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March 7th_Physiology II.docx

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Department
Kinesiology & Health Science
Course
KINE 2011
Professor
Gillian Wu
Semester
Fall

Description
Review: Arterioles side of the location can be thought of a as a reservioir, and the vol of it is affected by (i)cardia input (ii)cardic output. Arterioles are gateway to the rest of the circulation. This flow outwards is going to determine the vol that remains within arteries, and as a result of that vol we are going to have certain pressure. The pressure witin the arteriole system is determind by the filling volume. So arterioles do have an impact on the MAP. Two different sceiniors (arteriole are creating high resistance pathway, very constricted, highly limited with what can leave arteries) High resistance is called by the sympathetic nervous system which releases norepinephrine binding to alpha adregneric receptors on the smooth muscle which will cause arterioles to constrict. (i) of consequence of high resistance pathway, and impeded blood flow from getting out WE WILL INCREASE MAP. (ii) Due to high resistance capillaries will have less blood flow that is going to have two different impacts which will (i) minimize the amount of less gas/nutrient exchange since there is not enough blood moving through them allowing diffusion to occur (IMPACT ON TISSUE METABOLISM) (ii) When arterioles valves are shut off which limits the blood to enter, we are reducing capillary pressure (since not enough blood is filling them anymore) . We are reducing the hydrostatic pressure, but our osmotic protein pressure is the same. We will have greater fluid reabsorption from the interstitim into the capillaries compared to the filteration process. Those are two effects on the capillaries and are independent effect. (IMPACT ON BLOOD VOLUME & INERSITAIL FLUID VOL) Low Resistance When the arterioles become low resitance, they vasodilate, allowing large radius tubes , which lowers resistance and allowing more blood to go. When do we have low resistance pathway? Generally occurs whe we have accumulation of metabolites. Metabolites are major form of vasodilating.When they accumulate they intitate a signal which is greater than sympathetic signal. That allows vasodilation to occur and more blood to exist the arteries and go to arterioles. Cardiac out to be steady its not changing. The MAP when we open up the values , more blood is existing but same amount is coming in, vol is going to reduced that stays in the arteries. MAP wil be lower than before. The more arterioles that vasodilate, the more effect there will be on MAP. A lot of blood will go and move up to capillaries. Capillaries are now experiencing higher flow. The blood is going to be O2 rich and nutrient rich and remove CO2 and metabolies. We weill get enchaned exchange. The filling pressure of the capillaries is higher (more blood fills up capillaries. The hydrostatic pressure is higher , and its going to affect the fluid exchange . When we have more pressure in the capillaries because arterioles have jus let more blood enter them. There is going to be higher filteration than absorption( more water will be pushed into surrounding interstitium). The water will be accumulating and tissue will be swelling up =adema (CHECK SPALLING) Or the lymph vessels will take that fluid and move it back through the lymph system SO IT RETRUNS BACK TO THE CIRCULATION ------------------------------------------------------------------------------------------------------------------------------- --- Page 81 Systolic pressure isincreasing because of Valsalava Manoeuvre (forced expiration against closed glottis, increasing thoracic pressure will also increase MAP) Active & Reactive hypermia= both things cause vasodilation; both negative feed backs designed to restore the metabolic profile of the tissue. Active Reactive Hypermia -there is an accumulation of Hyperemia in a part resulting from the metabolites(adenosine, Co2) locally within the restoration of its temporarily blocked blood tissue , those metabolites since they cause the flow. smooth muyscle to relax which cause (e.g cuffs during blood pressure) vasodilation to occur. DIFFERENCE What has caused the accumulation is the difference between the two. Tissue has enhanced its metabolic Reactive hypermia, is happening in absence of activity; more consumption of O2 and change of metabolic activity. So in a muscle that greater production of metabolites. Active occurs when you have strong contraction , it can becase the cells are actively consuming happen in skeletal muscle, it temp blocks blood more oxygen and nutrients from entering that region because the blood vessels have been compressed by the muscle. Cells are still metabolizing , the cells are accumulating because they are not being WASHED OUT. *When you restore blood flow then you see REACTIVE HYPERMIA both things cause vasodilation; both negative feed backs designed to restore the metabolic profile of the tissue. The increase in blood flow will help to washaway metabolites and bring O2 back to that region blocked due to accumulation of metabolites. Arterioles VASODILATION does not affect the venous return because the veins lie in between the two (arterioles and the heart) . The veins determine VENOUS RETURN. Sympathatic Nervous effect on arterioles and how it fits in with exercise. Sympathetic nerves release norepinephrine which will cause vasoconstriction, when symp nervous activates adrenal glands they release epinephrine and in the skeletal muscles that will allow , for epinephrine to bind to beta adgregneric receptor which will cause some vasodilation. Balancing amount of norepinephrine vs. epinephrine because of that sympathetic nervous system to vasoconstricte skeletal muscle blood vessel. When sympathetic is active both are being released and two have a conflict with each other EXERCISE EXAMPLE Locally produced metabolites are added , that’s the additional point that tips the balance between vasoconstriction and vasodilation. So when you are excercising we have norepihinepihne and ephonrine balance. Metabolites will add to the vasodilation part and you will see vasodilation in the excercising muscle. In non-exercising is muscle, when sympathetic nerve activity is high in the body, you will see vasoconstriction in other muscles not EXCERCISING . There we just have norepinephrine due to more receptors as compared to epinephrine which causes VASOCONSTRICTION. Net total is vasoconstriction that no
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