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MICROCIRCULATION – (CAPILLARY CIRCULATION) Dr.Mohammed Sharique Ahmed Quadri Asst Prof – Physiology Al Maarefa College.

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Presentation on theme: "MICROCIRCULATION – (CAPILLARY CIRCULATION) Dr.Mohammed Sharique Ahmed Quadri Asst Prof – Physiology Al Maarefa College."— Presentation transcript:

1 MICROCIRCULATION – (CAPILLARY CIRCULATION) Dr.Mohammed Sharique Ahmed Quadri Asst Prof – Physiology Al Maarefa College

2 Arterioles Major resistance vessels Arteriolar Resistance converts the pulsatile systolic to diastolic pressure swings in the arteries into the non-fluctuating pressure present in the capillaries Radius supplying individual organs can be adjusted independently to – Distribute cardiac output among systemic organs, depending on body’s momentary needs – Help regulate arterial blood pressure

3 Arterioles Mechanisms involved in adjusting arteriolar resistance – Vasoconstriction Refers to narrowing of a vessel – Vasodilation Refers to enlargement in circumference and radius of vessel Results from relaxation of smooth muscle layer Leads to decreased resistance and increased flow through that vessel

4 Arteriolar Vasoconstriction and Vasodilation

5 Mechanisms for control of blood flow to the various organs Blood flow to organ depends on the demands of each organ. a) Local control of blood flow is the primary mechanism that matches the blood flow to the metabolic needs of the organ. b) Neural or Hormonal control is the other mechanism.

6 Arterioles Only blood supply to brain remains constant Changes within other organs alter radius of vessels and adjust blood flow to organ Local chemical influences on arteriolar radius – Local metabolic changes – Histamine release Local physical influences on arteriolar radius – Local application of heat or cold – Chemical response to shear stress – Myogenic response to stretch

7 ARTERIOLES Many factors can increase or decrease the tone and can cause vasoconstriction and vasodilation. Causes of VASOCONSTRICTION - Sympathetic Stimulation - Epinephrine and Nor Epinephrine - Angiotensin II - Vasopressin - Endothelin [from endothelial cells] - O 2 - CO 2 - Cold 7

8 Arterioles Specific local chemical factors that produce relaxation of arteriolar smooth muscle – Decreased O 2 – Increased CO 2 – Increased acid – Increased K + – Increased osmolarity – Adenosine release – Prostaglandin release

9 Arterioles Local vasoactive mediators – Endothelial cells Release chemical mediators that play key role in locally regulating arteriolar caliber Release locally acting chemical messengers in response to chemical changes in their environment Among best studied local vasoactive mediators is nitric oxide (NO)

10 Arterioles Extrinsic control – Accomplished primarily by sympathetic nerve influence – Accomplished to lesser extent by hormonal influence over arteriolar smooth muscle

11 SYMPATHETIC CONTROL OF ARTERIOLE Sympathetic Control of Arterioles is important in regulating blood pressure. Sympathetic ANS supplies arteriolar smooth muscle all over body except brain. Increase sympathetic stimulation causes arteriolar vasoconstriction. Decrease sympathetic stimulation causes arteriolar vasodilation. There is no parasympathetic innervations to arterioles. 11

12 CONTROL OF REGIONAL BLOOD FLOW

13 LOCAL CONTROL OF BLOOD FLOW A) Autoregulation – maintenance of constant blood flow to an organ in spite of fluctuations in BP. E.g. brain – auto regulation is best kidney – auto regulation is good skeletal muscle – auto regulation is poor

14 LOCAL CONTROL OF BLOOD FLOW B) Active Hyperemia - When any tissue becomes highly active [eg. Skeletal muscle during exercise]. the rate of blood flow through the tissue increases. C) Reactive hyperemia When blood flow to a tissue is blocked for few seconds and then is unblocked, the flow through tissue increases almost 4-7 times normal. The excess blood flow lasts long enough to repay the tissue oxygen deficit that has occurred during occlusion.

15 Two basic mechanisms that explain local control of blood flow 1. Myogenic theory Increase in blood flow  Stretches the vessel  Contraction of vascular smooth muscle  Decrease blood flow back to normal

16 2. Metabolic theory Increase in rate of metabolism  Accumulation of vasodilator substances in active tissues  Blood vessels dilate  Increase blood flow Vasodilator metabolites  O2 tension,  H,  CO2 tension,  Temperature, K+, lactate, Adenosine, Histamine.

17 The term Microcirculation refers to the functions of the capillaries and the neighboring lymphatic vessels. 5 % of circulating blood volume is present in the capillaries at any given time. This takes part into the exchange of nutrients, gases and waste products between the blood & tissues.

18 The Microcirculation ●Important in the transport of nutrients to tissues ●Site of waste product removal ●Over 10 billion capillaries with surface area of 500-700 square meters ●Solute and fluid exchange

19 Arteriole  Meta arteriole  Capillaries  Venules. Pre capillary sphincter is present at the junction where the capillary arises from the Meta arteriole. This opens and closes the entrance of capillary and hence regulates the blood flow through the capillary. The capillary wall is thin & consists of a single layer of endothelial cells on basement membrane. Pores are present between the endothelial cells that allow transport of substances including water.

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21 Types of capillaries Classified according to the size of the pores Brain – the pores are very tight and allow only very small molecules to pass thru. Kidney & Intestine - the pores are wider – fenestrations Liver - the endothelium is discontinuous with wide gaps between the cells.

22 EXCHANGE OF SUBSTANCES ACROSS THE CAPILLARY WALL This occurs by. Simple diffusion Lipid soluble gases such as O2 & CO2 readily diffuse thru the endothelial cells. Bulk Flow - the most important mechanism for fluid transfer driven by Starlings forces.

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24 The rate of filtration at any point along the capillary depends on a balance of forces – STARLINGS FORCES. 1. Capillary hydrostatic pressure Arterial end = 37 mmHg Venous end = 17 mmHg 2. Plasma colloid osmotic pressure = 25 mmHg 3. Interstitial hydrostatic pressure = 0 -1 4. Interstitial colloid osmotic pressure = 0 mmHg

25 Fluid movement = Kf [ (Pc – Pi) – ( Πc - Πi ) Kf = filtration coefficient

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27 Arteriolar end  fluid moves out into tissue spaces Venous end  fluid enters into capillaries. Any decrease in plasma proteins (hypoproteinemia) or increase in capillary hydrostatic pressure (cardiac failure) causes edema. (abnormal increase in interstitial fluid volume ) Histamines, bradykinin increases capillary permeability  edema.

28 Starling’s forces across capillary wall 6/4/2016 28 Filtration Absorption

29 Lymphatic circulation Lymphatic system is responsible for bringing the interstitial fluid to vascular compartment. Normal 24 hrs lymph flow is 2-4 L Lymphatic capillaries lie in interstitial fluid close to vascular capillaries,these capillaries merge into large lymphatic vessels & eventually into largest vessel, thoracic duct which empties into large veins. 29

30 6/4/2016 30

31 Lymphatic circulation The interstitial fluid enter lymphatic capillaries through loose junctions between endothelial cells. Lymph flow back to the thoracic duct is promoted by contraction of smooth muscle in wall of lymphatic vessels & contraction of surrounding skeletal muscle. Failure of lymphatic drainage can lead to Edema. 6/4/2016 31

32 What is Edema? Accumulation of fluid beneath the skin or in a body cavity Palpable swelling produced by expansion of the interstitial fluid volume

33 Causes of Edema Increase capillary pressure – Increase vascular volume Heart failure Kidney disease Pregnancy Environmental heat stress – Venous obstruction Thrombosis Liver disease Decrease colloidal osmotic pressure – Increase loss of proteins Nephrotic syndrome Burns – Decrease production Starvation, Malnutrition Liver disease

34 Causes of Edema Increase capillary permeability – Inflammation – Allergic reaction – Tissue injury – Malignancy Obstruction of lymphatic flow – Surgical removal of lymph nodes – Malignant obstruction – Infection ( filariasis)

35 References Human physiology by Lauralee Sherwood, seventh edition Text book physiology by Guyton &Hall,11 th edition Text book of physiology by Linda.s contanzo,third edition


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