especially in the veins, as the arteries contract as soon as the heartaction ceases.

Overaction of the heart is less frequent than weakness. Temporary overaction occasions increased activity of the circulation and elevation of blood-pressure, sometimes sufficient to cause hemorrhage. More prolonged overaction due to overwork, to excessive feeding, or to nervous stimulation, as in Graves's disease, causes hypertrophy of the left ventricle, and later of the whole organ. In consequence the circulation may be more or less permanently overactive.

Arterial Disorders.-Both organic and nervous disturbances are important. Of the organic disturbances the most frequent is sclerosis of the arteries, which offers a constant impediment to the arterial circulation. Hypertrophy of the heart overcomes the obstacle, but when the heart fails venous congestions and dropsy ensue. Sclerosis may also affect the veins, but much less commonly. Local diseases of the aorta, as congenital narrowing, compression by enlarged glands or tumors, aneurysms, and blood-clots may obstruct the flow of blood to the arteries, and thereby cause stagnation of the blood in the heart, lungs, and venous system.

Vasomotor disturbances are dependent upon the nervous system. Under the influence of certain diseases of the nervous system or of poisons (as carbonic acid gas in asphyxia) acting locally on the vessels or upon the vasomotor center in the brain, contraction of the smaller arterioles occurs; and in consequence the blood-pressure is greatly elevated, the heart is impeded, and venous congestion results. On the other hand, the arterioles may distend from vasomotor paresis, the blood-pressure falls, and unless the heart is active there is a tendency to hypostatic congestion.

Changes in the Blood.-Increase and decrease of the quantity of the blood are generally merely passing conditions to which the circulation readily adapts itself by dilatation or contraction of the vessels. Sudden losses of blood, if large, may be fatal by syncope. Smaller losses are soon repaired by absorption of water from the tissues and by regeneration of blood. Increases in the quantity of the blood by ingestion of liquids never disturb the circulation greatly. Rapid excretion soon reduces the quantity

to the normal.

Changes in the character of the blood may affect its circulation. The accumulation of carbonic acid and probably other effete products of tissue-change impede the flow by exciting vasomotor contraction. This is probably brought about by the action of the poisons on the terminal nerve-filaments in the blood-vessels or directly on the walls of the vessels. This is the best explanation of the increase of pressure in cases of Bright's disease without arteriosclerosis. The poisons in this case are the retained renal

excreta.

LOCAL HYPEREMIA.

Local hyperemia is increase in the quantity of blood in a part of the body. This may be due to increase of the flow to that part, or to obstruction of the outflow. The former is called active or arterial hyperemia or congestion; the latter, passive or hyperemia.

venous

Active hyperemia occurs in organs during periods of functional activity, the increased blood-supply here being due to increased demand for nutrition. Pathologically, active hyperemia is due to canses which lead to dilatation of the arteries of a certain part. This dilatation may be due to influences acting through the vasomotor nervous system or to local affections of the vessel-walls. The vasomotor nervous system may be affected at its center in the medulla or peripherally. The latter is seen when the sympathetic nerves, which contain vasoconstrictor fibers, are severed or compressed by tumors, the vessel-walls thereby becoming paralyzed (neuroparalytic hyperemia). The superficial congestive hyperemia in fevers is probably due to the central vasomotor action of the toxic causes of fever. On the other hand, the vasodilator fibers in the spinal nerves may be stimulated, as in certain cases of neuritis, with a similar result (neurotonic hyperemia). Direct injury to the vessel-walls by heat, traumatism, inflammation, drugs, or by the vascular fatigue following temporary stoppage of the circulation, is a frequent cause.

Active hyperemia is spoken of as collateral when anemia in one part leads to overfilling of the vessels of an adjoining or even distant part.

The hyperemic area is bright red in color, the temperature is elevated, and there is slight swelling. After death the distended arteries and capillaries may contract and the part grows paler. Arterial hyperemia is one of the phenomena of beginning inflammation, and in any case if prolonged may terminate in inflammation. Functional activity is increased by moderate conges

tions.

Passive hyperemia is due to impediments to the outflow of the blood through the veins. This may be brought about by compression of veins by tumors, by thickening of their walls, or by thrombi within. Little disturbance results from obstruction of a small vein, because of the freedom of collateral circulation, provided the heart is active. In cases of weak heart-power, however, slight obstructions may determine local venous hyperemia, or by gravity alone the blood may accumulate in dependent parts. The latter constitutes hypostatic congestion (see page 46).

Areas the seat of passive hyperemia are dark red (cyanosis) and lowered in temperature. The veins are distended, and very soon the watery elements of the blood transude and the part becomes

edematous and swollen. In severe cases red blood-corpuscles escape by diapedesis.

This occurs in the small veins and capillaries, but not in the arteries. In consequence of the increased intravascular pressure the red corpuscles are pushed through the wall of the vessel at the points of junction of adjacent endothelial cells. At these points the cement substance is found in greater abundance than along the borders of the cells, and the escape of the corpuscle takes place through the semi-solid cement substance.

In

Later fatty degeneration results from the imperfect nutrition of the tissues; or even necrosis and gangrene may occur. long-continued moderate passive hyperemia overgrowth of connective tissue and pigmentation of the tissue by broken-down blood-corpuscles is observed (brown induration).

Complete stoppage of the circulation in a localized area is called stasis (Fig. 1). This may be an extreme grade of passive hyperemia. The blood-corpuscles accumulate in the small vessels (arteries, capillaries, and veins), and the plasma is slowly pressed through the vessel-wall or onward in the vessel. There results a filling of the vessel with a homogeneous red material, which is composed of the red corpuscles so closely packed as to be indistinguishable. On relief of the stasis the corpuscles become free again. Stasis may also be produced by chemical agents which rapidly withdraw the plasma from the vessels, leaving the corpuscles unable to circulate; or similarly by rapid evaporation of the liquor sanguinis from internal structures (as the peritoneum) exposed to the air.

Passive congestion of any grade and stasis interfere with functional activity in two ways: by the reduction of nutrition of the cells and by the pressure exercised upon them by the accumulating blood and serum.

LOCAL ANEMIA.

Local anemia or ischemia is the condition in which a tissue contains less than its proper quantity of blood. This may be direct when it results from causes obstructing the flow into the arteries, or collateral when it is due to withdrawal of blood into hyperemic areas in other parts of the body. Of the causes acting

directly, pressure is the most frequent. There may be general pressure upon an organ or localized area of the body, as in the application of elastic bandages; or pressure upon the vessels within the tissue itself, as in amyloid disease, the amyloid substance compressing the arteries and capillaries, or there may be direct compression of an artery by tumors. The circulation in an artery may be impeded by sclerosis of the vessel-walls and by emboli or thrombi within the vessel. Local anemia of moderate or even severe grade may be due to nervous influences acting through the vasomotor system, as in the earlier manifestations of Raynaud's disease. Collateral anemia is well illustrated by the anemia of the brain occurring in animals in which the splanchnic nerves have been cut, with the consequent production of abdominal hyperemia. When ischemia is due to obstruction of a single vessel the circulation is generally soon restored by collateral anastomosis; the collateral vessels sometimes reach considerable dimensions (Fig. 2). When an artery which has few anastomoses and which soon splits up into capillaries is obstructed the phenomena of infarction (see page 55) ensue.

FIG. 2.-Anastomoses three

months after ligation of the

An anemic area is pale, reduced in size and temperature, and functionally less active than normal. If the condition persists, fatty degeneration and necrosis result. When a severe local anemia is relieved it is apt to be followed by hyperemia of the same area, due to exhaustion or degenerative weakness of the vessel-walls.

femoral artery of a dog (Porta).

HEMORRHAGE.

By hemorrhage is meant the escape of the several constituents of the blood from the blood-vessels. It is said to be arterial, venous, or capillary according to the vessel from which the flow of blood takes place, and parenchymatous when it comes from all of the vessels. Hemorrhage may occur either by diapedesis and extravasation through intact vessels (hemorrhage per diapedesim) or by actual rupture of a vessel (hemorrhage per rhexin). The former process is seen only in the capillaries and smaller veins; the latter occurs mainly in the arteries and veins.

Diapedesis and Emigration.-Under normal conditions a certain number of white corpuscles by virtue of their ameboid movements escape from the capillaries, and become wandering cells which move about in the tissues or are carried by the lymph

stream. This process is called emigration. There is at the same time some transudation of plasma, which, with the leukocytes, enters the lymphatic circulation. Under certain abnormal conditions the red corpuscles also pass through the vessel-wall and collect in the tissues. This is known as diapedesis (Fig. 3). It may be studied very readily under the microscope in the mesentery of a living frog. It is noticed that the red corpuscles approach certain parts of the wall of the capillary or vein and become fixed; then a small projection appears outside the vessel, opposite the corpuscle, and as this increases the corpuscle within grows smaller, until the whole body has gradually passed through. Not rarely several

FIG. 3.-Diapedesis of the red blood-corpuscles through a capillary of a frog's tongue (after Thoma).

corpuscles pass through in one mass; as has been particularly noted by Thoma. Outside the vessel the corpuscle at once assumes its ordinary shape.

Diapedesis was first studied by Stricker and Cohnheim. Arnold, whose investigations are most important, first believed that the emergence of the red corpuscles takes place through orifices or stomata; but later recognized, as is now generally believed, that the supposed stomata are merely accumulations of intercellular substance in certain places between adjoining endothelial cells or at the junction of several cells. The active cause of the extrusion of the red corpuscles is the pressure of the blood.

The leukocytes emigrate from the vessel in exactly the same way as the red corpuscles, but mainly by their own ameboid movements. At the same time there is a more or less copious outflow of plasma.

Diapedesis is readily induced by mechanical compression of a vein, which elevates the blood-pressure; or it may follow elevation of blood-pressure from any other cause. On the other hand, with normal pressure increased permeability of the vessel-walls may occasion diapedesis. Such degenerative conditions of the vessels may be due to the action of poisons, to various infectious diseases, to moderate traumatism, or to temporary obstruction to the flow of blood into a certain area. Perhaps also altered states of the