Local irritation is such an influence, and it may excite the ganglia to increased activity, so producing a contraction of the vessel and consequent pallor; or it may suspend the action of the ganglia, so producing a dilatation of the vessel and consequent flushing.
Another influence is irritation acting from a distance and conveyed to the local ganglia by nerve-fibres. These nerve-fibres can be distinguished from all others by their structure, being non-medullated, and by the fact that they have an indirect course, passing from the central nervous system to the sympathetic ganglia, and from these to the local ganglia in the vessels. The impulses sent along these nerves may affect the local ganglia in one of two ways, and either cause contraction by exciting the ganglia, or dilatation by inhibiting the action of the ganglia. The result produced has determined the names given to the impulse, to the fibre transmitting it, and to the centre whence the impulse proceeds, and hence vaso-constrictors and vaso-dilators are distinguished from one another.
The history of the development of the sympathetic nervous system,1 as well as its gross anatomy, affords distinct proof that it is not an independent system, as Bichat supposed, but is closely connected in its physiological action with the spinal cord and brain. Impulses which reach the sympathetic ganglia from a distance along the vaso-constrictor or vaso-dilator fibres originate in the central nervous system. The nervous mechanism which controls the local vascular tone is therefore a complex one, consisting not only of the set of local ganglia connected with larger sympathetic ganglia, but also of centres in the spinal cord connected with higher centres in the brain. The brain-centres in turn are complex, consisting of an automatic mechanism in the medulla regulating the action of all the subordinate parts below it, and of a series of cortical centres whose function it is to stimulate or inhibit the medullary mechanism. It therefore becomes evident that local vascular tone may be modified by local causes acting on the ganglia in the vessels—e.g. cold or heat; by changes in the sympathetic ganglia—e.g. the hyperæmia of the face in lesions of the cervical ganglia; by reflex action through the spinal cord—e.g. pallor produced by pain; by reflex action through the medulla oblongata—e.g. glycosuria following sciatica; or by conscious or unconscious impulses coming from the cortex—e.g. the blush of shame, the vaso-motor paralysis of hemiplegia.
1 W. R. Birdsall, “Embryogeny of the Sympathetic System,” Arch. of Med., vol. i. where a bibliography of the subject is to be found.
Vaso-constrictors.—Such a mechanism, however complex in structure, would be easily comprehended if the constant manifestation of energy in the maintenance of arterial tone had its only source in the action of the local ganglia in the vessels, and was affected only occasionally by impulses from a distance, as has been thus far supposed. This, however, is not the case, as has been demonstrated by a series of experiments beginning with the brilliant researches of Claude Bernard. The classical experiments of the French physiologist were made upon the sympathetic cord in the neck of a rabbit. Division of this was found to produce a dilatation of the vessels of the ear. Irritation of the peripheral end of the divided cord produced a contraction of the vessels. Division of the spinal nerves connected with the cervical sympathetic and of their anterior roots, or irritation of the cut ends, produced effects similar in character to those caused by division or irritation of the cervical sympathetic. Destruction of the spinal cord in the lower cervical region, or division of the cord at any higher level up to the medulla, was followed by dilatation of the vessels. If the segment of the divided cord just below the section was irritated the vessels contracted. Destruction of the medulla at the calamus scriptorius and above it for three centimeters produced a general dilatation of all the vessels in the body, but division above this level had no effect. The initial congestion produced by these various experiments was accompanied by a rise of temperature in the part. It was followed after a time by a partial recovery of vascular tone, which was more complete the farther the division from the local ganglia. These facts warranted the conclusion that the energy expended by the local ganglia in holding the vessels in a state of constant moderate contraction is derived from the central nervous system, primarily from the automatic centre in the medulla, which in turn is reinforced by each of the secondary centres in the spinal cord and sympathetic ganglia; and also that while the medullary centres control the entire body, the cord and sympathetic centres control only those parts with which they are especially related. In order, therefore, to the maintenance of normal vascular tone the local ganglia must be intact, and they must be in connection with the sympathetic ganglia; these must be active, and must be connected with the spinal cord; the cord must be normal, and its tracts from the medulla must be capable of conduction; the medullary centre must be active, and not hindered or spurred by cortical impulses of a conscious or unconscious nature. Any injury to one or more of these parts will produce a vascular dilatation by interfering with the transmission of vaso-constrictor impulses from within outward, and any irritation of one or more of these parts may cause a contraction of the vessels by increasing the normal stimulus sent to the local ganglia by the vaso-constrictors.
Vaso-dilators.—The action thus far considered has been wholly of a vaso-constrictor kind, and the dilatation which has been mentioned has been due to cessation of the constrictor energy normally passing outward. This may be termed a passive dilatation. It is the kind produced by division of any one of the sympathetic ganglia or cords. But further experiments have shown that another kind of dilatation may be produced, traceable not to a mere cessation of constrictor impulses, but to an impulse of a positive kind sent to the local ganglia and resulting in a sudden suspension of their activity. Such an impulse is really an inhibitory impulse arresting the action of the ganglia in spite of the continued stimulus sent to them from the central nervous system. Its result is a dilatation of the arteries, produced by the blood-pressure within them, which may be termed an active dilatation. Thus, Bernard found that irritation of the chorda tympani caused an immediate flow of blood to the submaxillary gland because of the dilatation of its vessels. And Dastre and Morat2 have demonstrated a similar effect in the head and extremities after irritation of portions of the cervical sympathetic and of the peripheral nerves.
2 See Archives de Physiologie, “Vaso-dilateurs,” 1879, 1880, 1882; Comptes rendus de l'Academie des Sciences, 1880, pp. 393 and 441.
Much confusion has arisen from the use of the term active dilatation, and many explanations of its mechanism have been offered. At first it was supposed that a system of longitudinal fibres in the vessel-wall acted as opponents to the circular constrictor fibres. This theory, originating with Stilling and Duchenne,3 has been lately revived by Anrep and Cybulski.4 They hold that since a vessel elongates as well as dilates with every heart-beat, its total distension is the result of two factors—viz. transverse and horizontal distension. If one of these is neutralized, they claim that the other will be increased. Longitudinal fibres in the wall by preventing elongation may thus allow the entire force of the heart to be expended in dilating the vessel. This theory has not, however, been accepted, and with that of Schiff, that contractile elements of the connective tissue surrounding the vessel-walls could pull outward the walls and thus dilate the vessel, has lapsed, because of lack of demonstration of the necessary anatomical structure in all arterioles. Another theoretical explanation, that dilatation of the arteries is caused by contraction of the veins damming back the blood, is disproved by the fact proven by Dastre and Morat, that blood-pressure increases instead of diminishing in the veins during vaso-dilator action. Legros5 and Onimus,6 noticing the normal occurrence of a peristaltic motion of centrifugal direction in the arteries of the retina, which if increased produced a certain degree of hyperæmia, attempted to explain the phenomena of dilatation by supposing a sudden increase of peristalsis. But Vulpian has proved that the peristalsis is both too slight and too slow in its effects to account for the rapid action of the vaso-dilators, and Dastre and Morat have shown that the peristalsis, not being synchronous with the heart-beat, really impedes the flow of blood. The last theory to be mentioned has a chemical basis, and is known as the theory of attraction (Brown-Séquard, Severini.) According to this, the organs, when active, manifest increased metabolism, to maintain which the blood is drawn toward them by the chemical changes in progress. This theory was based on the fact that irritation of the chorda tympani causes an increased secretion of saliva as well as a congestion of the submaxillary gland. It is now known, however, that these two acts are independent of each other, as either can be suspended while the other continues. Hence this theory too has lapsed.
3 Von Recklinghausen, Handbuch der Pathologie des Kreislaufs und der Ernahrung, 1883, where a full bibliography is to be found.
4 St. Petersburg Med. Wochenschrift, 1884, i. 215.