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TAMU BIOL 320 - Vascular Tissues & Hemodynamics
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BIOL 320 1st EditionLecture 9Outline of Last Lecture I. Cardiac CycleII. Cardiac Output- Flow Chart to Increase Cardiac OutputIII. Regulation of Stroke Volume (SV)- Three Factors that Regulate SV:IV. Effects of Calcium in Cardiac MuscleV. Heart DevelopmentVI. Congenital Heart DefectsVII. Aging of the HeartI. Blood Vessels- StructureII. ArteriesIII. Capillary Beds: sites of gas exchange- Thoroughfare channel: bypass capillary bedOutline of Current Lecture IV. Capillary ModificationsV. Venules & VeinsVI. HemodynamicsVII. Blood Flow- Long-Term Auto-regulation of Blood Flow- Blood Flow: Skeletal Muscles- Blood Flow: BrainVIII. Blood PressureIX. Venous ReturnX. Blood Pressure Regulation- Cardiac Output Regulation by BP- Short-Term BP Controls- VMC Regulation: Baroreceptor Reflex- Long-Term BP Regulation: RenalCurrent LectureCapillary Modifications- Continuous Capillarieso Structure: endothelial tissue wrapped around exterior, tight junctions, tight intra-cellular clefts that allow diffusion (blood-brain barrier)o Located: skin, muscle- Sinusoidso Structure: loose and leaky, large intra-cellular cleft (cell, solutes, etc. can pass through easily)o Located: liver, bone marrow, spleen- Fenestrationso Structure: portholes, windows, or pores present; intermediate leakiness between the three types; solutes and chemicals can pass through poreso Located: near endocrine glands, kidney, small intestineVenules & Veins- Have valves (anti-backflow valves)- Veins have a large diameter, thin-walled, are low pressure with high volume tubes, and hold the most blood at any point in time (throughout the body)- What do varicose veins and hemorrhoids have in common?o Both have damage to these anti-backflow valves- Vascular anastomoses: a cross-connection between other vascular tubeso Brain, heart, abdominal organs, jointsHemodynamics- Blood flow: volume of blood through a define area- Blood pressure: force exerted on vessel wall- Resistance (peripheral resistance): opposition to flow (highest in arterioles)- Resistance factors: most important factor in blood flowo Viscosity: changes with hydrationo Blood Vessel Lengtho Blood Vessel Diameter: changes most frequentlyBlood Flow- Blood flow through entire CVS = cardiac output (CO)- At rest…relatively constant- Blood flow in individual organs…varies with need- Flow is directly proportional to change in pressure (greater the difference the faster the flow)- Poiseuille’s Lawo Inversely proportional to resistance Inversely proportional to viscosity Inversely proportional to vessel length Directly proportional to vessel diametero Directly proportional to ∆ pressure- Regulation of Blood Flowo Intrinsic mechanisms (auto-regulation): distribute blood flow to individual organs and tissues as needed Metabolic Controls- Decreaseo pH (dilates)o O2 (dilates)- Increaseo CO2 (dilates)o K+ (dilates)o Prostaglandins (dilates)o Adenosine (dilates)o Nitric oxide (dilates)o Endothelins (constricts) Myogenic Controls- Increase:o Stretch (contricts)o Extrinsic mechanisms: maintain mean arterial pressure (MAP); redistribute blood during exercise and thermoregulation Nerves- Sympathetic (constricts) Hormones- Epinephrine/Norepinephrineo α receptors (constricts)o ß receptors (dilates)- Angiotensin II (constricts)- Antidiuretic hormone [ADH] (constricts)- Atrial natriuretic peptide [ANP] (dilates)- Long-Term Auto-regulation of Blood Flowo Angiogenesis: growing of new blood vessels Occurs when short-term auto-regulatory can’t meet tissue needs Increase number of vessels to region & existing vessels enlarge- Blood Flow: Skeletal Muscleso At rest: myogenic & general neural mechanisms predominateo During muscle activity: Blood flow increase relative to tissue activity Local controls over-ride sympathetic vasoconstrictiono Muscle blood flow can increase 10x or more during physical activity- Blood Flow: BrainBlood Pressure- Pulse pressure (PP) = SP (Systolic pressure) – DP (Diastolic pressure)- MAP = DP + 1/3PP- MAP: Mean Arterial Pressure…pressure that propels blood to target- Biggest pressure difference occurs in the arterioles (since they spread the blood out…disperse to capillary beds)Venous Return- Allowed by these factors:o Respiratory “pump”o Muscular “pump”o Valves: anti-backflow- These help increase EDV (get the heart more full)Blood Pressure Regulation- Why bother:o Maintains flow through capillary bedso To change regional blood flow based on needso Counteract gravity- Factors:o Cardiac Output (CO)o Peripheral Resistance (vasoconstriction/vasodilation…dehydration)o Blood volume (regulation via kidneys)- Cardiac Output Regulation by BPo Normal: HR control: P-ANS (CIC) SV (stroke volume) control: venous return (EDV)o Under Stress: HR control: S-ANS (CAC) SV (stroke volume) control:- Epinephrine/neural regulation: increase contractility  SV (decrease ESV)- Venous return: increase due to increased activity (muscle/respiratory pumps)- Short-Term BP Controlso Neural controls: Specific demands- Overcome pooling in legs when suddenly stand (after sitting for a while)- Direct blood to active areas (muscles, skin,…)- Recover pressure (lost with hemorrhage) Maintenance of MAP (via altering blood vessel diameter) Operate via reflex arcs- Receptor: baroreceptors- Integration center: vasomotor center- Effector: smooth muscle on outside of vessels (arteries/arterioles)o Vasomotor center: cluster of S-ANS neurons in medulla…never an on/off…always maintains constant low level of activity to be readyo Cardiovascular center: Vasomotor center CAC & CICo S-ANS activity increase: vasoconstriction; increase BPo S-ANS activity decrease: P-ANS takes over; decrease BPo Vasomotor center regulation: Chemoreceptor Reflex:- Location: aorta, carotid artery- Measure: oxygen and carbon dioxide- Stimuli: low oxygen or elevated carbon dioxide- Action: activate VMCenter- Result: vasoconstriction  speed blood back to heart- Coupled with: increased HR- VMC Regulation: Baroreceptor Reflexo High BP: Increase CIC Vasodilation S-ANS: decrease HR/contractility  COo Low BP: VMC stimulate vasoconstriction Increase CAC (decrease CIC) S-ANS: increase HR and contractility  CO- Long-Term BP Regulation: Renalo Control mechanism: via blood volumeo Direct Pathway: with time,


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TAMU BIOL 320 - Vascular Tissues & Hemodynamics

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