium vs ventricle

  46. The importance of cardiac output (Q) Respiratory function: O2 uptake = Q x (A-V O2 difference) (Cao2-Cvo2); tissue O2 extraction Q10 effect: O2 uptake doubles for +10oC Species variability in routine & maximum Q values Humans @ 37oC 70-300 ml/min/kg Hagfish @ 10oC 10-30 ml/min/kg Trout @ 10oC 15-50 ml/min/kg Tuna @ 28oC 100-200 ml/min/kg Icefish @ 0oC 100 ml/min/kg Q10 effect~ x8 ~ x8 ~ x2~ x16 [Hb] is a primary determinant of Cao2

  47. Contribution of Q during exercise Human exercising O2 uptake = Q x (A-V O2 difference) Q = [heart rate] x [cardiac stroke volume] Q = 3-fold increaseHR = 2.5-fold increaseSVH = 20% increase A-VO2 = 3-fold increase Volume = O2 delivery to tissues 10-fold increase

  48. Regulation of Q during exercise • Intrinsic pacemaker rate Temperature Body mass • Extrinsic modulation of pacemaker • CNS • Hormones Ions • Intrinsic contractile properties Cardiac stretch Temperature • Extrinsic modulation of contractility • CNS Hormones Ions Q = [heart rate] x [cardiac stroke volume]

  49. Acute temperature effect on heart rate 60 HR,bpm 20 0 20 40 Temperature, oC Ectotherms & Endotherms human trout Cooling by D10oC 2x decrease Q10 ~ 2

  50. Temperature acclimation (resetting of pacemaker rate) 60 HR,bpm 20 0 20 40 Temperature, oC Ectotherms 1. Compensation eg, trout, Q10 = 1-2 trout 2. Downregulation eg, turtles, Q10 > 3 Acute Q10 ~ 2

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