Lecture 9 - Circulation III

Lecture 9 - Circulation III - JAN 20 LECTURE (THURS)...

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Unformatted text preview: JAN 20 LECTURE (THURS) Biology 2A03 Lecture 9 Circulation III 1 Total Peripheral Resistance (TPR) Combined resistance of all blood vessels within the systemic circuit Resistance across a network of blood vessels depends on resistance of all vessels Flow through network varies with resistance Vasoconstriction in network increase resistance decrease flow Vasodilation in network decrease resistance increase flow 2 - volume of blood injected by heart per unit time = cardiac output - cardiac output is product of stroke volume and heart rate - stroke volume = volume injected by heart when contracts Relating Pressure Gradients and Resistance in the Systemic Circulation Flow = ΔP /R –  Flow = cardiac output = CO –  ΔP = mean arterial pressure = MAP –  R = total peripheral resistance = TPR Cardiac Output (CO) = MAP / TPR MAP = CO x TPR 3 Vascular system small microcirculation Inner radius arteries 12mm Low resistance, little pressure drop, acts as a pressure reservoir arterioles 15µm Major site of resistance, controls bloodflow patterns helps regulate arterial blood pressure capillaries 3µm venuoles Exchange site of nutrients and metabolic biproducts 10µm Exchange Low resistance, thin walled, distensible, adjusts blood return to heart, acts as a blood reserve (60% of blood volume) All parts of the circulatory system have endotheluim (inner layer), all but capillaries have smooth muscle and connective tissue (outer layer) veins 5mm connective tissue smooth muscle With varying degrees of elastic and collagen fibers - elastin? endothelium (single layer of cells) 4 See Fig 15-6 - arteries are fairly large, relatively low resistance - little decrease in pressure?? - can store some of the presssure generated by heart in elastic walls - arterioles control blood flow pattern and help regualte MAP - capillaires -> very small but abundant - exchange site for nutrients and metabolic byproducts - since very close to cells, diffusion is sufficient - venuoles -> some exchange as well - veins -> lowest resistance in body -> thin walls -> very distensible - arteries are large and have lots of smooth muscle, travels next into arterioles (many brachings into atrerioles, then thousands of capiliarries) - pre-capillary sphinter help regualte blood flow - veins have less smooth muscle, and valves (to ensure unidirectional movement) - blow-up of capillary - shows its just a thin layer of cells so diffusion is possible 5 Fig 15-5 Arteries Muscular, highly elastic - High elastin /collagen in connective tissue (outisde layer) Compliance = ΔV ΔP moderate compliance to smooth out pressure fluxuations from heart Large changes in pressure with small changes in volume make arteries pressure reservoirs Large changes in volume with small changes pressure make veins volume reservoirs The higher the compliance the greater a vessel can be stretched Fig 15-20 6 - Arteries are first vessel coming out of the heart - veins have high complicane and arteries have low compliance - other way to think abt it is you have two baloons - pink balloon is made out of think rubber and cant blow it up (walls hold up pressure - known as low compliance = artery - upper pic = contraction of heart -> genetrating huge pressure when contracting and pushing blood into artery -> atery store this pressure into wall and release it when relaxing (use it to push blood out) -> valve makes sure that the elastic recoil of blood does not go backwards - if blood flow wasnt constant, it would be squirting Arteries as a pressure reservoir Stores pressure which is then released between ventricle contractions (diastole) Only 1/3 of the stroke volume leaves the arteries at this time - rest leaves when arterial walls recoil - helps maintain blood flow constant Arterial walls recoil during diastole and this maintains blood flow constant Fig 15-7 7 See 14-9 3rd ed. systolic PP HEALTHY PERSON diastolic Pressure peaks during ventricular ejection (systole) = systolic pressure (SP), lowest is diastole pressure (DP) btw contractions SP-DP = pulse pressure (PP) Depends on stroke volume, speed of ejection and compliance of arteries - (low compliance high PP) e.g. hardening of arteries decreases compliance and increases PP 8 - beasure atery is harder, cant store pressure any more - doctors measure blood pressure in arteries, thus lowest is ~70 not zero - MAP is weighted average of these since spends more time in diastole pulse pressure = difference between the two - pressure at aterioles decreases significanlty because its a major source of resistance - thus biggest drop in pressure Relative flood flow -> rest to extercise example 5L/min was resting value -> exercise increases it to 20L/min innervated -> nerves that terminate - smooth muscle has baseline contraction controlled by nervous input, sympathetic nervous system has a baseline for it - increasing or decreasing signal is done to control it Arterioles 2 roles: 1) determines relative bloodflow to tissues e.g. rest – exercise muscle bloodflow 1L/min – 20L/min 2) Helps regulate Mean Arterial Pressure (MAP) -Major site of resistance in cardiovascular system Largest ΔP -Adjust resistance of vessels going to tissues by adjusting radii both passively (stretch) and actively (nerves, hormones etc..) -Are well innervated and contain smooth muscle that contracts (vasoconstriction) or relaxes (vasodilation) -Always some intrinsic tone (basal tone) plus tonic constriction due to basal firing of Sympathetic Nervous System Control of vascular smooth muscle Local (intrinsic) paracrine e.g. Active hyperemic extrinsic 1) SNS through neurotransmitter Norepinephrine (NorEpi) 2) PSNS not very important 9 3) hormones See Fig 15-13 Active hyperemia Local chemical change causes bloodflow to increase in proportion to metabolic activity of that organ * O2, CO2, pH, adenosine, etc.. Occurs in heart & skeletal muscle since it has large variation in metabolic rate vasoconstriction Other intrinsic factors: Endothelin-1, vasodilation NO (nitric oxide) Affects contraction of smooth muscle in vessel wall 10 Fig 15-12 Local chem change -> vinicity of arterioles *(atp hydrolosis -> adenosine) - if tissue becomes metabolically active, and consumes oxygen, delivery of oxygen by vessels will not be sufficient for metabolic need of cells, triggers vessels to vasodialate and greater delivery of oxygen -> and once oxygen levels increase, stops vasodialating Reactive hyperemic causes metabolites to change and trigger an increase in bloodflow Decrease in blood flow Myogenic response Change in vascular resistance in response to vessels in absence of any external factors stretch of blood Flow is kept constant = flow autoregulation BLOOD calcium enter cell and contract BLOOD 11 Fig 15-14 END OF LECTURE Table 15-2 Extrinsic controls SNS: -Arterioles highly innervated and have receptors (post-synaptic) which trigger through neurotransmitter -Changes above or below tonic constriction (nerves always active) -Important role in controlling whole body arterial blood pressure PSNS: Not a big role in vascular smooth muscle regulation Hormones: - from adrenal medulla causes - via receptors, -Skeletal muscle has both In most vascular beds outnumber via -adrenergic receptors (except in skeletal muscle) Epinephrine has greater affinity for β2 receptors 12 Rest Exercise -High concentration of Epi – binds to both α and β2 -Vasodilation in skeletal and cardiac muscle vascular beds -Decrease TPR -Vasoconstriction in most other vascular beds -Maintain/increase TPR Maintain blood pressure -Dominant effect usually vasoconstriction 13 Other vasoconstrictor hormones See Table 15-1 Angiotensin (ANG)II – renin – ANG system Vasopressin – from posterior pituitary Endothelin-1 (mostly acts as peptide paracrine agent release by endothelial cells) Vasodilator hormones Atrial natriuretic hormone – secreted by the heart 14 ...
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This note was uploaded on 06/21/2011 for the course BIO 2A03 taught by Professor Tba during the Spring '10 term at McMaster University.

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