Heart and Blood Vessels

HEART LAYERS

A. Endocardium

3.. Endocardium is lined by endothelium.

2. It is underlain by the subendocardial layer, which contains blood vessels, nerves, and Purkinje myocytes.

3. It is continuous with the tunica intima of blood vessels.

B. Myocardium consists of the following cell types:

1. Cardiac myocytes (see Chapter 6 II A)

a. Cardiac myocytes contract through intrinsically generated action potentials, which are then passed on to neighboring myocytes by gap junctions; that is, the heart beat is myogenic.

b. The action potentials are generated by ion fluxes in the cardiac myocytes (Figure 8-1), and can be divided into phases:

(1) Phase 0 is due to the influx of sodium ions into the cardiac myocyte through fast sodium channels. Tetrodotoxin and many drugs that treat cardiac arrhythmias block fast sodium channels.

(2) Phase 1 is due to a brief efflux of potassium ions through potassium channels, which can be blocked by 4-aminopyridine.

(3) Phase 2 is due to the influx of calcium ions into the cardiac myocyte through L-type calcium channels located on the cell membrane and T tubule. This influx of calcium ions is involved in contraction of cardiac myocytes. Verapamil and diltiazem block calcium channels, thereby reducing the strength of contraction. However, these drugs are used in patients with congestive heart failure (CHF) to inhibit vascular smooth muscle contraction, causing vasodilation (not because of their effect on cardiac myocytes). The peripheral vasodilation reduces the load on the heart. These drugs are often referred to as afterload-reducing drugs.

(4) Phase 3 is due to an efflux of potassium ions that is greater than the influx of calcium ions.

(5) Phase 4 is due to removal of the excess sodium ions that entered in phase 0 by Na+-K+-adenosine triphosphatase (ATPase) and removal of the excess calcium ions that entered in phase 2 by the Na+/Ca2+ exchanger. Cardiac glycosides (e.g., digitalis, ouabain) block Na+-K+-ATPase, thereby elevating intracellular sodium level. The elevated sodium level overwhelms the Na+/Ca2+ exchanger so that more calcium ions can be reaccumulated by terminal cisternae (TC). During the next contraction,

-100

Fast Na+ K+ L-type Ca2+ Na+-K+ Na+-Ca2+ channel channel channel -ATPase exchanger

Figure 8-1. (A) Phases of the action potential generated by cardiac myocytes and pattern of sodium (Na+), potassium (K+), and calcium (Cai + ) ion fluxes. (B) The ion fluxes are mediated by various ion channels in the cell membrane and T tubule of the cardiac myocyte. The influx of Ca2+ in phase 2 acts as trigger calcium that stimulates the release of a large pool of Ca2+ from the terminal cisternae. This leads to cardiac myocyte contraction. Various drugs are indicated that act as blockers of specific ion channels.

Fast Na+ K+ L-type Ca2+ Na+-K+ Na+-Ca2+ channel channel channel -ATPase exchanger

Figure 8-1. (A) Phases of the action potential generated by cardiac myocytes and pattern of sodium (Na+), potassium (K+), and calcium (Cai + ) ion fluxes. (B) The ion fluxes are mediated by various ion channels in the cell membrane and T tubule of the cardiac myocyte. The influx of Ca2+ in phase 2 acts as trigger calcium that stimulates the release of a large pool of Ca2+ from the terminal cisternae. This leads to cardiac myocyte contraction. Various drugs are indicated that act as blockers of specific ion channels.

Influx of Na

Influx of Ca2+

-100

Efflux of K

Influx of Na

Influx of Ca2+

Efflux of K

more calcium ions are released from TC, increasing the strength of contraction. Cardiac glycosides are used in patients with CHF to increase the strength of contraction.

2. Purkinje myocytes are modified cardiac myocytes that are specialized for conduction. Purkinje myocytes are not neurons. They are joined hy gap junctions.

3. Myocardial endocrine cells are found in the right and left atria and have secretory granules containing atrial natriuretic peptide (ANP).

a. ANP is secreted in response to increased blood volume or increased venous pressure within the atria (e.g., atrial distention due to left atrial failure).

b. ANP functions

(1) ANP increases glomerular filtration pressure and glomerular filtration rate (via vasoconstriction of the efferent arteriole) and decreases sodium resorption by the proximal convoluted tubule (PCT). These actions produce natriuresis (increased sodium excretion) in a large volume of dilute urine.

(2) ANP inhibits secretion of antidiuretic hormone (ADH) from the neurohypophysis.

(3) ANP inhibits secretion of aldosterone from the adrenal cortex (zona glomerulosa).

(4) ANP inhibits secretion of renin from juxtaglomerular cells.

(5) ANP causes vasodilation of peripheral and renal blood vessels.

C. Epicardium consists of connective tissue and a layer of mesothelium. In gross anatomy, the epicardium is called the visceral layer of the pericardial sac.

II. CONTRACTION OF CARDIAC MYOCYTES (Figure 8-1)

A. A diad consists of a T tubule located at the Z disk and flanked by one terminal cisterna. A T tubule is an invagination of the cell membrane. TC are dilated sacs of sarcoplasmic reticulum that store, release, and reaccumulate calcium ions.

B. The influx of calcium ions that occurs at the cell membrane and T tubule in phase 2 of the action potential is not sufficient to cause contraction, but acts as trigger calcium, which stimulates the release of a large pool of calcium ions stored in TC.

C. Calcium ions bind to troponin, which allows the myosin cross-bridge—ADP—PO|~ complex to bind to actin (see Figure 6-2).

D. ADP-PO|~ is released, leaving the myosin cross-bridge bound to actin.

E. The myosin cross-bridge binds ATP, which detaches the myosin cross-bridge from actin.

F. ATP is hydrolyzed by myosin ATPase, and the products (ADP and PO^~) remain bound to the myosin cross-bridgc, thereby reforming the myosin cross-bridge-— ADP—PO|" complex.

G. As the influx of calcium ions begins to decrease at the end of phase 2, TC reaccumulate calcium ions.

H. Troponin is freed of calcium ions.

III. CONDUCTION SYSTEM (Figure 8-2)

A. The sinoatrial (SA) node is the pacemaker of the heart. It is located at the junction of the superior vena cava and the right atrium.

1.. Phase 0 of the action potential generated by the SA node is not produced by an influx of sodium ions, and is therefore not sensitive to tetrodotoxin.

SA node

AV node

SA node

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Bundle Of His

Pwave PR interval

QRS complex QT interval

ST segment Twave

AV node

Bundle Of His

(posterior)

(posterior)

(anterior)

Heart Action

Represents atrial depolarization

Is the interval from start of atrial depolarization to the start of ventricle depolarization

Gets shorter as the heart rate increases

Gets longer as conduction velocity through AV node is slowed (e.g., heart block)

Represents ventricle depolarization

Represents the entire period of ventricle depolarization and ventricle repolarization

Represents the period when the entire ventricle is depolarized Represents ventricle depolarization

D First-degree AV block

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Figure 8-2. (A) The action potential generated by rhe sinoatrial (SA) node consisting of phases 4, 0, and 3. Compare this action potential with action potential of cardiac myocytes in Figure 8-1 (A). (B) A diagram of the heart conduction system. (C) Normal electrocardiogram measured from lead II and table of the heart actions. (D) Electrocardiogram of first-degree heart block in which the I'R interval is 0.28 seconds (> 0.20 seconds is abnormal). Electrocardiogram of second-degree heart block in which all QRS complexes are preceded by P waves, but not all P waves are followed by QRS complexes. Electrocardiogram of third-degree heart block in which P waves and QRS complexes are disassociated. (Reprinted with permission from Berne RM, Levy MN: Physiology, 4th cd. St. Louis, Mosby, 1998, p 355.) AV = atrioventricular node; LBB = left bundle branch; RBB = right bundle branch; SA = sinoatrial node.

2. Phase 4 of the action potential generated by the SA node is a slow diastolic depolarization that proceeds until threshold is reached.

3. From the SA node, the impulse spreads throughout the right atrium to the left atrium, and eventually to the atrioventricular (AV) node.

4. Ectopic pacemakers are present in the normal heart, and their added activity may induce continuous rhythm disturbances, such as paroxysmal tachycardias. When the ectopic pacemaker stops functioning, the SA node may remain quiescent for a period of time (called SA node recovery time). In patients with sick sinus syndrome, the SA node recovery time is prolonged with a period of asystole (absence of heartbeat) and loss of consciousness.

5. If all SA node activity is destroyed, the AV node assumes the pacemaker role.

B. The AV node is located on the right side of the interatrial septum near the ostium of the coronary sinus.

1. The delay between the start of the P wave (atrial depolarization) and the QRS complex (ventricle depolarization) occurs at the AV node. This normal delay allows for optimal ventricular filling during atrial contraction.

2. A first-degree heart block occurs when there is an abnormally long delay at the AV node.

C. AV conduction

1. A second-degree heart block occurs when only a portion of atrial impulses are conducted to the ventricles.

2. A third-degree heart block occurs when no atrial impulses are conducted to the ventricles.

3. Wolff-Parkinson-White syndrome is a congenital disorder in which an accessory conduction pathway between the atria and ventricles exists. This syndrome is ordinarily asymptomatic. However, a re-entry loop may develop in which impulses travel to the ventricles via the normal conduction pathway but return to the atria via the accessory pathway, causing supraventricular tachycardia.

D. Bundle of His, bundle branches, and Purkinje myocytes

1. The bundle of His travels in the subendocardial layer on the right side of the interventricular septum.

2. It divides into right and left bundle branches. The left bundle branch further divides into a thin anterior division and a thick posterior division.

3. The right and left bundle branches terminate in a complex network of the Purkinje myocytes.

IV. NEURAL REGULATION OF HEART RATE. The autonomic nervous system modulates the myogenic heartbeat.

A. The parasympathetic system decreases the heart rate.

1. The cell bodies of preganglionic neurons are located in the dorsal nucleus of the vagus and nucleus ambiguus of the medulla. The axons of preganglionic neurons run in the vagus (X) nerve and use acetylcholine (ACh) as a neurotransmitter.

2. The cell bodies of postganglionic neurons are located near the SA node and AV conduction tissue. The axons of postganglionic neurons terminate on the SA node and AV conduction tissue and use ACh as a neurotransmitter.

3. ACh binds to the muscarinic ACh receptor (mAChR), which is a G protein-linked receptor that inhibits adenylate cyclase and decreases cyclic adenosine monophosphate (cAMP) levels.

4. The SA node and AV conduction tissue contain high levels of acetylcholinesterase (degrades ACh rapidly) such that any given vagal stimulation is short-lived.

5. Atropine is an mAChR antagonist; therefore, atropine increases the heart rate.

6. Vasovagal syncope is a brief period of lightheadedness or loss of consciousness due to an intense burst of vagus (X) nerve activity that decreases the heart rate.

B. The sympathetic system increases the heart rate.

1. The cell bodies of preganglionic neurons are located in the intermediolateral columns of the spinal cord. The axons of preganglionic neurons enter the paravertebral ganglion and travel to the stellate/middle cervical ganglia and use ACh as a neurotransmitter.

2. The cell bodies of postganglionic neurons are located in the stellate and middle cervical ganglia. The axons of postganglionic neurons are distributed to the myocardium-accompanying blood vessels and use norepinephrine (NE) as a neurotransmitter.

3. NE binds to (i-adrenergic receptors, which are G protein-linked receptors that stimulate adenylate cyclase and increase cAMP levels. Consequently, protein kinases are activated, which promotes phosphorylat ion of various proteins that activate calcium channels of the cardiac myocytes to increase the influx of calcium ions.

4. Released NE either is carried away by the bloodstream or is taken up by the nerve terminals so that sympathetic stimulation is relatively long-lived.

5. Propranolol is a ^-adrenergic antagonist; therefore, propranolol decreases the heart rate.

V. ENZYME LEVELS IN MYOCARDIAL INFARCTION (Table 8-1). Creatine kinase

(CK) and lactate dehydrogenase (LDH) semm isoenzyme levels are useful in diagnosing myocardial infarction. These isoenzymes normally are confined to the cytoplasm of cardiac myocytes; however, ischemia allows for the leakage of these isoenzymes into the serum. Isoenzymes catalyze the same reaction but have different amino acid sequences and properties.

A. CK levels. CK consists of M and B subunits. CK-1 (MM suhunits) is found in skeletal muscle and cardiac muscle. CK-2 (MB subunits) is found in cardiac muscle. CK-3 (BB subunits) is found in brain. An elevated total CK-1 and CK-2 fraction provides early confirmation of myocardial infarction.

B. LDH levels. LDH consists of H and M subunits. LDH[ (HHHH subunits) is found in cardiac muscle and red blood cells. LDH2 (HHHM subunits) is found in cardiac muscle and red blood cells. LDH3 (HHMM subunits) is found in brain and kidney. LDH4 (HMMM subunits) is found in liver and skeletal muscle. LDH5 (MMMM subunits) is found in liver and skeletal muscle. A reversed LDH,:LDH2 ratio at 24 hours after admission is a characteristic sign for confirmation of myocardial infarction.

VI. BLOOD VESSELS

A. Tunics

1. Tunica intima consists of endothelium, a basal lamina, loose connective tissue, and an internal elastic lamina.

Table 8-1

Changes in Creatine Kinase and Lactate Dehydrogenase Serum Levels in Myocardial Infarction

Time Total CK-2 Fraction LDH

Admission

12 hours after admission

24 hours after admission

290 U/L

Normal values

U/L = units/liter; CK = creatine kinase; LDH = lactate dehydrogenase; N/A = not applicable.

2. Tunica media consists of smooth muscle cells, type III collagen, elastic fibers, and an external elastic lamina.

3. Tunica adventitia consists of fibroblasts, type I collagen, and some elastic fibers.

B. Elastic (conducting) arteries (e.g., pulmonary artery, aorta) have a tunica media with a prominent elastic fiber component that responds to the high systolic pressure generated by the heart.

C. Muscular (distributing) arteries have a tunica intima with a prominent internal elastic lamina and a tunica media with a prominent smooth musclc cell component.

D. Arterioles have a tunica media that consists of only one to two layers of smooth muscle cells and play a major role in regulation of blood pressure. Metarterioles arc the smallest (or terminal) branches of the arterial system and play a role in regulation of blood flow ro capillary beds.

E. Arteriovenous anastomoses (AVA) allow arteriolar blood to bypass the capillary bed and empty directly into venules. AVA are found primarily in the skin to regulate body temperature. Constriction of the arteriolar component directs blood to the capillary bed causing depletion of body heat. Dilation of the arteriolar component directs blood to the venules causing conservation of body heat.

F. Capillaries consist of a single layer of endothelial cells surrounded by a basal lamina and are the site of exchange (e.g., C02, 02, nutrients) between blood and cells. Mi-crovasculature damage associated with type 1 and type 2 diabetes is due to nonenzy-matic glycosylation of various proteins, which causes the release of harmful cytokines. The different types of capillaries include the following:

1. Continuous capillaries consist of a single layer of endothelial cells joined by a zonula occludens (tight junction) and contain no fenestrae (or pores). They are found in lung, muscle, and brain.

2. Fenestrated capillaries consist of a single layer of endothelial cells joined by a zonula occludens (tight junction) and contain fenestrae (or pores) with diaphragms. They are found in endocrine glands, intestine, and kidney. Fenestrated capillaries without diaphragms are found solely within the kidney glomerulus.

3. Discontinuous capillaries (sinusoids) consist of a single layer of endothelial cells that arc separated by wide gaps (i.e., no zonula occludens present) and contain fenestrae. They are found in the liver, bone marrow, and spleen.

VII. FUNCTIONS OF ENDOTHELIUM

A. Secretion of the following substances:

1. von Willebrand factor is stored in Weibel-Palade granules and promotes platelet adhesion to subcndothelial collagen at an injury site, as well as blood coagulation, von Willebrand disease is a common bleeding disorder in humans.

2. Nitric oxide (NO) affects smooth muscle cells of the tunica media and causes vasodilation.

a. NO is synthesized by the reaction:

Arginine -NO + Citrulline b. NO activates guanylare cyclase in smooth muscle cells, causing increased levels of cyclic guanosine monophosphate (cGMP) and vasodilation.

C. NO is involved in the vasodilation associated with penile erection. Viagra used in the treatment of erectile dysfunction is a cGMP phosphodiesterase inhibitor. With its use, increased cGMP levels are maintained, d. The vasodilation effects of nitroglycerin and amyl nitrates occur through their conversion to NO.

3. Prostacyclin (PGI2) causes vasodilation and inhibits platelet aggregation. PGI2 is synthesized from arachidonic acid using the enzymes cyclooxygenase and PGI synthase.

4. Endothelin 1 affects smooth muscle cells of the tunica media and causes vasoconstriction.

B. Conversion of the following substances:

1. Angiotensin I to angiotensin II, which causes vasoconstriction and secretion of both aldosterone and ADH

2. Bradykinin, serotonin, norepinephrine, prostaglandins, and thrombin to inert compounds

C. Breakdown of lipoproteins to triglycerides and cholesterol VIII. BLOOD FLOW

A. Modification. Blood flow to an organ is modified in a number of ways.

1. Autoregulation is the phenomenon whereby blood flow to an organ remains constant over a wide range of pressures.

2. Active hyperemia is the phenomenon whereby blood flow to an organ is proportional to its metabolic activity.

3. Reactive hyperemia is the phenomenon whereby blood flow to an organ is increased after a period of occlusion.

B. Modification theories. Modification of blood flow to an organ is explained by the following:

1. The metabolic hypothesis states that vasodilator metabolites are released upon an increase in tissue activity.

2. The myogenic hypothesis states that vascular smooth muscle contracts upon stretching.

IX. TYPES OF CIRCULATION (Table 8 2)

Table 8-2

Types of Circulation

Percent of Cardiac Blood Flow Circulation Output Demonstrates Control

Table 8-2

Types of Circulation

Percent of Cardiac Blood Flow Circulation Output Demonstrates Control

Coronary

5

Autoregulation Active hyperemia Reactive hyperemia

Hypoxia and adenosine cause vasodilation

Cerebral

15

Autoregulation Active hyperemia Reactive hyperemia

Increased Pco2 or decreased pH cause vasodilation

Skeletal muscle

20

Autoregulation Active hyperemia Reactive hyperemia

During exercise, lactate, adenosine, and K+

cause vasodilation At rest, sympathetic innervation through NE release stimulates a-adrenergic receptors, causing vasoconstriction At rest, sympathetic innervation through NE release stimulates 3-adrenergic receptors, causing vasodilation

Kidney

25

Autoregulation

Renal blood flow remains constant from 100-200 mm Hg arterial pressure.

Respiratory

100

Hypoxic vasoconstriction

Hypoxia causes vasoconstriction so that blood is directed away from poorly ventilated areas to well-ventilated areas of the lung It is the only circulation that responds to hypoxia by vasoconstriction

Skin

5

Temperature regulation

Increase the temperature: sympathetic innervation causes vasodilation, directing blood to the surface

NE = norepinephrine.

NE = norepinephrine.

X. SELECTED PHOTOMICROGRAPHS

A. Normal muscular artery (Figure 8-3; see VI C)

Figure 8-3. Light micrograph of a muscular artery. The tunica intima (i), tunica media (M), and tunica ad ventitia (Ail) are indicated, eel = external elastic lamina; iel = internal elastic lamina.

B. Coronary artery atherosclerosis (Figure 8-4)

Figure 8-4. (A) Coronary artery with atherosclerosis. The entire coronary artery is shown with a eccentric, narrow lumen (L) due to the presence of an atheromatous plaque (tunica intima thickening). Atherosclerosis is considered an intimal disease. (B, C, D) High magnification of the boxed areas (shown in A) of the atheromatous plaque. The fibrous cap (/c) is composed of smooth muscle cells, a few leukocytes, and a relatively dense deposition of collagen. The deeper necrotic core (see C) consists of a disorganized mass of lipid material, cholesterol crystals (cc), cell debris, and foam cells. Ad = tunica adventitial M = tunica media. [An atheromatous plaque may undergo many histologic changes, such as: (1) calcification that turns arteries into brittle pipes, (2) hemorrhage into the plaque that occurs and induces focal rupture of ulceration, (3) focal rupture at the luminal surface that results in thrombus formation, whereby the thrombus may partially or completely occlude the lumen, leading to approximately 90% of all myocardial infarctions. In this situation, thrombus formation is initiated by platelet aggregation induced by thromboxane (TXA2). TXA2 is synthesized from arachidonic acid using the enzyme cyclooxygenase. Aspirin covalently inhibits cyclooxygcnase, and nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and acetaminophen reversibly inhibit cyclooxygenase and thereby block the synthesis of TXA,. Consequently, low doses of aspirin and NSAIDs are effective in prevention of myocardial infarction. Thrombolysis is stimulated by tissue plasminogen activator (TPA) treatment, which successfully decreases the extent of ischemic damage due to myocardial infarction. TPA stimulates the conversion of plasminogen to plasmin. Plasmin is a protease that digests fibrin within the thrombus.) (Reprinted with permission from East Carolina University, School of Medicine, Department of Pathology slide collection.)

C. Myocardial infarction (Figure 8-5; see V)

Figure 8-5. Myocardial infarction. (A) Low magnification of the myocardium (24-36 hours after ischemia) showing normal (undamaged) cardiac myocytes and damaged cardiac myocytes (Mi). (B) High magnification of normal cardiac myocytes, which are relatively straight with some branching and contain a centrally located nucleus and very little intercellular space. (C) High magnification of damaged cardiac myocytes, which show the following characteristics: wavy appearance, no conspicuous nucleus, loss of striations, and an intercellular space filled with inflammatory exudate (*) composed mostly of neutrophils. The necrosis associated with myocardial infarction begins in the myocardium closest ro the endocardium. (D, E) Old myocardial infarction. The damaged cardiac myocytes are replaced with collagenous scar tissue (sc). The cardiac myocytes adjacent to the scar represent a compensatory hypertrophy. These myocytes usually show bizarre-shaped nuclei, as indicated in E (cross-section of cardiac myocytes). (Reprinted with permission from the East Carolina University, School of Medicine, Department of Pathology slide collection.)

Figure 8-5. Myocardial infarction. (A) Low magnification of the myocardium (24-36 hours after ischemia) showing normal (undamaged) cardiac myocytes and damaged cardiac myocytes (Mi). (B) High magnification of normal cardiac myocytes, which are relatively straight with some branching and contain a centrally located nucleus and very little intercellular space. (C) High magnification of damaged cardiac myocytes, which show the following characteristics: wavy appearance, no conspicuous nucleus, loss of striations, and an intercellular space filled with inflammatory exudate (*) composed mostly of neutrophils. The necrosis associated with myocardial infarction begins in the myocardium closest ro the endocardium. (D, E) Old myocardial infarction. The damaged cardiac myocytes are replaced with collagenous scar tissue (sc). The cardiac myocytes adjacent to the scar represent a compensatory hypertrophy. These myocytes usually show bizarre-shaped nuclei, as indicated in E (cross-section of cardiac myocytes). (Reprinted with permission from the East Carolina University, School of Medicine, Department of Pathology slide collection.)

D. Purkinje myocyte (Figure 8-6; see III D 3)

Figure 8-6. Purkinje cell. (A) Light micrograph of Purkinje cclls (P) traveling within the myocardium (nvy). By light microscopy, Purkinje cells appear pale because the large amount of glycogen that is normally contained in the cytoplasm is lost during histologic processing. (B) Electron micrograph of a Purkinje cell (P) showing large amount of glycogen (gly) and few myofilaments (mf). A portion of a cardiac myocyte within the myocardium (my) is also shown. (Courtesy of Dr. S. Viragh, Postgraduate Medical School, Budapest, Hungary.)

Figure 8-6. Purkinje cell. (A) Light micrograph of Purkinje cclls (P) traveling within the myocardium (nvy). By light microscopy, Purkinje cells appear pale because the large amount of glycogen that is normally contained in the cytoplasm is lost during histologic processing. (B) Electron micrograph of a Purkinje cell (P) showing large amount of glycogen (gly) and few myofilaments (mf). A portion of a cardiac myocyte within the myocardium (my) is also shown. (Courtesy of Dr. S. Viragh, Postgraduate Medical School, Budapest, Hungary.)

E. Fenestrated capillary with diaphragm (Figure 8-7; see VI F 2)

Figure 8-7. Fenestrated capillary with diaphragms. (A) Low-magnification electron micrograph of a fenestrated capillary within the pancreatic islets of Langerhans (an endocrine gland) adjacent to a beta cell. The fenestrae with diaphragms are indicated at the arrows. L = lumen of the capillary. (B) High-magnification electron micrograph of a fenestrated capillary showing insulin (/) within a secretory granule and its route of release through the fenestrae (large arrow) into the lumen (L) of the capillary. The small arrow indicates fenestrae with diaphragm, endo = endothelial cell.

Figure 8-7. Fenestrated capillary with diaphragms. (A) Low-magnification electron micrograph of a fenestrated capillary within the pancreatic islets of Langerhans (an endocrine gland) adjacent to a beta cell. The fenestrae with diaphragms are indicated at the arrows. L = lumen of the capillary. (B) High-magnification electron micrograph of a fenestrated capillary showing insulin (/) within a secretory granule and its route of release through the fenestrae (large arrow) into the lumen (L) of the capillary. The small arrow indicates fenestrae with diaphragm, endo = endothelial cell.

F. Kaposi sarcoma (Figure 8-8)

Figure 8-8. Kaposi sarcoma. Kaposi sarcoma is a relatively rare vascular tumor but has come to the forefront because of its high frequency of occurrence in AIDS patients. Multiple red-to-purple skin plaques are observed clinically. (A,B) Low- and high-magnification light micrographs show an inract epidermis (epi) of the skin covering the malignant vascular lesion in the dermis consisting of numerous vascular channels (vc), spindle-shaped neoplastic stromal cclls (*), and extravasated red blood cells (arrows). (Reprinted with permission from the East Carolina University, School of Medicine, Department of Pathology slide collection.)

Figure 8-8. Kaposi sarcoma. Kaposi sarcoma is a relatively rare vascular tumor but has come to the forefront because of its high frequency of occurrence in AIDS patients. Multiple red-to-purple skin plaques are observed clinically. (A,B) Low- and high-magnification light micrographs show an inract epidermis (epi) of the skin covering the malignant vascular lesion in the dermis consisting of numerous vascular channels (vc), spindle-shaped neoplastic stromal cclls (*), and extravasated red blood cells (arrows). (Reprinted with permission from the East Carolina University, School of Medicine, Department of Pathology slide collection.)

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