Summary

This document describes local, humoral, and neural mechanisms to control blood flow. It details the needs of tissues, factors impacting blood flow, and specific tissue examples.

Full Transcript

Chapter 17: Local and Humoral Control of Blood Flow by Tissues Each tissue has ability to control its own local blood flow based on metabolic needs. Remember: sum of all local tissue flow determines cardiac output Needs: 1. 2. 3. 4. 5. 6. O2 delivery Other nutrients: glucose, amino acids, fatty aci...

Chapter 17: Local and Humoral Control of Blood Flow by Tissues Each tissue has ability to control its own local blood flow based on metabolic needs. Remember: sum of all local tissue flow determines cardiac output Needs: 1. 2. 3. 4. 5. 6. O2 delivery Other nutrients: glucose, amino acids, fatty acids CO2 removal H+ removal Proper ion concentrations Hormone transport How: 1. Local Mechanisms (metabolic) 2. Humoral Mechanisms (angiotensin II) 3. Neural Mechanisms (sympathetic stimulation) Slide 51 Acute vs. Long Term Control of Blood Flow Acute control - rapid changes occur within seconds to minutes to cause local vasodilation or vasoconstriction of small arterioles and pre-capillary sphincters to allow rapid maintenance of local tissue flow. Long term control - slow controlled changes over period of days, weeks, months. These changes usually involve changes in vessel size and number and allow even better control of flow in proportion to the needs of the tissues. Slide 52 Organ blood flow is dependent on metabolic rate Organ Blood Flow Organ Percent Brain Heart Kidneys Liver Skeletal muscle (resting) Skin Other 14 4 22 27 Total 100% Figure 17-1 > rate of metabolism ® > blood flow 15 6 12 Flow matches metabolic needs Slide 53 Acute Control of Local Blood Flow “Metabolic Theory” O2 one of the most necessary metabolites In the absence of O2, blood vessels relax and dilate. Oxygen availability < availability of O2 to tissues ® > blood flow Figure 17-2 Figure 17-3 Slide 54 Ohms Law F = ∆P/R Acute Control of Local Blood Flow “Metabolic Theory” ­metabolism / ¯O2 O2 deficiency vasodilator substance release vasodilation ­ blood flow Slide 55 Mediators? Adenosine CO2 K+ , H+ Histamine Phosphate compounds Examples of Metabolic Control Hyperemia: > blood flow Examples of Metabolic Control 1. Reactive Hyperemia Increase in flow following short term occlusion. 2. Active Hyperemia Increased flow with increased metabolic rate. Exercise--20x increase in skeletal muscle flow. Slide 56 Autoregulation of Blood Flow An acute increase in pressure causes an immediate increase in flow (remember: F = ∆P / R). But, within a minute, flow in most tissues returns to normal. Tissues regulate their own blood flow. = Autoregulation Blood flow remains constant despite changes in pressure. Note: Acute represents “steady state” response, not an instantaneous response. Flow responses are measured a few minutes (3-10 min) after change in pressure. Slide 57 Autoregulation of Blood Flow Acute Components: Metabolic Component: Hypoxia is central mediator. Too much O2 ® vasoconstriction. Myogenic Component: (not related to O2) ­pressure ® vascular smooth muscle stretch ® contraction ® vasoconstriction ® ¯ diameter Figure 17-4 Tissues with strong autoregulatory flow control: Kidney Brain Mesenteric Heart Slide 58 >AP→ >BF, autoregulation restores BF 75 175 Long term regulation is more complete. Chronic Control of Local Blood Flow Chronic ­metabolism / ¯O2 Chronic O2 deficiency Angiogenic factor release Changes in vessel # and size begins within days to weeks angiogenesis Long-term: Remodeling of vasculature Angiogenesis: Formation of new vessels/ Change in tissue vascularity. ­Maximum blood flow Degree of change in vascularity is dependent on maximal need, not average need. Slide 59 ¯Diffusion distances ­ demand ® ­ vascularity ¯ demand ® ¯ vascularity Examples 1. Chronic exercise 2. Development of collateral circulation after obstruction Hormonal Regulation of Blood Flow Control by substances secreted or absorbed into body fluids Vasoconstrictor (VC) Agents NE-powerful, Epi-less powerful, SNS and can also have vasodilatory effect, ie. coronary circulation. arteries, arterioles and veins Epinephrine/Norepinephrine Angiotensin II Ang II - acts on arterioles Vasopressin (aka Anti-Diuretic Hormone) Endothelin Endothelin Released from damaged endothelium to cause severe vasoconstriction-helps prevent excessive bleeding (hemorrhage) Slide 60 ADH - more powerful VC than Ang II Released from hypothalamus Also aids water reabsorption in kidney Hormonal Regulation of Blood Flow Control by substances secreted or absorbed into body fluids Vasodilator Agents Bradykinin Tissue damage ®kallikrein activation® Bradykinin release ® vasodilation, capillary permeability Histamine Prostaglandins Allergic reaction ® histamine release ® vasodilation and capillary permeability Nitric Oxide Nitric Oxide – released from healthy cells in response to a number of different stimuli Ions Calcium -- vasoconstriction Potassium, Magnesium, Hydrogen, Carbon Dioxide -- vasodilation Slide 61 Control of Local Blood Flow in Specific Tissues: Kidney- Control of blood flow linked to a mechanism called tubuloglomerular feedback – see Chapter 26. Brain- Control of blood flow linked to tissue oxygen concentration, concentrations of carbon dioxide and hydrogen ions. ↑ CO2 and H → dilation of cerebral vessels to allow rapid washout of excess CO2 or H+ from brain tissues. Skin- Control of blood flow is closely linked to regulation of body temperature – see Chapter 73. Slide 62 Why are these pressure-flow curves different? Chapter 14 F = ∆P/R Slide 63 Chapter 17 Why are these pressure-flow curves different? Chapter 14 Chapter 17 Left - Passive vessel with no adjustment to change in arterial pressure. Right - Response of a vessel/tissue that reacts to the change in pressure. Occurs in tissues with strong autoregulatory control. Examples: kidney, brain, mesenteric, heart. Slide 64