Blood and lymphatic circulatory systems and heart

Introduction

The main transport systems are the circulatory systems, in which substances are dissolved or suspended in liquid and carried from one part of the body to another in a series of tubes (vessels). There are two main circulatory systems: the blood circulatory system and the lymphatic system.

The blood circulatory system is the main method of transporting oxygen, carbon dioxide, nutrients and metabolic breakdown products, cells of the immune and other defence systems, chemical messengers (hormones) and many other important substances (e.g. clotting factors). Transfer of transported substances from blood to tissue and vice versa occurs in the systemic and pulmonary capillary systems ( Fig. 9.1 ). These tiny thin-walled vessels permit the passage of fluid, small and large molecules, dissolved gases and even cells across their walls in both directions. The circulatory network that transports blood to the capillaries is called the arterial system, and the network that carries blood away from the capillaries is called the venous system.

The lymphatic circulatory system drains extracellular fluid from the tissues, returning it to the blood circulatory system after passage through lymph nodes. This system is also involved in absorption of nutrients from the gut.

Blood circulatory system

There are three types of blood circulatory systems, two of which (systemic and pulmonary circulations) depend on a central pump, the heart, to push the blood around (see Fig. 9.1 ). The third system is the portal system, discussed later.

The systemic circulation transfers oxygenated blood from a central pump (the heart) to all the body tissues (systemic arterial system) and returns deoxygenated blood with a high carbon dioxide content from the tissues to the central pump (systemic venous system).

The pulmonary circulation transfers deoxygenated blood with a high carbon dioxide content from a central pump (the heart) to the lungs (pulmonary arterial system) and transfers re-oxygenated blood from the lungs back to the central pump (pulmonary venous system).

The portal systems are specialized vascular channels that carry substances from one site to another, but do not depend on a central pump (see p. 166).

Systemic blood vessels

There are two main types of large blood vessels:

• Arteries, which carry blood away from the heart toward the capillary systems at relatively high pressure

• Veins, which carry blood back to the heart from the capillary systems at relatively low pressure

The systemic arterial circulation is an extensive high-pressure system. The structure of its vessels reflects the high pressures to which they are subjected.

The output of the left ventricle is carried in large-diameter vessels with a high component of elastic tissue in their walls that smooths the systolic pressure wave. These are called the large elastic arteries (i.e. the aorta and its large branches, such as the carotid, subclavian and renal arteries).

Distal to these large elastic arteries are smaller vessels in which the artery walls become proportionately more muscular. These muscular arteries gradually decrease in size as they branch within tissues until they form arterioles. The arterioles then open into a system of very fine vessels termed capillaries.

From capillaries, blood moves into venules and then into veins, which become progressively larger as they approach the heart. The large veins carry blood at low pressure and hence have a small amount of muscle in their wall compared with arteries.

The pulmonary circulation transfers blood a short distance from the right ventricle of the heart to the capillary systems of the lung, and from there back to the left atrium of the heart. The pressures within the pulmonary circulation are lower and the walls of the main vessels are generally thinner than seen in the systemic circulation. The detailed histology of the pulmonary vasculature is discussed in Chapter 10 .

The walls of blood vessels are made up of three identifiable layers (tunica): intima, media and adventitia.

The tunica intima is composed of a lining layer of highly specialized, multifunctional, flattened epithelial cells termed endothelium . This sits on a lamina ( the internal elastic lamina ); beneath this is a very thin subendothelial layer of fibrocollagenous support tissue containing occasional contractile cells with some of the properties of smooth muscle cells but which are also capable of synthesizing collagen and elastin (like fibroblasts) and which also can have phagocytic properties (like histiocytes/macrophages). These cells are called myointimal cells and become very important in the development of the most common arterial disease, atherosclerosis (see p. 162).

The media is the middle layer in a blood vessel wall and is composed predominantly of smooth muscle reinforced by organized layers of elastic tissue, which form elastic laminae. The media is particularly prominent in arteries, being relatively indistinct in veins and virtually non-existent in very small vessels. In vessels that are close to the heart, receiving the full thrust of the systolic pressure wave, elastic tissue is very well developed, hence the term elastic arteries. In muscular arteries and arterioles, the elastic lamina separating the tunica media and the tunica adventitia is the external elastic lamina.

The tunica adventitia is the outer layer of blood vessels. It is composed largely of fibroblasts and collagen, but smooth muscle cells may be present, particularly in veins. The adventitia is often the most prominent layer in the walls of veins. Within the adventitia of vessels with thick walls are small blood vessels, the vasa vasorum, which send penetrating branches into the media to supply it with blood. These are not seen in thinner vessels, which obtain their oxygen and nutrients by diffusion from the lumen. The adventitia also carries autonomic nerves, which innervate the smooth muscle of the media.

The differences between the layers in the wall of a small artery and a small vein are illustrated in Fig. 9.2 . Although the smaller vessels progressively lose the media and adventitia, all blood vessels have a tunica intima lined internally by the flat endothelial cells. The smallest vessels, the capillaries, have only a layer of endothelial cells sitting on a basal lamina. The endothelial cells lining the entire blood circulatory system are vitally important cells, with many functions.

The endothelium is composed of flattened cells with diverse functional roles. In routine histological sections, the cytoplasm of most endothelial cells is barely visible and only the small flattened nuclei are seen. Ultrastructurally, each cell can be seen to be anchored to an underlying basal lamina; individual cells are anchored together by adhesion junctions, including prominent tight junctions, which prevent diffusion between cells. A prominent feature of endothelial cells is the presence of many pinocytotic vesicles, which are involved in the process of transport of substances from one side of the cell to the other. In small blood vessels of the nervous system, the endothelial cells express transport proteins, which are responsible for the active transport of all substances, for example, glucose, into the brain. Ultrastructurally, endothelial cells also contain smooth and rough endoplasmic reticulum and free ribosomes, with occasional mitochondria and variable numbers of microfilaments. The characteristic cytoplasmic organelle of the endothelial cell is an electron-dense ovoid structure called the Weibel–Palade body, which are storage granules containing von Willebrand factor, P-selectin and other vascular modulators ( Fig. 9.3 b).

Endothelial cells can sense changes in blood pressure, oxygen tension and blood flow. Each endothelial cell has chemoreceptors and mechanoreceptor elements linked to signalling structures of the primary cilium (see p. 37). In response to changes in local factors, endothelial cells respond by secreting substances which have effects on the tone of vascular smooth muscle. Vasodilators that cause relaxation of vascular smooth muscle and increase local blood flow include nitric oxide (NO), prostacyclin (PGI ₂ ) and less well-defined factors that cause hyperpolarization of vascular smooth muscle (endothelium-derived hyperpolarizing factors [EDHFs]). Factors that cause vasoconstriction include thromboxane (TXA ₂ ) and endothelin-1 (ET-1).

Endothelial cells are important for control of blood coagulation, and under normal circumstances the endothelial surface prevents blood clotting. This is done by high expression of factors that prevent blood clotting and low expression of factors that activate this process (see Fig. 9.3 a).

KEY FACTS

Endothelium

• Cells are bound together by junctional complexes and have many pinocytotic vesicles.

• Cells have many functional roles despite their apparent structural simplicity.

• Normally secretes factors which prevent blood clotting.

• Normally secretes factors which maintain the tone of vascular smooth muscle.

• Can be activated by cytokines to express cell adhesion molecules, which allow white blood cells to stick.

ADVANCED CONCEPT

Activated Endothelium

The endothelium can adapt rapidly to changes in its environment. Under certain circumstances, especially in response to inflammation, the endothelium may become activated and change its function.

The endothelium responds to blood flow and external stimuli to secrete factors which alter the state of contraction of vascular smooth muscle (vasoconstriction and vasodilatation).

Endothelium may become activated by cytokines and develop specialization for emigration of lymphoid cells. The endothelial cells become cuboidal in shape and express surface adhesion molecules, which facilitate lymphocyte adhesion and migration. This type of endothelium is normally seen in the specialized venules in the lymph node paracortex (high endothelial venules).

Endothelium may become activated by cytokines and express cell adhesion molecules for neutrophils. This normally occurs after any form of tissue damage and allows neutrophils to migrate into local tissues in the process of acute inflammation. The substance P-selectin, a cell adhesion molecule, is stored in special vesicles (Weibel–Palade bodies) inside the endothelium (see Fig. 9.3 b). With appropriate stimulation, these vesicles dock with the endothelial cell membrane. P-selectin is then available on the cell surface for neutrophil adhesion.

Endothelium is normally locally impermeable to substances in the blood. Under the effects of certain factors – for example, histamine – endothelial cells lose attachment to each other and retract. This allows fluid and proteins to diffuse out into the local tissues, causing tissue swelling, termed oedema. This reorganization of cell–cell junctions is rapid and reversible and takes place in the space of a few minutes.

Elastic arteries are the largest arteries and receive the main output of the left ventricle; thus they are subjected to high systolic pressures of 120–160 mmHg. Furthermore, these large vessels are adapted to smooth out the surges in blood flow, as blood is impelled through them only during the systolic phase of the cardiac cycle. The elastic tissue in their walls provides the resilience to smooth out the pressure wave.

The intima of large elastic arteries is composed of endothelium with a thin layer of underlying fibrocollagenous tissue.

Elastic arteries have a thick, highly developed media of which elastic fibres are an important component. These are arranged in interrupted, lamellar circumferential sheets between layers of smooth muscle throughout the thickness of the media. In the largest artery, the aorta, there are often 50 or more layers ( Fig. 9.4 ).

The elastic fibres are arranged in sheets so that they run circumferentially rather than longitudinally to counteract the tendency of the vessel to overdistend during systole. Return of the elastic fibres from the stretched to the unstretched state during diastole maintains a diastolic pressure within the aorta and large arteries of about 60–80 mmHg. Interposed between the elastic layers are smooth muscle cells and some collagen.

With age, and particularly in association with the common disease of the intima, atherosclerosis (see p. 162), the elastic fibres and smooth muscle fibres of the media of an elastic artery undergo degeneration and are replaced by non-elastic, non-contractile collagen. The most severe complication of the loss of elastic and smooth muscle is the permanent pathological dilatation of the elastic artery (usually the aorta). This is called aneurysm formation (see Clinical Example box, p. 162).

The adventitia of the large vessels carries vasa vasorum and nerves.

The large elastic arteries gradually merge into muscular arteries by losing most of their medial elastic sheets, usually leaving only two layers, an internal elastic lamina and an external elastic lamina, at the junction of the media with, respectively, the intima and the adventitia. The general structure of a muscular artery is shown in Figs 9.5 a and 9.5 b.

In a muscular artery the media is composed almost entirely of smooth muscle. These arteries are therefore highly contractile, with their degree of contraction or relaxation being controlled by the autonomic nervous system and by endothelium-derived vasoactive substances. A few fine elastic fibres are scattered among the smooth muscle cells but are not organized into sheets. These are most numerous in the large muscular arteries, which are a direct continuation of the distal end of the elastic arteries (see Figs 9.5 c and 9.5 d).

Muscular arteries vary in size from about 1 cm in diameter, close to their origin at the elastic arteries, to about 0.5 mm in diameter. In the larger arteries there may be 30 or more layers of smooth muscle cells, whereas in the smallest peripheral arteries there are only two or three layers. The smooth muscle cells are usually arranged circumferentially at right angles to the long axis of the vessel.

CLINICAL EXAMPLE

Atherosclerosis

Atherosclerosis is a disease of the arteries which starts in the intima. It is characterized by infiltration of the intima by oxidized lipids, which accumulate in macrophages and myointimal cells, accompanied by increased deposition of collagen. Such intimal thickening forms a so-called atheromatous plaque.

There are three common consequences of atheroma:

Impaired blood flow

Atheromatous change leads to a reduction in the size of the lumen of the vessel so that blood flow is decreased.

Thrombus formation

Another complication of atherosclerosis is that it damages the smooth internal lining of endothelial cells, exposing circulating blood to the underlying intimal collagen. This can trigger coagulation to form a mass of blood clot, termed a thrombus, within the vessel. Thrombus further reduces the lumen of the vessel and may block it completely ( Fig. 9.6 ), resulting in death of the tissue (infarction) supplied by the vessel. The myocardium is particularly vulnerable to infarction (see Fig. 9.22 ), as are the brain (stroke) and the feet and toes (gangrene).

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here