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NROSCI/BIOSC 1070 and MSNBIO 2070 September 27, 2017 NROSCI/BIOSC 1070 and MSNBIO 2070 September 27, 2017 Cardiovascular 6 Special Circulations Coronary Muscle The coronary arteries branch directly from the aorta, and provide the perfusion of the heart. Although blood actually is pumped through the heart, only ~ 100 µm of the inner endocardial surface can obtain significant amounts of nutrition directly from the blood supply in the cardiac chambers. Blood flow through the coronary capillaries during systole and diastole is different than in most other tissues of the body. The blood flow to the ventricles falls during systole, and increases during diastole. During ventricular contrac- tion, blood flow through the capillaries is obstructed by compression of the vessels. Thus, blood flow increases during diastole when the muscle around the vessels relaxes. Autoregulatory mechanisms are paramount in adjusting the blood flow through the heart. Another major influence on dilation of the coronary arteries is epinephrine released from the adrenal gland. Cerebral Circulation The cerebral circulation is almost completely insensitive to neural and hormonal influences that produce vasoconstriction elsewhere in the body. By far the predominant factor that controls blood flow through the cerebral circulation is paracrine release. In particular, carbon dioxide has a strong vasodilation effect on the cerebral vessels. Skeletal Muscle Circulation Control of blood flow to skeletal muscle is in many respects similar to that in the heart. Paracrine fac- tors have strong influences, and vasodilation is induced by the release of epinephrine from the adrenal gland. A major difference between the two circulations is that skeletal muscle arterioles are richly in- nervated by sympathetic vasoconstrictor fibers, and are major resistance vessels to contribute to total peripheral resistance. Because skeletal muscle mass is so large, vasodilation of muscle vessels would greatly diminish total peripheral resistance unless vasoconstriction occurs in other vascular beds. It is thus necessary that the central nervous system provides control of blood flow through skeletal muscle. 9/27/17 Page 1 Cardiovascular 6 Body Fluid Compartments: Fluid in the body is located in three distinct compartments: Plasma (~ 3 L) Interstitial fluid (~12 L) Intracellular fluid (~25 L) To reach that intracellular compartment from the plasma, a molecule must diffuse across the capillary plasma membrane into the interstitial compartment, and then across the cell membrane into the intracellular fluid. Capillaries are composed of a single layer of endothelial cells and a basement mem- brane; the thickness of the wall is only about 0.5 micrometers. Small intercellular clefts typically separate the endothelial cells. Capillaries are often associated with elongated, highly branched cells that form a meshlike layer between the endothelium and interstitial fluid. These cells are called pericytes. The pericytes contribute to restricting capillary permeability. Exchange of materials through capillaries usually occurs through diffusion. Small and uncharged and lipid-soluble molecules (including O2 and CO2) have no problem passing through the capillary wall. Larger and charged molecules may pass through the intercellular clefts or via vesicular transport. Water crosses the capillary through both in- tercellular channels and specialized water channels (aquaporins) in the endothelial cell membrane. In general, large molecules have a very difficult time escaping from capillaries, as shown in the table to the left. There are some exceptions, however. Some capillaries have receptors for particular proteins; once the protein binds it is carried across the membrane via a process called transcytosis. 9/27/17 Page 2 Cardiovascular 6 However, in some organs, very large proteins (and even cellular elements) need to enter or leave the circulation. Thus, some capillaries are fenestrat- ed (or have large pores) to facilitate this exchange. For example, the intestine contains fenestrated capil- laries so that large molecules can be moved from the GI tract to the bloodstream. In other organs (e.g., bone marrow and the spleen), the endothelial cells are discontinuous to permit red blood cells to enter the circulation. Osmotic Relationships Between Compartments Osmolarity is a measure of the absolute concentration of osmotically active particles. A solution of one mole/liter of non-dissociable solute is equivalent to 1 osmole/liter (1 Osm). Normal osmolarity of body fluids is about 300 mOsm. The osmotic pressure of a 1 Osm solution is 22.4 Atm, or 22.4 x 760 = 17,024 mmHg. Thus a 300 mOsm solution has an osmotic pressure equivalent of 17,024 x 0.3 = 5,107 mmHg. The only molecular species for which there is a significant concentration difference between the plasma and interstitial fluid is protein. All of the other solutes, which make up the major component of plasma osmolarity (Na+, Cl-, HCO3-), are present in approximately equivalent concentrations on both sides of the capillary membrane. Hence differences in protein concentration provide the only osmotic driving force at the capillary level. The plasma protein concentration is about 7 gm/100 cc plasma (7 gm%). The osmotic pressure generated by this protein is known as the oncotic pressure and is in the range of 25-28 mmHg. The oncotic pressure difference between the capillary plasma and the interstitial fluid tends to draw fluid INTO the capillary. However, another major force is at play in capillaries: hydrostatic pressure, which is due to the pressure in the blood imparted primarily by the contraction of the ventricle. The hydrostatic pressure is higher in the capillary than in the interstitial fluid, and tends to force fluid OUT of the capillary. The balance between oncotic pressure and hydrostatic pressure across the capillary will determine whether there is a net gain or loss of fluid across the vessel. This balance can be expressed quantita- tively via Starling’s equation (from the same Starling who formulated “Starling’s Law of the Heart.”) 9/27/17 Page 3 Cardiovascular 6 The Starling equation reads as follows: Jv = Kf ([Pc—Pi] — s [pc—pi]) Where: Pc = Capillary hydrostatic pressure Pi = Interstitial hydrostatic pressure pc = Capillary oncotic pressure pi = Interstitial oncotic pressure Kf = Filtration coefficient s = Reflection coefficient Jv = Net fluid movement between compartments In essence the equation says that the net filtration (Jv) is proportional to the net driving force. By con- vention, outward force is defined as positive, and inward force is defined as negative. Ifv J is positive, fluid will tend to leave the capillary (filtration). If Jv is negative, fluid will tend to enter the capillary (absorption). This equation has a number of important physiologic implications, especially when pathologic processes grossly alter one or more of the variables. The first four variables in the list above (Pc, Pi, pc, pi ) are the forces that contribute to the net driving force. The filtration coefficient f(K ) is the constant of proportionality. A high Kf value indicates a highly wa- ter permeable capillary. A low value indicates a low capillary permeability. The filtration coefficient is the product of two components: capillary surface area and capillary hydraulic conductance. The val- ues for both of these components are usually relatively high, and are fixed for a vascular bed, but there are exceptions. As you will learn during the renal section, the number of aquaporin channels inserted into the distal convoluted tubule and collecting ducts of the kidney nephrons is dependent on the levels of circulating vasopressin. In the absence of vasopressin, few aquaporins are present and Kf is low. The reflection coefficient (s) is often thought of as a correction factor. The idea is that the difference in oncotic pressures contributes to the net driving force because most capillaries in the body are fairly impermeable to the large molecular weight proteins. In fact, some smaller proteins can leak across the capillary membrane through the intercellular clefts, which must be accounted for as it diminishes the driving force. The reflection coefficient (s) is used to ‘correct for’ the ineffectiveness of some of the oncotic pressure gradient. It can have a value from 0 up to 1. Non-fenestrated vessels have a reflection coefficient close to 1, whereas the value is lower for fenestrated capillaries. Across a particular capillary, Kf and s are usually constant. As such, when we are considering the dynamics in a particular vascular bed, Starling’s equation can be restated as: Jv ≈ ([Pc—Pi] — [pc—pi]) Let’s consider a situation where the blood entering the arterial end of a capillary has a hydrostatic pressure of 25 mmHg, and also carries an oncotic pressure of 25 mmHg. In the adjacent interstitial space, hydrostatic pressure is usually slightly negative (approximately -3 mm Hg). Let’s also assume that interstital oncotic pressure is 5 mm Hg. In this case, Jv ≈ ([25 — (-3)] — [25 — 5]), or 8 mmHg. Since Jv is positive, fluid will tend to leave the capillary and filtration will occur. 9/27/17 Page 4 Cardiovascular 6 As blood passes along a capillary, it loses hydrostatic pressure due to friction. At the venule end, hy- drostatic pressure is often near 10 mmHg, If there has been no appreciable shift in protein balance be- tween the capillary and interstitial compartments, the relative oncotic pressures won’t change. Thus, at the venule end of the capillary, Jv ≈ ([10 — (-3)] — [25 — 5]), or -7 mmHg. Since Jv is negative, fluid will tend to enter the capillary and absorption will occur. Note that there is an imbalance in filtration and ab- sorption (8 mmHg of filtration at the arterial end and 7 mmHg of absorption at the venule end). As such, the net filtration pressure is 1 mmHg. In general, we tend to lose 2-4 liters of fluid per day into the interstitial space due to the filtration-absorption imbalance. The process is illustrated in the figure to the left. Luckily, the excess fluid lost into the interstitial space is collected by the lymphatic system, as de- scribed below.
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