BISC 307L 2nd Edition Lecture 28 Current LectureBlood VesselsAneurysms only occur in arteries, because only in arteries is the wall strain high enough to cause an aneurysm. Only 3 out of these 5 vessels havesmooth muscle in their walls: arteries,arterioles, and veins. Capillaries andvenules don’t (they consist of a singlelayer of endothelial cells). The vascularsmooth muscle is capable of contractingor not – when contracting, it is calledvasoconstriction. When not contracting,the pressure inside the vessel causesthem to inflate, and this is calledvasodilation. The vasoconstriction of thearteries and especially the arterioles isgoing to increase the resistance to bloodflow. These changes in resistance toblood flow make it possible to redirectblood flow in the systemic circulation, which has many paths - so regional vasoconstriction can redirect blood flow one way or another. For example, after lunch vasodilation causes blood to flow toward the digestive organs. MicrocirculationCirculation of small vessels. Can seean artery feeding into an arteriole intocapillaries – flow is down from thetop, across to the right, then back up. Arteries are strongly reinforced byconnective tissue sheaths. Arteriolesdo not have this – also, they cangenerate force very efficiently for longperiods of time. They are always contracted to some extent, 24 hours a day – their level of contraction is called vascular tone. Capillaries have no smooth muscle except at the place where the arterioles meet the capillaries,there are bands of smooth muscles called pre-capillary sphincters, and they regulate how much blood is going through the capillary network. In most tissues, every cell in the tissue is no more than a few cells away from a capillary – so there is dense vascularization of capillaries through most tissues. Under most conditions, most of the capillaries do not have blood flowing through them – the precapillary sphincters are constricted. Only 10-20% of capillaries at a time have blood flowing through them. Blood has to get from arteriole side to venous side to get back to the heart, so if the capillaries are sealed off, how does the blood get by? They get through thoroughfare channels formed by metarterioles or arteriovenous bypasses. Metarterioles have some smooth muscle around it, but not as much as a normal arteriole. These are bigger vessels and tend to be thicker walled than capillaries so they don’t contribute much to gas/nutrient exchange. Because they are bigger, leukocytes(which are larger than RBC’s) use them instead of capillaries to get around. AngiogenesisThere’s a lot of research recently on angiogenesis – the formation of new blood vessels. This is important in tumor research – a tumor attracts blood vessels so that it can grow. So there has been a lot of advances on the growth factors that promote angiogenesis. Important stimulants: -vascular endothelial growth factor (VEGF) – this can happen in the retina due to vascular damage caused by diabetes that forces VEGF to be used to vascularize the area in orderto fix it. -fibroblast growth factor (FGF) -matrix metalloproteinases (MMPs) – these are extracellular proteases that digest molecules in the extracellular matrices. These are important in angiogenesis because things like VEGF stimulate endothelial cells to de-differentiate from their normal, mature phenotype, to proliferate and migrate to form new blood vessels. The migration of endothelial cells to tissue toa site that needs vascularization requires these MMP’s to digest their way through the space.-a dozen other factorsInhibitors of angiogenesis:angiostatin, endostatin(a proteolytic fragment of a blood clotting protein called plasminogen), many othersPressure in Blood VesselsLooking at pressure change in systemic circulation. Graph shows pressure in mmHg in various places in the systemic circulation starting from left ventricle to right atrium. In general, pressure fluctuates from 120+ to 0. During systole, left ventricle pressure is high, and during diastole, it is at or close to 0. Blood comes out of LV and enters aorta. There are still pressure fluctuations here, but they are much less, between 120/80. Why the arterial pressure fluctuates less is because arteries are moderately compliant (tendency of a material to deform under pressure-a rubber balloon would have much less compliance than aplastic bag, which would take much less air pressure to blowup) and highly elastic (property of a material to recoil to itsoriginal size after its been deformed – rubber balloon wouldbe highly elastic and plastic bag not at all). This means whenblood comes into artery, they expand due to the moderatecompliance. During isovolumic ventricular relaxation, and thepressure in the ventricle is falling because it is in diastole,there is no more blood being ejected into the aorta becausethe higher backpressure has closed the semilunar valve. The stretching of the elastic wall had stored some of the energy that the blood, and during diastole of the ventricle, the aorta squeezes down on the blood and keeps the pressure from going as low as it is in the ventricle (hence the 120->80 instead of the 120->0). The pulse pressure is the difference between systolicpressure and diastolic pressure. MAP(mean arterial pressure) is not the halfway between the systolic and diastolic pressure because the systolic and diastolic phases are different in length, and because the falling phase ofpressure is slower than the rising phase. Result:Mean Arterial Pressure (MAP) = diastolic P + 1/3 (pulse P)= 80 + 1/3 (120 – 80= 93 mm Hg.93 can be thought of as the arterial pressure that is pushing blood through the vascular system. We have two ways of calculating mean arterial pressure now. The way above, and the formula: MAP = CO x peripheral resistance. As the blood leaves the arteries and enters the arteriole, the pulses dampen out because the arterioles are much smaller. Resistance of the arterioles are high, which diminishes the pressurefluctuations. Deeper you go into the arterioles, they get more damped. By the time you reach the capillaries, there are no more fluctuations. This allows for more efficient exchange of nutrients/gases in capillaries. If you were to lose elasticity, due to disease like arteriosclerosis(hardening of arteries), the pressure fluctuations on the artery would be bigger (because it was the elasticity thatdampened the pressure pulse) and would pulse further