Any agent which is released into the vessel wall may alter the mechanical characteristics of the wall. In some conditions, neuro-chemical agents and temperature changes may counteract. For example, in some pathologic conditions, like sepsis or heat stroke, clinical data show that splanchnic vessels become constricted despite increase in body temperature upto However, clinical evidences show that higher temperature over Moreover, in all conditions in which vessels are isolated and relatively free of the counteracting effects of neuro-chemical agents, the diameter of vessels, even splanchnic vessels, increases in response to moderate increase in temperature, even below Therefore, through the mechanical modeling of any vessel, temperature-induced changes in vessel diameter can be explained more accurately than that through neurochemically-mediated approaches alone.
Moreover, the analysis of the vascular response to different temperatures can be done more precisely and comprehensively. The authors would like to acknowledge Sadra-Sina interdisciplinary scientific group for helpful discussions. Conflict of Interests: The authors do not have any conflict of interests, and any funding source. National Center for Biotechnology Information , U. J Biomed Phys Eng. Author information Article notes Copyright and License information Disclaimer.
This article has been cited by other articles in PMC. Abstract Autoregulation of blood flow is a marvelous phenomenon balancing blood supply and tissue demand. Introduction Autoregulation of blood flow to body tissues is a marvelous phenomenon regulating blood flow in proportion to tissue demand: supplying high blood flow to a hyperactive tissue as well as low blood flow to a hypoactive tissue [ 1 ].
R dyne. Open in a separate window. Figure 1. Hypothesis When parenchymal cells of a tissue become more active, higher amount of heat energy is emitted from the hyperactive cells making the tissue warmer. Discussion The present explanations for autoregulation of blood flow are commonly based on chemically-mediated approaches [ 2 - 5 ].
Acknowledgment The authors would like to acknowledge Sadra-Sina interdisciplinary scientific group for helpful discussions. References 1. Textbook of medical physiology. Philadelphia: W. Saunders Company; Autoregulation of the total systemic circulation following destruction of the central nervous system in the dog.
Circ Res. Circulation: overall regulation. Annu Rev Physiol. Control of microcirculation and blood-tissue exchange. Handbook of Physiology. Sec 2, Vol. Bethesda: American Physiological Society; Astrocytes function in matching blood flow to metabolic activity. News Physiol Sci. Hosford WF. This equation may be applied not only to a single vessel, but can also be used to describe flow through a network of vessels i.
It is known that the resistance to flow through a cylindrical tube or vessel depends on several factors described by Poiseuille including: 1 radius, 2 length, 3 viscosity of the fluid blood , and 4 inherent resistance to flow, as follows:.
It is important to note that a small change in vessel radius will have a very large influence 4th power on its resistance to flow; e. If one combines the preceding two equations into one expression, which is commonly known as the Poiseuille equation, it can be used to better approximate the factors that influence flow though a cylindrical vessel:.
Importantly, flow will only occur when a pressure difference exists. Hence, it is not surprising that arterial blood pressure is perhaps the most regulated cardiovascular variable in the human body, and this is principally accomplished by regulating the radii of vessels e. Although understanding the math behind the relationships among the factors affecting blood flow is not necessary to understand blood flow, it can help solidify an understanding of their relationships.
Please note that even if the equation looks intimidating, breaking it down into its components and following the relationships will make these relationships clearer, even if you are weak in math. One of several things this equation allows us to do is calculate the resistance in the vascular system. Normally this value is extremely difficult to measure, but it can be calculated from this known relationship:.
The important thing to remember is this: Two of these variables, viscosity and vessel length, will change slowly in the body. Only one of these factors, the radius, can be changed rapidly by vasoconstriction and vasodilation, thus dramatically impacting resistance and flow.
Further, small changes in the radius will greatly affect flow, since it is raised to the fourth power in the equation. The relationship between blood volume, blood pressure, and blood flow is intuitively obvious. Water may merely trickle along a creek bed in a dry season, but rush quickly and under great pressure after a heavy rain. Similarly, as blood volume decreases, pressure and flow decrease.
As blood volume increases, pressure and flow increase. Under normal circumstances, blood volume varies little. Low blood volume, called hypovolemia, may be caused by bleeding, dehydration, vomiting, severe burns, or some medications used to treat hypertension. It is important to recognize that other regulatory mechanisms in the body are so effective at maintaining blood pressure that an individual may be asymptomatic until 10—20 percent of the blood volume has been lost.
Treatment typically includes intravenous fluid replacement. Hypervolemia, excessive fluid volume, may be caused by retention of water and sodium, as seen in patients with heart failure, liver cirrhosis, some forms of kidney disease, hyperaldosteronism, and some glucocorticoid steroid treatments. Restoring homeostasis in these patients depends upon reversing the condition that triggered the hypervolemia. Viscosity is the thickness of fluids that affects their ability to flow.
Clean water, for example, is less viscous than mud. The viscosity of blood is directly proportional to resistance and inversely proportional to flow; therefore, any condition that causes viscosity to increase will also increase resistance and decrease flow. For example, imagine sipping milk, then a milkshake, through the same size straw. You experience more resistance and therefore less flow from the milkshake.
Conversely, any condition that causes viscosity to decrease such as when the milkshake melts will decrease resistance and increase flow. Normally the viscosity of blood does not change over short periods of time. The two primary determinants of blood viscosity are the formed elements and plasma proteins. Since the vast majority of formed elements are erythrocytes, any condition affecting erythropoiesis, such as polycythemia or anemia, can alter viscosity.
Since most plasma proteins are produced by the liver, any condition affecting liver function can also change the viscosity slightly and therefore decrease blood flow. Liver abnormalities include hepatitis, cirrhosis, alcohol damage, and drug toxicities.
While leukocytes and platelets are normally a small component of the formed elements, there are some rare conditions in which severe overproduction can impact viscosity as well.
The length of a vessel is directly proportional to its resistance: the longer the vessel, the greater the resistance and the lower the flow. As with blood volume, this makes intuitive sense, since the increased surface area of the vessel will impede the flow of blood. Likewise, if the vessel is shortened, the resistance will decrease and flow will increase. The length of our blood vessels increases throughout childhood as we grow, of course, but is unchanging in adults under normal physiological circumstances.
Further, the distribution of vessels is not the same in all tissues. Adipose tissue does not have an extensive vascular supply. One pound of adipose tissue contains approximately miles of vessels, whereas skeletal muscle contains more than twice that.
Overall, vessels decrease in length only during loss of mass or amputation. An individual weighing pounds has approximately 60, miles of vessels in the body. Gaining about 10 pounds adds from to miles of vessels, depending upon the nature of the gained tissue. One of the great benefits of weight reduction is the reduced stress to the heart, which does not have to overcome the resistance of as many miles of vessels. In contrast to length, the diameter of blood vessels changes throughout the body, according to the type of vessel, as we discussed earlier.
The diameter of any given vessel may also change frequently throughout the day in response to neural and chemical signals that trigger vasodilation and vasoconstriction.
The vascular tone of the vessel is the contractile state of the smooth muscle and the primary determinant of diameter, and thus of resistance and flow. The effect of vessel diameter on resistance is inverse: Given the same volume of blood, an increased diameter means there is less blood contacting the vessel wall, thus lower friction and lower resistance, subsequently increasing flow.
A decreased diameter means more of the blood contacts the vessel wall, and resistance increases, subsequently decreasing flow. The influence of lumen diameter on resistance is dramatic: A slight increase or decrease in diameter causes a huge decrease or increase in resistance. This means, for example, that if an artery or arteriole constricts to one-half of its original radius, the resistance to flow will increase 16 times.
Recall that we classified arterioles as resistance vessels, because given their small lumen, they dramatically slow the flow of blood from arteries. In fact, arterioles are the site of greatest resistance in the entire vascular network. This may seem surprising, given that capillaries have a smaller size. How can this phenomenon be explained? Figure 4 compares vessel diameter, total cross-sectional area, average blood pressure, and blood velocity through the systemic vessels.
Although the diameter of an individual capillary is significantly smaller than the diameter of an arteriole, there are vastly more capillaries in the body than there are other types of blood vessels. Part c shows that blood pressure drops unevenly as blood travels from arteries to arterioles, capillaries, venules, and veins, and encounters greater resistance.
However, the site of the most precipitous drop, and the site of greatest resistance, is the arterioles. This explains why vasodilation and vasoconstriction of arterioles play more significant roles in regulating blood pressure than do the vasodilation and vasoconstriction of other vessels.
Figure 4. The relationships among blood vessels that can be compared include a vessel diameter, b total cross-sectional area, c average blood pressure, and d velocity of blood flow. Part d shows that the velocity speed of blood flow decreases dramatically as the blood moves from arteries to arterioles to capillaries. This slow flow rate allows more time for exchange processes to occur. As blood flows through the veins, the rate of velocity increases, as blood is returned to the heart. Compliance allows an artery to expand when blood is pumped through it from the heart, and then to recoil after the surge has passed.
This helps promote blood flow. In arteriosclerosis, compliance is reduced, and pressure and resistance within the vessel increase. This is a leading cause of hypertension and coronary heart disease, as it causes the heart to work harder to generate a pressure great enough to overcome the resistance.
Arteriosclerosis begins with injury to the endothelium of an artery, which may be caused by irritation from high blood glucose, infection, tobacco use, excessive blood lipids, and other factors. Artery walls that are constantly stressed by blood flowing at high pressure are also more likely to be injured—which means that hypertension can promote arteriosclerosis, as well as result from it.
Recall that tissue injury causes inflammation. As inflammation spreads into the artery wall, it weakens and scars it, leaving it stiff sclerotic. As a result, compliance is reduced. Moreover, circulating triglycerides and cholesterol can seep between the damaged lining cells and become trapped within the artery wall, where they are frequently joined by leukocytes, calcium, and cellular debris.
Eventually, this buildup, called plaque, can narrow arteries enough to impair blood flow. Figure 5. Sometimes a plaque can rupture, causing microscopic tears in the artery wall that allow blood to leak into the tissue on the other side.
When this happens, platelets rush to the site to clot the blood. This clot can further obstruct the artery and—if it occurs in a coronary or cerebral artery—cause a sudden heart attack or stroke. Alternatively, plaque can break off and travel through the bloodstream as an embolus until it blocks a more distant, smaller artery.
Ischemia in turn leads to hypoxia—decreased supply of oxygen to the tissues.
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