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Vertebrate Closed Circulatory Systems • Closed circulatory systems • Cardiac anatomy & its O2 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 • Blood is forced out into the circulation • Diastole – relaxation • Blood enters the heart Closed vertebrate circulatory system • Multi-chambered heart • Capillaries connect arterial & venous systems • Respiratory pigments present in red blood cells Lower BP, thinner walled Tunica media = vascular smooth muscle + elastin fibres Anatomy of the chambered heart All vertebrates • Similar developmental pathway • Myogenic contractions • Similar intrinsic properties Venous blood pressure Arterial blood pressure Fish: The simplest/earliest design • Four cardiac chambers bulbus/conus arteriosus • 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) 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 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 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 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 Cardiac muscle blood & O2 supply Most fish = Trabeculae = venous Mammals = compact = coronary Variable compact/spongy Octopus coronaries 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 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 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 Increasing Heart Rate Decreasing Heart Rate Modulation of heart rate Depolarization travels through heart in two ways 1. Directly between cardiomyocytes • Cardiomyocytes are electrically connected via gap junctions • Electrical signals can pass directly from cell to cell 2. Specialized conducting pathways • Modified cardiomyocytes that lack contractile proteins • Specialized for electrical impulse conduction 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 Impulse conduction – step 1 Impulse conduction – step 2a Impulse conduction – step 2b Impulse conduction – step 3 Impulse conduction – step 4 Conducting Pathways EKG 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 Excitation-contraction coupling Cardiac action potentials 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 Vertebrate Hearts Vertebrate hearts have 3 main layers • Pericardium • Myocardium • Endocardium Myocardium 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) Vertebrate hearts - Myocardium • Muscle layer • Composed of cardiomyocytes • Specialized type of muscle cell 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 Mammalian cardiac anatomy Two atria Two ventricles 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 Electrical and Mechanical Events in the Cardiac Cycle • Heart sounds: opening and closing of valves Figure 9.26 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 Heart Pressures Heart Pressures 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 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: 1) Extrinsically (by nervous system and hormones) 2) Intrinsically (via local mechanisms) Modulation of cardiac output Control of cardiac output: Intrinsic control mechanisms • The importance of cardiac output (Q) • Heart rate Pacemaker rate: temperature; body size • Cardiac stroke volume Species variability Effects of filling (venous) pressure 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 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 [Hb] is a primary determinant of Cao2 Q10 effect ~ x8 ~ x8 ~ x2 ~ x16 Contribution of Q during exercise O2 uptake = Q x (A-V O2 difference) Q = [heart rate] x [cardiac stroke volume] Human exercising Q HR SVH A-VO2 = 3-fold increase = 2.5-fold increase = 20% increase = 3-fold increase Volume = O2 delivery to tissues 10-fold increase Regulation of Q during exercise Q = [heart rate] x [cardiac stroke volume] • 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 Acute temperature effect on heart rate Ectotherms & Endotherms human 60 trout Cooling by D10oC 2x decrease Q10 ~ 2 HR, bpm 20 0 20 Temperature, oC 40 Temperature acclimation (resetting of pacemaker rate) Ectotherms 1. Compensation eg, trout, Q10 = 1-2 60 trout 2. Downregulation eg, turtles, Q10 > 3 HR, bpm 20 0 20 Temperature, oC 40 Acute Q10 ~ 2 Control of intrinsic pacemaker rate Body mass & heart rate Endotherms HR = k . BM-0.25 hummingbird (1 g) 1,000 Rate, bpm human 60 bpm Body Mass whale 20 bpm Ectotherms 120 bpm is maximum for many ectotherms Intrinsic control of stroke volume Roles 1. Automatic matching output of chambers ventricular output must match atrial output – all vertebrates right & left ventricular matching – crocodiles, birds & mammals 2. Varying stroke volume Alter cardiac emptying (end-systolic volume) = D muscle contraction Alter cardiac filling (end diastolic volume) = D venous pressure Many fishes (2-3x increase) Small increases (<50%) other vertebrates How? The Frank-Starling mechanism: Control of Stroke Volume Frank-Starling effect – an increase in end-diastolic volume results in a more forceful contraction of the ventricle and an increase in SV • Due to length-tension relationship for muscle • Allows heart to automatically compensate for increases in the amount of blood returning to the heart (autoregulation) Level of sympathetic activity shifts the position of the cardiac muscle lengthtension relationship Frank-Starling mechanism: An intrinsic property of all vertebrate cardiomyocytes Venous pressure cardiac filling myocyte stretch stronger contraction actin z myosin contractile unit passive stretch SV Venous filling pressure z Control of Stroke Volume The nervous and endocrine system can cause the heart to contract more forcefully and consequently pump more blood with each beat Control of stroke volume Control of cardiac output & flow distribution Extrinsic control mechanisms • Cardiac stroke volume Change in contractility - importance of calcium •Heart rate Sympathetic & parasympathetic neural controls - mechanisms - species diversity • Blood flow distribution Arteriolar controls neural, humoral, paracrine, autocrine Changing heart rate (vagal inhibition) Pacemaker rate rarely equals measured HR Inhibition & excitation Vagus innervation of pacemaker & atrium All vertebrate hearts Except hagfish & lampreys Sympathetic innervation of pacemaker, atrium & ventricle Some advanced, athletic teleost fishes, Amphibians, reptiles, birds & mammals Cardiac stores: primitive fish Innervated Chromaffin tissue: other fishes Adrenal medulla Negative chronotropic effects (vagal inhibition) 0 mV -60 mV Positive chronotropic effects (adrenergic stimulation) 0 mV -60 mV