reflexly by the mechanical injury to peripheral sensory neurones, plays the chief role in inaugurating a state of shock. The loss of control over the general arterial tone which results from this weakening of the center results in a determination of blood in certain vascular fluids. Of these the largest and most important is the great spanchnic territory, the flooding of which side-tracks, as it were, such an amount of blood that there results an anemia of the brain and lungs, a weakened cardiac action, on the "empty pump" principle of Goltz, and a consequent great fall in blood-pressure.

As has been stated in the brief discussion of the two cases, which, early in this paper, have been cited at some length, there are certain predisposing factors which are influential in favoring this reflex loss of vasomotor tone. It is, in the first place, a well recognized physiological fact that stimulation, of one sort or another, of a peripheral sensory nerve of an animal in normal condition occasions a rise of blood-pressure or so-called "pressor" response due to a reflex constriction of the smaller arteries of certain vascular territories. Such a pressor response is frequently seen in clinical cases, and we have had the opportunity of plotting many such curves in correspondence with the experimental observations such as Dr. Crile has carried out. A patient in an attack of biliary colic, for example, will have a rise of blood-pressure from its normal level, corresponding possibly to 120 millimeters of mercury, to a level of 200 millimeters or over. A corresponding response occurs, as I have many times observed it experimentally, when there is a forcible injection of fluid into, and so as to distend, the biliary passage of an animal under anesthesia. Similarly an attack of pain, such as is experienced in a paroxysm of trigeminal neuralgia, will raise the blood-pressure to inordinate heights. The increase in arterial tension under these circumstances may be unassociated with alteration in pulse-rate. Certain simple operative

procedures as well, such as dilating the sphincter or stretching the sciatic nerve, as has been already instanced (Fig. 14), will call forth a pressor response.1

From the experimental side many observations have been made to determine the conditions which favor the calling out of the depressor rather than the normal pressor response to a given stimulus. The loss of blood or a coexistent primary anemia, the exhaustion of an extensive operation or of prolonged anesthetization, the repeated calling out of pressor responses from painful stimuli with consequent fatigue of the vasoconstrictor mechanism, and a great variety of other conditions might be mentioned in illustration; conditions which have long been recognized as prejudicial to the safe-conduct of certain operations.

Comparatively recent observations, chiefly those coming from Howell's laboratory, have been largely instrumental in establishing the view that in each bundle of mixed peripheral nerves there exist definite centripetal ("pressor") fibers, stimulation of which calls forth by reflex action a vasoconstrictor response, and others equally definite, which on the other hand produce when stimulated a depressor effect from reflex vasodilatation with consequent fall in blood-pressure. In the neck of the rab bit, as is well known from the classical experiments made in Ludwig's laboratory, afferent fibers subserving in a certain measures these different functions run apart and may be indi-. vidually stimulated. One of these nerves has become known in

1When one sees recorded the pressor effects, which often occur in operative cases under anesthesia, with a rise of arterial tension to double or more its normal level, it becomes a matter of astonishment that rupture of blood-vessels does not more often occur, especially in the feebly supported vessels of the central nervous system, and in patients who show evidence of alteration in the arterial walls. It is not improbable that the cases of sudden death, which on rare occasions have followed such simple procedures as stretching the sphincter ani for fistula, may be attributable to such an occurence. Cases furthermore of anesthesia-apoplexy are by no means rare.

consequence as "the depressor-nerve," and must not be confused with the depressor fibers supposed to be present in other mixed nerves. Under ordinary circumstances, however, in the neck as well in the nerves of the extremities, both pressor and depressor fibers run together in the same trunk and due to the fact that the former under normal conditions respond more readily and effectually to most forms of stimulation, a rise in blood-pressure is usually produced. Of these two sets of fibers, those having a pressor action seem to be the first to suffer from injury or overstimulation, and when, in consequence, they have become exhausted, the same irritation to the mixed nerve which previously would have called forth a vasoconstrictor action, then elicits a fall in blood-pressure from stimulation of the still active depressor fibers.

Howell, for instance, has shown, when such a mixed nerve has been subjected to the effects of cold applied locally in its course, that it no longer calls forth pressor responses to peripheral stimulation, but that depressor effects may still be evoked. He and his pupils 'demonstrated, furthermore, in illustration of the fact that these two sets of fibers are functional entities, that after division of a peripheral mixed nerve those fibers calling forth reflexly a vasodilator response regenerate more rapidly than do those producing on stimulation a vasoconstrictor action.

Hunt2 subsequently, working in the same laboratory, has further elaborated these studies, and has brought out the fact that in a fresh animal the depressor fibers may apparently be stimulated in excess of those subserving a pressor function by the action of weak electric currents. Strong currents, on the other hand, would produce the usual rise in blood-pressure from vaso'Howell, Budgett, and Leonard, Journal of Physiology, 1894, Vol. xvi, p. 298.

"The fall of blood-pressure resulting from the stimulation of afferent nerves, Journal of Physiology, 1895, Vol. xviii, p. 381.

constrictor action. He has shown, also, in agreement with Kleen, that the mechanical bruising of muscles is apt to lead to a depressor effect. In confirmation of the observations

of Latschenberger and Deahna1 and others, Hunt's experiments demonstrate that on the repetition of a particular stimulus or injury, each of which, singly, would cause a rise in blood-pressure, a point is reached at which a pressor effect no longer occurs, but at which the same stimulus calls out a depressor response with fall in blood-pressure.

It must be confessed that there is no present uniformity of opinion among physiologists as to the nature of the depressor response. Conclusive proof even of the presence of depressor fibers, in the sense of Latschenberger and Deahna, is yet forthcoming. It is believed by some investigators that the fall in blood-pressure is due to alterations in the center itself rather than the result of a reflex dilator action of specific afferent fibers. Whatever the mechanism of the response may be, however, the fact of its occurrence is sufficient for practical require ments; and, although the matter may have been presented here in an amateurish fashion, it needs but a glance to appreciate the importance to the operating surgeon of these laboratory observations. Their relation also to the clinical notes which have been given in the first part of this paper, demands no written inter-. pretation.

The facts remain that injuries of most diverse nature to peripheral nerves may, especially in some physical states, produce reflexly a fall in blood-pressure; that this loss of vascular tone, when it endures, is the most characteristic feature of shock, the symptom-complex of which is largely due to this one factor; that local anesthetization of a nerve-trunk will block the transmission of these centripetal impulses which otherwise might bring about this reflex loss of vascular tone.

'Latschenberger and Deahna,

"Beitrage zur Lehre von der reflectorischen Erregung der Gefrassmuskeln," Pflüger's Archiv, 1876, Band xii, p. 157.

THE DUTY OF THE GENERAL PRACTITIONER IN RESPECT TO AURAL DISEASES.

BY FRANK H. EDSALL, M. D., OF MADISON.

In the presence of aural disease the general practitioner has a somewhat difficult question to determine as to what his course should be in respect to the case. In the light of the present-day knowledge of ear diseases the old policy of trusting the case to nature will scarcely answer. Of old, with an incipient middleear abscess, the family physician was wont to purge, perhaps to bleed, and then if the patient were unrelieved, to wait with whatever of calmness the sufferer's condition would allow "for it to break." More likely than not the diagnosis had been equally as inexact as was the treatment, and as the latter failed ofttimes even to assist nature the victim of aural affections was in an unfortunate position, for what was true of the diagnosis and treatment of aural abscess was even more emphatically true of most of the other affections of the ear. Nor was the old-time family physician culpable in that better treatment were not given the patient. His instruction while a student of medicine did not furnish him with the necessary ground-work upon which he could build a better superstructure, and, indeed, until rather recent times the aurist, if he could have been reached, would have helped but little, and in those "good old times" aurists were few and far between, and by reason of these things the oldtime doctor's duty in the presence of aural disease was to go in and do the best he could and trust the outcome to God. Is this condition changed at the present time? Yes and No.

Knowledge of aural affections has multiplied in recent times and, also, aural specialists abound. For well-nigh a generation reasonably satisfactory instruction in the diagnosis and treatment of aural diseases has been open to the medical student, at