1625915643-5d53d156c9525bd62bd0d3434ecdc231 (843955), страница 34
Текст из файла (страница 34)
12.2). Muscular arteriolesmay directly feed into capillaries or into metarterioles thatstructurally are between capillaries and arterioles. Precapillarysphincters are bands of smooth muscle found at the point atwhich blood enters capillaries. Constriction and relaxation ofthe smallest arteries, arterioles, and precapillary sphinctersregulates flow into capillary beds (see “Regulation of BloodFlow”).The thin wall of capillaries consists of a single layer of endothelial cells and the associated basement membrane.
Thissimple structure is well adapted for the diffusion of gases,nutrients, and wastes between blood and the interstitial fluidof tissues, which occurs only in capillaries. The exchange ofThe histological differences between various types ofvessels reflect their functional roles. The thin wall of thecapillaries, consisting of only an intimal layer, allows the efficient exchange of nutrients, waste, and dissolved gases betweenblood and tissues. On a relative basis, the muscular tunicamedia is more prominent in small arteries and arterioles thanin large arteries or veins, reflecting their role in regulation ofblood flow. Larger arteries have thick adventitia with significantelastic tissue, consistent with their role as “distributing vessels,”whereas veins have more compliant adventitia.
The tunicamedia of veins contains smooth muscle arranged both circularlyand longitudinally, reflecting the function of veins as “capacitance vessels.” Similarly, elastic tissue in the adventitia of veinsis less prominent than in arteries.fluid between the vascular space and interstitial space alsooccurs across the capillary wall by simple diffusion (seeFig. 2.1). The net filtration pressure for diffusion of fluid outof capillaries is governed by the Starling equation. Entering thecapillary at the arteriolar end, hydrostatic pressure is approximately 30 mm Hg; it falls to approximately 10 mm Hg at thevenular end of the capillary.
Interstitial hydrostatic pressure isuniform within a local region; plasma oncotic pressure is highin plasma and substantially lower in the interstitial space. Thus,there is usually net filtration of fluid out of the capillary at thearteriolar end. Toward the venular end of the capillary, wherecapillary hydrostatic pressure is lower, net reabsorption of fluidinto the capillary usually occurs.Excess interstitial fluid is returned to the circulation throughthe lymphatic system (Fig. 12.3).
Movement of fluid from theEdema is the swelling associated with an increase ininterstitial fluid in a tissue or body cavity. The amountof fluid in the interstitial space depends on the rate at whichinterstitial fluid is produced and the rate at which it is removed.When high capillary hydrostatic pressure, low capillary oncoticpressure, or leakage of proteins from the vascular space (producing high interstitial oncotic pressure) results in excessivefluid in the interstitial space, it is ordinarily removed by thelymphatic system.
Edema may occur with blockage of the lymphatic system or excessive flux of fluid from the vascularspace.126Cardiovascular PhysiologyEndothelial cellsBasement membraneTunica adventiaInternal elastic membraneSmooth muscle cellsExternal elastic membraneTunica mediaConnective tissueTunica intimaFigure 12.1 The Vascular Wall The vascular walls of arteries and veins have three tissue layers, withthe relative thickness of medial and adventitial layers varying among various vessel types.
The capillary wallconsists of only the intimal layer of endothelial cells and basement membrane. The vessel illustrated aboveis a large artery, with prominent medial smooth muscle. The walls of large arteries and veins have their ownvascular supply (vasa vasora).
The tunica media of arteries is bounded by an internal elastic membrane (IEL)and an external elastic membrane (EEL).ArterioleSmooth muscle cellsPrecapillary sphinctersMetarterioleCapillariesVenuleFigure 12.2 Components of the Microcirculation Arterioles, metarterioles, capillaries, and venulesconstitute the microcirculation. Direction of blood flow is indicated by arrows. Blood flow is regulated byconstriction and dilation of smooth muscle of the arterioles, metarterioles, and precapillary sphincters.Sympathetic nerves extend to arterioles, metarterioles, and venules in the microcirculation.The Peripheral CirculationLymphatic flow127Lymphatic circulationInterstitialfluidc = 28 mm HgPc = 10 mm HgPc = 30 mm HgCapillary wallPlasmai = 8 mm Hg=0L = 8 mm Hg8–12L/dayPi = ⫺3 mm Hg1–4L/dayPL = ⴚ4 mm Hg4–8 L/dayLymph vesselArterioleVenuleLymph nodeFigure 12.3 The Lymphatic Circulation Diffusion of fluid from the vascular space to the interstitialspace is governed by the Starling equation (see Chapter 1).
Excess fluid in the interstitial space is transportedby the lymphatic system back to the central venous circulation. Movement of fluid from interstitium to thelymphatic system is driven solely by the hydrostatic pressure gradient, because there is no oncotic pressuregradient (protein flows freely through the lymphatic vessel wall). (Pc = HPc, hydrostatic capillary pressure.)interstitium into the capillaries is driven by the hydrostaticpressure gradient between the interstitial space and the lymph,because there is no significant oncotic pressure gradient (theprotein reflection coefficient of lymphatic capillaries is zero),and there are one-way valves through which fluid and proteinflow into lymphatic vessels. Lymph flows into larger lymphatic vessels and is returned into the central venous circulation through the thoracic duct.REGULATION OF BLOOD FLOWFlow through a specific tissue can be altered either by changesin perfusion pressure or changes in resistance of the arterialvessels perfusing the tissue.
Obviously, when blood flowrequirements of a specific tissue are altered, the most efficientmechanisms for adjusting blood flow will involve a change inregional resistance. On the other hand, when systemic metabolic needs vary, for example during exercise, regulation offlow is accomplished through changes in both systemic hemodynamics (blood pressure and cardiac output) and regionalresistances, resulting in changes in both overall flow (cardiacoutput) and flow distribution between various tissues.At the tissue level, both intrinsic and extrinsic factors mayinfluence smooth muscle tone in the resistance vessels (arterioles, precapillary sphincters, and small arteries) in responseto local and systemic events. Both smooth muscle and endothelial cells participate in this regulation.
Basic aspects ofsmooth muscle structure and function are discussed inSection 2.Regulation of Vascular Tone byEndothelial CellsThe role of the endothelium in regulation of smooth musclecontraction and relaxation is a relatively recent discovery. Theendothelium participates in this regulation through theseprocesses (Fig. 12.4):■■■release of vasodilators such as nitric oxide andprostacyclinrelease of the vasoconstrictors endothelinconversion of angiotensin I to angiotensin IIOf particular importance is the endothelium’s role in vascularregulation through production of nitric oxide (NO). Whenendothelial cells are exposed to endothelium dependent vasodilators such as acetylcholine, histamine, and bradykinin, theenzyme nitric oxide synthetase (NOS) is activated, resultingin the production of the short-lived but powerful vasodilatorNO from the amino acid arginine:NOSL-arginine → NO + L-citrullineNitric oxide diffuses to adjacent smooth muscle cells andacts on smooth muscle guanylyl cyclase, elevating cGMP.cGMP causes reduction in free intracellular Ca2+, producing128Cardiovascular PhysiologyVasopressin (ADH)ANPConstrictDilateSmooth muscle cellEndothelial cellA-IIProstacyclin(PGI2)NitricoxideACEEndothelinA-IShear stressHistamineAcetylcholineBradykininPurinergics (e.g., ATP)Pulmonary hypertensionVessel injuryFigure 12.4 Control of Arteriolar Tone The greatest resistance to flow occurs in the small arteriesand arterioles.
The state of constriction or relaxation of these vessels is regulated in part by the sympatheticnervous system and the release of norepinephrine. Circulating hormones, including vasopressin (ADH) andangiotensin II (A-II), may contribute to constriction through their actions on vascular smooth muscle; atrialnatriuretic peptide (ANP) is a smooth muscle dilator. The endothelium plays an important role in regulatingvascular tone by its release of nitric oxide (NO) and prostacyclin (PGI2) in response to many factors, includingshear stress, acetylcholine, and bradykinin. Endothelin is a potent, endothelium-derived vasoconstrictorimportant in some pathophysiologic states. The endothelial cell surface also has angiotensin-convertingenzyme, which forms angiotensin II by cleavage of circulating angiotensin I (A-I, an inactive precursor).relaxation of smooth muscle and thus vasodilation.
![](https://s.studizba.com/z.php?f=/templates/si/i/noavatar.png&w=100&h=100&t=1"){kind=avatar}
