BSC 2086 1st Edition Lecture 13 Outline of Last Lecture I. Capillaries ContinuedII. VeinsIII. Blood Distribution in Vessels IV. Pressure and ResistanceV. Arterial Blood PressureVI. Venous Pressure and ReturnVII. Capillary PressuresOutline of Current Lecture I. Pressure and ReabsorptionII. Cardiovascular RegulationIII. Cardiovascular Response to Exercise and HemorrhagingIV. Other Cardiovascular AdaptationsV. Pulmonary and Systemic PatternsVI. Effects of Aging Current LectureI. Pressure and Reabsorptiona. Filtration and Reabsorptioni. Makes sure that plasma and IF are in constant communication and are mutually exchanging 1. Enters lymphatic system which drains extra fluid from tissues ii. Accelerates the distribution of nutrients, hormones and dissolved gases intissuesiii. Assists with the transportation of tissue proteins and insoluble lipids that cant cross capillary walls to enter the bloodstreamiv. Carries bacterial toxins and chemical stimuli to the lymphatic tissues and those organs responsible for disease immunity b. Net hydrostatic pressure i. ΔP between the inside and the outside of a capillaryii. Forces water out of solutioniii. Pushes blood out of capillaries and into IF iv. Factors that contribute: 1. Capillary hydrostatic pressure (CHP)2. Interstitial fluid hydrostatic pressure (IHP)c. Net osmotic pressurei. Forces water into solution ii. Pushed blood into the capillariesd. Net Capillary Colloid Osmotic Pressurei. Difference between blood colloid osmotic pressure (BCOP) and interstitialfluid colloid osmotic pressure (ICOP)1. Usually see that BCOP is higher than ICOPii. Pushes water and solutes into capillary from IF e. Net Filtration Pressure (NFP)i. Difference between net hydrostatic pressure and net osmotic pressureii. IHP and ICOP is usually 0 mmHgiii. NFP = CHP – BCOPf. Capillary Exchangei. At the arterial end of a capillary NFP > 01. Fluid moving from the capillary into IFii. At the venous end of a capillary NFP < 01. Fluid moving from IF into capillary iii. The transition point between filtration and reabsorption is closer to the venous end of the capillaryiv. Filter more than they reabsorb 1. Excess fluid enters lymphatic vessels g. Capillary Dynamicsi. Hemorrhaging will reduce CHP and NFP and increase reabsorption of IF 1. Fluid recallii. Dehydration will increase BCOP because proteins will remain stuck in the blood1. Accelerate reabsorption because you now have a larger component drawing liquid back into the capillaryiii. Increase in CHP or decrease in BCOP will move fluid out of blood and cause a build up in peripheral tissues (edema)1. Edema results from starvation or liver disease due to no production of plasma proteinsII. Cardiovascular Regulationa. Tissue Perfusioni. Blood flow through tissues that involves carrying O2 and nutrients to the tissues and organs while carrying CO2 and wastes away ii. Affected by: 1. How much blood is reaching tissues cardiac output2. Peripheral resistance the greater the peripheral resistance the less blood reaches tissues3. Blood pressure depends on cardiac outputb. Regulation changes the amount of blood flowing to a specific area at an appropriate time and in the right area without changing blood pressure and blood flow to vital organs c. Cardiac output and blood pressure regulated by:i. Autoregulation immediate, localized homeostatic adjustments 1. Don’t need stimulation of neural system2. Adjusted by peripheral resistance while the cardiac output stays the same a. Functions of local vasodilators Accelerate blood flow at tissue level due to:i. Low O2 or high CO2ii. Low pH when cell is metabolically active the pH becomes more acidic iii. Nitric oxide (NO)iv. High K+ or H+ concentrations 1. The higher the H+ the lower the pHv. Chemicals like histamine that are released due to inflammation vi. Elevated local temperature 1. Associated with increase metabolic activityb. Local vasoconstrictorsi. Will only affect local, single capillary bedsii. Released by damaged tissues and contrict precapillay sphincters iii. Examples: prostaglandins and thromboxanes ii. Neural mechanisms 1. Quick responses to changes at specific sites2. Short term3. Cardiovascular (CV) centersa. Medulla oblongatab. Cardiac centers:i. Cardioacceleratory centers increase cardiac outputii. Cardiacinhibitory center reduces cardiac outputc. Vasomotor centers:i. Vasoconstriction is controlled by stimulation of smooth muscle contraction in arteriole wallsii. Vasodilation controlled by relaxing smooth muscle d. Monitor arterial blood through:i. Baroreceptor reflexes: respond to blood pressure changes1. Stretch receptors found in the walls of:a. Carotid sinusesi. Maintains flow of blood to brainb. Aortic sinusesi. Monitors the start of the systemic circuitc. Right atrium i. Monitors end of systemic circuitii. Used in Bainbridge reflex to increase heart rate 2. When blood pressure rises, cardiac output decreases and vasodilation begins3. When blood pressure falls, cardiac output increases and vasoconstriction begins ii. Chemoreceptor reflexes: respond to chemical composition changes, especially due to pH and gases 1. Peripheral chemoreceptors found in carotid bodies and aortic bodiesa. Monitor blood2. Central chemoreceptors found below medulla oblongataa. Monitor CSFb. Control flow of blood to brain3. Reduce changes in pH, O2, and CO2 concentrations4. Thought processes and emotional states will cause cardiac stimulation and vasoconstriction due to elevated blood pressure iii. Endocrine mechanisms long term changes 1. Some have short term effects while others are long term 2. E and NE stimulate vasoconstriction and cardiac output3. Antidiuretic hormone (ADH)a. Released by posterior pituitary neurohypophysis b. Elevates blood pressure and reduces water loss at kidneysc. Responds to:i. Low blood volumeii. High plasma osmotic pressureiii. Circulating angiotensin II4. Angiotensin IIa. Responds to fall in kidney blood pressureb. Stimulates: i. Aldosterone production from adrenal cortexii. ADH productioniii. Thirst causes an increase in fluid intake and raisein blood volumeiv. Cardiac output and vasoconstriction 5. Erythropoietin (EPO)a. Released at kidneys and responds to low blood pressure and low O2 content in the bloodb. Stimulates RBC productioniv. Natriuretic peptides1. Atrial natriuretic peptide (ANP) produced by cells in right atrium2. Brain natriuretic peptide (BNP) produced by ventricular muscle cells3. Respond
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