The Windkessel action is most spectaculars aorta but is also seen in its branches too In old age (and some times in young persons too)

ries Their functions areas follows . As the heart pumps out its stroke volume into the aorta (which already contains some blood), an additional 70 ml or so (= the stroke volume) is thrust into it (aorta) The aorta is therefore suddenly more distended This means a part of the energy released by the heart during the ventricular systole is stored as potential energy in the walls of the aorta. in the next moment, during diastole, the aortic wall recoils due to its elasticity and the potential energy is re leased into the blood, causing it to surge forward with a renewed' vigor This is called Windkessel Effect' Because of this Wmdkessel Eflect. the velocity of blood is reduced to some eilent during systole but the velocity of blood during diislole is increased (owing to the elastic recoil of aorta), where the Windkessel Effect is deficient (as in arteriosclerosis, see below), the systolic velocity or blood is very high and the aorta becomes more empty in distole( The Windkessel Effect, reduces the requirement of energy expenditure by the heart dunng the systole The pumping action of heart the elastic recoil, of the aorta, taken together, is the driving force which drives the blood forward and is called Vis a tergo' Vis a largo is the most important factor for the onwar movement of blood Evidently, the magnitude of the elastic recoil depends upon the presence of sufficient number of elastic fibers in the aorta and its branches. The Windkessel action is most spectaculars aorta but is also seen in its branches too In old age (and some times in young persons too) the aorta becomes the seat of the disease called atherosclerosis In this disease there is lipid deposition in the tunica itima and media and subsequently there is calcification. There is much loss of elastic tissue. As a result of all these events. The arterial walls become hardened ('arteno-sclerosis) and The aorta loses its elasticity In such cases, owing to the lack of stretchability of the aorta, the systolic BP be comes very high but as the eitra blood leaves these vessels very quickly, the diastolic pressure is low Clinically, such cases are called systolic hypertension, the condition is characterized by high systolic, and a normal or subnormal diastolic pressure (e.g. ,200/70 mm Hg) and a high pulse pressure. This may be thus, viewed as a type of 'water hammer pulse' (chap 9 sec V, pulse', for details) The Windkessel vessels do not offer any serious resistance to The flow of blood (fig. 5 .7. 4.) Any change in their diameter has only a negligible effect on the total penpheral resistance. II Precapillary resistance vessels in short, this means the arterioles Most of the peripheral resistance encountered by the advancing column of blood is at the level of arterioles (fig. 5.7.4.) Therefore, arterioles are aften spoken of as the 'seal of the peripheral resistance' NB In the disease, essential hypertension, the arterioles are narrowed -4 BP increases. The walls of the ariterioles, practically speaking do not contain any elastic tissue, hence they are also called muscular arteries. They are richly supplied by the sympathetic system, There is a basic tone of The smooth muscles, on the top of which there is the added effects of the sympathetic nerves. Further, the sympathetic nerves themselves discharge Tonically. Due To the action of the sympathetic nerves (and also due to The actions of such naturally occurring vasoactive agents like adrenalin) the diameter of the artenoles after from time to time which in turns causes change of total peripheral resistance from time to time Some special points in relation to the artenoles are discussed below. 1. Critical closing pressure (of Burton) it can be shown by arguments that there is a critical diameter for every blood vessel, and if the diameter is Further reduced [below this critical diameter (due to the achon of sympathetic or vesopressor agent), the blood vessel will totally collapse. Evidently, arterioles therefore face the possibility of closing when subjected to The excessive action of vasoconstrictors Explanation: Recall the Laplace's law (fig. 5. 12.1 ) however the mathematical expression of Laplace's law for cylinder like arteriole is little different from that of a sphere, but this may be ignored for the time being). Smaller the radius, r. of the cylinder (or sphere) greater is The transmural pressure, P (which here is due to the tone of the arteriolar muscle) at a low perfusion pressue the arteriole collapses. If the vascular tone is constant, lower the BP. greater is the propensity to collapse (Here. the BP is the P1 of fig. 5.12.1) 2. Autoregulation Apparently it appears that if the perfusion pressure in the aorta falls there will be reduction of blood flow in the individual organs and vice versa. In practice, at least in some organs (brain, heart, kidney) the blood flow does not after unless the perfusion pressure is severely changed That is. minor or even moderate rise or fall of perfusion pressure does not affect the perfusion of the organ This ability of the individual organ to keep its blood flow reasonably constant, despite fair degree of changes in the perfusion pressure, is called autoregulation Mechanism of autoremulation is not clear Some popular the ones are discussed below (i) One of the widely believed theories is as follows Suppose the perfusion pressure in the feeding artery of the organrises — This causes more stretch of the arterial wall. In the arterioles. this leads To stretch of the smooth muscles in the well — vigorous contraction of the smooth muscles, (because a property of the smooth muscles of arterioles is that when it is stretched, it risponds to the stretch by contracting). This theory, called myogenic Theory is not new