An example of this interaction are the elastic arteries* (as the ascending aorta,arch of aortaall the arteries close to the heart,..

Transcription

1 بسم رلاهللا Maintaining the blood flowto the organsis done by interaction of both: 1)The heart 2)and the blood vessels An example of this interaction are the elastic arteries* (as the ascending aorta,arch of aortaall the arteries close to the heart,..) *They are called elastic because they have a media that is very rich in elastic tissue,conversely, the Muscular arteries the media is rich in smooth muscle The ascending aorta stems from the left atrium (in between there is the aortic valve),and the left atrium is connected to the left ventricle by the bicuspid valve. Those two (the aortic valve and the bicuspid valve) work in correlation to each other so that in early systole(systole and diastole have stages **) both are closed **systole stages(pumping of blood***): In ventricular systole we have 1)Isovolumetric contraction :where the ventricular fibers contract without a change in their length(as we recall: we have two types of contraction,isotonic contraction; where the muscle s length is reduced and the tension remains the same, and isometric contraction where the tension increases and the length of the muscle remains the same.) Here in the isometric contraction first phase, the wall of the ventricle has contracted and the fibers length hasn t changed,and the blood pressure inside is increased as a result of tension increase.this increase in the ventricular pressure push the blood back so the bicuspid valve close and so preventing the blood return to the atrium In the second phase the pressure s increase inside the ventricle makes it more than the pressure in the aorta, as a result the aortic valve opens and the second stage of systole begins. 2) Ejection of blood to the ascending aorta and the arch of the aorta (remember they are elastic fibers) making them expand as a result of their elasticity.by this the systole ends and the diastole begins. The Diastole (filling of blood****): The heart muscle relaxes so the blood pressure in the ventricle decreases so it become less than the pressure of the atrium and this leads to opening the bicuspid valve.simultaneously, the aortic valve is closed to prevent the blood return from the aorta to the ventricle

2 As we said earlier in Diastole the ventricle relaxes, so it fills with blood,the blood is not pumped to the body, while in systole the blood is pumped out, so the blood flow from the heart is an intermittentflow, would the brain tolerate this? The answer is no, the brain won t tolerate a time in which it receives blood and another without blood, so we must transform this intermittent flow into a continuous flow and this is done by elastic artery. How does the elastic artery do that? During systole when the blood is pumped, the elastic artery expands while in diastole when there is no pumping of blood from the heart it recoils pushing the blood to the body (so even when there is no pumping from the heart, the blood still goes to the body).this is because of the abundance of elastic tissue in the elastic artery.here we see the structure function relationship and how the heart and blood vessels interact. ***at the end of systole 80 millilitrecubic of blood is pumped (called stroke volume)***** ****at the end of diastole the each ventricle is filled with 130millilitre cubic of blood(called end diastolic volume) 50 millilitreis left (called end systolic volume) So at the end of systole the ventricle is not completely emptied from blood So if in every stroke 80mm is pumped, in 1 min 80X70=5.6 litres which is called Cardiac Output. *****this reflex the strength of the heart s contraction and this is called inotropic effect which means contractility, the muscle of the heart gets weak if the blood that reach it is less as when there is a thrombus in the coronary arteries,if this happen,the pumping action of the heart is weakened.we test this by a device in hospitals called echocardiograph we calculate the ejection fraction which is the percentage of what got out of the heart to what remained in it so 80/130 *100% =65-67%.and this is the simplest test done, if its this means that the heart is weak (there are many reasons for this like ischemia )and this could lead in the future to heart failure. If there is an increase it would be in the cardiac output as a result of an increase in the heart rate, some drugs may increase the force of contraction and so the stroke volume but the result is on the cardiac output, for the cardiac output is

3 composed of stroke volume and heart rate,any of them could increase but if the heart accelerates a lot the stroke volume will decrease as there won t be enough time for filling (the diastole is too short). Now we will compare the heart muscle to the skeletal muscle First, the cardiac muscles branch and these branches have no function they don t conduct cardiac impulse or anything. Second,every skeletal muscle fiber is a cell while the cardiac muscle fiber is a group of cells connected together by intercalated desks (which is a cell membrane connected to a cell membrane by macula adherence,fascia adherence and most importantly gap junctions which is an area in the membrane of low electrical resistance that allow rapid spread of action potential /cardiac output from cell to cell )so if we activated one cell in the atrium or in the ventricle all of the atrium or ventricle will contract,this property is not available in skeletal muscle(cause they don t have gap junctions) its only in cardiac and some smooth muscles. In skeletal muscles the nerve gets to the muscle and gives a branch to a group of fibers (so the muscle is divided to units)which is called a motor unitso we can stimulate one part of the muscle or more (this is the foundation of muscle tone which is a partial contraction of the muscle) but in cardiac muscle we don t have motor units (we have gap junctions instead) and the whole heart contracts as one mass and this is essential for the mechanism by which the heart functions. Third, in cardiac and skeletal muscle there are cross striations which indicate that there is actin and myosin arranged as sarcomeres (a and I band and z desk),in the smooth muscles they are not arranged as sarcomeres Forth,in cardiac muscle every cell contains single nucleus placed in the center while in skeletal they are multinucleated and the nuclei are peripherally located Fifth,calcium induced calcium release Sixth, the sarcolemma (the cell membrane of the skeletal muscle fiber ) has an invagination called the T tubule which is essential in skeletal and cardiac muscles fibers where it conducts the action potential deep into the muscle fiber.but in the cardiac muscle fibers it is wider and is associated with calcium channels and found at the level of the Z-line while in skeletal it's on the A-I junction. In skeletal fibers, on the sides of the T tubule the sarcoplasmic reticulum aggregate to form terminal cisternae(they are called triad) where the calcium (which is essential for contraction) is stored.in the cardiac muscle the sarcoplasmic reticulum is less well developed,they have diad,where there are no large terminal cisternae,instead there are small expansions

4 How do we get the calcium out of its storage? In skeletal muscle,on the inner surface of the T tubulethere are voltage sensors,and as the T tubule is a membrane it has proteins (channel proteins).on the terminal cisternae there are Ryanodine calcium release channels which is closed by a molecule called foot process.when the action potential reaches the T tubule a conformational change in Dihydropyridine receptor(named after the drug that act on it ) occur,this conformational change removes the foot process that was closing the ryanodine calcium release channel, and the calcium gets out. In the cardiac muscle, it s the same process but with few differences: The Dihydropyridine receptor has a calcium channel where the calcium enters from outside so in order for the calcium to exit from the cisternae (sarcoplasmic reticulum, the storage) there should be also calcium entering inside this is called calcium induced calcium release. Contraction in the cardiac muscle is sequential,not direct: First,the action potential reaches the T tubule causing the calcium induced calcium release Second, the calcium concentration increases in the heart muscle Finally,contraction occurs So the Inotropic effect (the strength of contractility) depends on : 1)the amount of calcium in the sarcoplasmic reticulum(the main factor) 2)the amount of calcium that entered from outside causing the calcium in the inside to get out For the muscle to relax the extra calcium that entered from the outside ( during contraction) must exit or the muscle will tetanize,this is done by: 1) ATPase Calcium pump,which is found in the wall of the sarcoplasmic reticulum. It pumps calcium back to the sarcoplasmic reticulum. 2) Sarcolemmal ATPase Calcium pump,on the plasma lemma (on the plasma membrane.it pumps the calcium outside 3) Sodium calcium exchanger.it pumps one calcium outside in exchange of entering three sodium, here we are pumping calcium against concentration so we need energy so we use the energy that resulted from entering the sodium, so the entering of sodium downhill works on calcium exit uphill. 4) Closing the calcium voltage channel that we opened for the calcium to enter from outside

5 Those four work on lowering intracellular calcium and so cause muscle relaxation. At one time in the old days they used to give IV calcium to cure almost anything,but if we do so the calcium will rush to the heart quickly (more than normal) causing tetanization of the heart it will remain in systole,there will be no pumping of blood, and this will kill the patient, so if we give Iv calcium it must be very very slow (ex. 10 ml must be given at a 10 min interval ).So physiologically the heart muscle don t tetanize * but if we give calcium from outside it may. *(cause tetanization depend on action potential, and action potential here continue with the contraction while in skeletal muscle its very short it ends then the contraction starts) Now we will move to the pictures part.

6 This is a section in the elastic artery,it is at low magnification so we can t distinguish the intima or the adventitia or media. Those spots inside are smooth muscle nuclei not fibroblast. This is at larger magnification, but still we can t distinguish structures The intima composed of the endothelium( which is characterized by its nucleus, its simple squamous), and basal lamina(that we don t see),then sub endothelial connective tissue Internal elastic lamina is the outer border of the intima which separate it from media Media is rich with elastic laminea (its fenestrated elastic laminea layer) inbetween there is little amounts of smooth muscle and collagen (we can t distinguish which is which as they are all pink as they are stained by eosin)but if we look closely we see wavy lines those are definitely the elastic laminea (cut crosswise),we can t say if there was collagen and smooth muscle(in the elastic artery all the media looks as if it was homogeneous) If we want to distinguish the elastic laminea and collagen and smooth muscle we should use a differential stain that will stain the the elastic laminea black, and collagen green, and smooth muscle red.

7 This is also the intima and adventitia looking homogeneous,stained with the classical H and E stain. We see the vasa vasorum (vessel of the vessel) which is found in adventitia or the outer media to supply the outer layers (that the diffusion don t reach ) with blood and nutrients and oxygen

8 Here we used Masson s trichrome stain, it stains elastic fibers black,collagen green,and smooth muscles red.when we look at the media of the aortic elastic artery we notice that its black at most, soit's mostly elastic tissue (as we recall, its layer of elastic laminea ) This is at higher magnification.we see black (elastic laminea) and in between there is little green and red. Q: what is the function of the pointed tissue? A; elastic tissue expands during systole and recoil during diastole, hence, it converts intermittent flow to continuous flow of blood. Once again we say those nuclei we see aren t of fibroblasts, they are smooth muscles nuclei. Smooth muscles (red) produce both collagen (green) and elastic fibers (black)

9 The media is mostly black while the adventitia is mostly green because its mostly collagen with some elastic fibers. Also we see here a small blood vessel which is vasa vasorum. Here we used Van Giesonstain, it stains elastic fibers black and smooth muscle and collagen yellow to brown but here it is atypical so the black lines are the collagen and in between them is the collagen and smooth muscles.

10 Here we have it at a higher magnification (35:45) Here we will compare medium sized artery and vein placed beside each other. Arteries are found between muscles and around them are the veneacomitantes The wall of the artery is thicker than that of the vein (its thin so it is collapsed), but the lumen of the vein is bigger. After death we see blood RBCs and WBCs in the vein not the artery. The layers of the artery are intima, media and adventitia.at this low magnification its hard to see the tunica intima,but the media is the thickest layer in the artery while in the vein the thickest layer is the adventitia and the media is relatively thin.this is related to the function as smooth muscle is a major component of the muscular artery(which is the medium sized artery as femoral and brachial arteries and the corresponding veins are the medium sized veins ).this smooth muscles contract under the effect of sympathetic and other factors,when they contract they narrow the lumen and limit the blood flow, so we call these arteries distributing arteries ; it either allow the passing of blood or not so it distribute it while in the vein the abundance of collagen gives the character of compliance so it expand with little recoil(60% of our blood is in veins),these medium sized veins are described as low resistance collecting vessels or system (they have low resistance because usually the smooth muscles are the ones that are responsible for resistance and they are little in veins) also called low pressure storage system,it has high compliance,if we added large amount of blood in it the pressure will rise slightly (the pressure in veins don t increase over 18 mmhg) while if we added a little amount of blood to an artery the pressure will increase a lot

11 In the artery the adventitia is nearly equal or less than the media, while in the vein the adventitia has the major thickness At higher magnification we see a tortious line this line is the internal elastic laminea, we only see this in the muscular arteries not the elastic arteries,or in the veins incomplete. The media in the vein is thin while in the artery its much thicker

12 Here at higher magnification we see the wavy line clearer (so we say we are most likely looking at a muscular artery, but if it's not continuous then it s a vein), the main thickness is for the media while the adventitia s thickness is equal or less. This is the typical muscular artery: 1) Tunica intima : characterized by nuclei of squamous epithelium,underneath there is basal lamina (not clear),little sub endothelial connective tissue,then we see the wavy line (the internal elastic laminea,if its continuous then we're usually looking at muscular artery) 2) Media : in a big arteriole there are 4 layers of muscles if more then it's an artery (we count layers by the nuclei,if we move horizontally then every nucleus is a layer here it's around layer).the layers are closely packed with little collagen inbetween (unlike the veins).the outer borders of the media are the external elastic laminea ( not a single lamina ) 3) Adventitia :to be continued

13 3) Adventitia :the muscles in the media are controlled by the network of sympathetic fibers in adventitia where they send their neurotransmitter (norepinephrine)to activate the muscles so there will be a vasoconstriction but when they relax( when there is no sympathetic stimulation,not by the parasympathetic) vasodilation occurs So when we see will defined internal elastic lamina and will defined external elastic laminea,then this is typical medium sized artery (distributing,muscular) This is at higher magnification

14 This is a muscular artery that we stained with Masson s trichrome, we know it s a muscular artery because of its borders of media(the black colors with the arrows pointing towards them) IEL(could be 2 layers) and the external elastic laminae (3-4 layers),we notice that the media is mostly red so its mostly composed of smooth muscles,we see little green (collagen),and if you look closely you will see black wavy lines, the elastic fibers(look at the turning arrow)and it is little unlike the elastic artery (where elastic fibers are abundant and muscles and collagen are little) The outer borders of the intima is the internal elastic lamina,and the outerborder of the media is the external elastic laminea that separate it from the adventitia. The intima is not clear, and the adventitia is thicker than the media.

15 When we magnify the media, we notice that there are a few smooth muscle layers (little) with abundant collagen between them, by this we say that this is a medium sized vein not an artery, we can see incomplete internal elastic laminae, we rarely see external elastic laminae.the major layer is the adventitia which is mostly collagen and little elastic and that what makes vein much more compliant than arteries (the abundance of collagen).compliance is the relationship of volume and pressure, it is a character of the vein not the artery,it is opposite to recoil. Arterioles and venules are similar to their parents the muscular artery and vein respectively.so the venule has a thin media and the adventitia is the major layer of its wall.the arteriole could be small (if it has one layer ) or large (if 2-4 layers).in arterioles, the media is exclusively smooth muscles (there is no collagen nor elastic) and its richly supplied with sympathetic this is true for the small and large arterioles and not the met arterioles nor the pre capillary sphincter that are influenced by metabolites more than the nerve.

16 We talked previously about the tone of the skeletal muscle which originates from the nerve if we cut the nerve there will be no tone.the tone is a partial contraction and a complete contraction and its neurogenic.we can also see tone in smooth muscle but it myogenic (a character in the muscle itself) which means that if we cut the nerve there will still be contraction in the smooth muscles (as in the arteries and intestines). In the arteriole there is myogenic tone which leads to partial contraction in the wall and so partial narrowing of the lumen,this contraction could be more leading to more and more vasoconstriction or it could be less and so leading to vasodilation,if there was no partial constriction then we couldn t have vasodilation just vasoconstriction,that s for its important. The best description of the large arteriole is the major resistance vessel for here the peripheral resistance and maintenance of blood pressure takes place. Blood pressure depends on three factors, the pumping of blood from the heart (cardiac output ), peripheral resistance (mainly in arterioles) and the blood volume (it plays a major role but more mainly are the other two factors, so the arterial pressure depends on the pumping action of the heart against the peripheral resistance).if the arterioles expanded the blood pressure decreases and blood won t reach the brain so the patient will be in danger, also the high blood pressure is dangerous. As long as the blood pressure is normal the patient is safe cause it means that the cardiac output and peripheral resistance are working well and there is blood reaching the brain. This is at higher magnification, here we have 4 layers so it s a large arteriole, we see a tortious (wavy) line not inside the smooth muscle it s the internal elastic lamina

17 Adventitia (green cause of abundance of collagen) Media red cause of smooth muscle but in between there is a lot of collagen Saphenous vein is superficial vein which means that its outside the deep fascia and the muscles and so it doesn t have support as do the deep veins that are surrounded by muscles and deep fascia. When we see smooth muscle and a lot of collagen in between (we see fusion of green and red )then this is vein as we don t see this in the artery.(this is characteristic) We have another character of the superficial veins,in the adventitia there are vertical muscles for support only,it strengthen the wall (unlike the horizontal ones that narrow the lumen)cause these superficial veins lack the support of muscles and deep fascia and the proof for this is that they cause varicosity (as when standing for long periods)

18 2 1 3 Microcirculation means the arteriole and what follows it,so its arteriole capillary then venule. 1:arteriole,thick wall, narrow lumen, 1-2 layers,small arteriole.(the Dr. can ask us a lot of Qs like major resistance vessels,what happens if excessive vasodilation occurs? Blood pressure drop.and they are richly supplied with sympathetic) 2:venule,thin wall,large lumen we could see some blood remaining,the muscles are relatively little 3:capillary, single endothelium resting on basal lamina,it doesn t have media nor adventitia ,2 :venules,they have thin walls 3:most probably it s an arteriole,its wall is thicker and we can see the nuclei of smooth muscles

19 This is the cardiac muscle at higher magnification, we see the muscle fibers branching and this character is not found in skeletal muscles More magnification, we see single nucleus located at the center.

20 This is a cross section of the cardiac muscle fibers, the cells that appear without a nucleus are cut at their sides that s why their nuclei don t appear (its located at the center). Intercalated desks are three components :macula adherence (desmosomes),fascia adherence and gap junctions(this gap junctions make the cardiac muscle a syncytium,as if there was no boundaries between cells functionally,cause there are cell membranes for each cell mso it is a functional syncytium not an anatomical one). The atrium is a syncytium and the ventricle is a syncytium in between there is a fibrous ring (it s the skeleton of the heart,valvus ring that the valves attach to), but there is a very small muscle called AV bundle that conduct the cardiac impulse from the atria to the ventricles(it s the only connection between them)

21 When we look closer we see evidence of cross striations that means that there are actin and myosin arranged as sarcomeres (in smooth muscles they are not arranged as sarcomeres) The heart has a conductive system for cardiac impulse (action potential):sanode,avnode, AVbundle, right and left branches(from which the Purkinje fibers branch ).So the heart muscle is either contractile or conductive.purkije fibers are larger than contractile fibers,and they are present under the

22 endocardium so its close to the blood, its most important characteristic is that it has little fibrils (fibers >fibrils> filaments actin and myosin ) for its function is contraction and Purkinje conducts, and lots of collagen. The collagen area takes the eosin stain Here its stained with PAS stain,it has glycogen(source of energy) with little fibrils ;so the central part of the fiber appears as if it was washed out.

23 This is at higher magnification. Sorry for mistakes Done by :Yarakhayyat Special thanks to : Anwar Hagar,Maha Al Mahdy.