TABLE 1

Carotid bloodflow during bath in cool water (Dog 9.5 kilos)

II. THE DISTRIBUTION OF THE BLOOD DURING STIMULATION OF THE

SPLANCHNIC NERVE

The quantitative measurements of the bloodflow in the portal vein and its tributaries (1) have proven conclusively that vasoconstrictor reactions in the viscera innervated by the splanchnic nerve caused a marked diminution in the influx of arterial blood into these organs. This stagnation is responsible for the increase in the arterial pressure.

Edwards (2) has shown, however, that the stagnation is not absolute and that a certain compensation is possible through the circuit of the carotid and femoral arteries, which tends to keep the venous system supplied with almost normal quantities of blood.

TABLE 2

Flow in inferior vena cava during stimulation of greater splanchnic nerve

This compensation in the distribution of the blood in consequence of splanchnic constriction is especially well betrayed in the inferior cava distally to the entrance of the hepatic veins. I have succeeded in showing this by calibrating the bloodstream in this vein before and

during the excitaton of the left greater splanchnic nerve. The stromuhr was inserted distally to the left renal vein. The distal cannula was connected with a membrane manometer which registered the venous pressure. The general arterial pressure was recorded by a mercury manometer connected with the left femoral artery. In illustration of the results I insert at this time the calculations for a part of experiment 2 of this series, as well as a reproduction of the phases recorded by the stromuhr during this time. As is clearly shown in figure 1, the stimulation of the aforesaid nerve A-B, is followed by a decided increase in the venous return, the normal flow of 5.4 cc. in a second, St, being gradually displaced by a flow equalling 9.0 to 11.0 cc. in a second. This change occurs during the period of high arterial pressure, C-D, i.e., at a time when the splanchnic organs are constricted. Under ordinary conditions the results of this constriction betray themselves in the central venous channels by a drop in pressure in consequence of the lessened influx of portal and renal blood, F. The present experiments, however, show that this central deficiency in blood is soon compensated for by a greater influx through circuits not dominated by the splanchnic nerve. In addition this change in the distribution of the blood acts as a check upon the pressures, preventing the occurrence of an undue arterial stagnation and hence of an injurious increase in the arterial pressure.

III. THE RELATION BETWEEN THE INTRAPERICARDIAL PRESSURE AND THE PORTAL BLOODFLOW

These experiments are intended to illustrate the clinical picture observed in pericarditis as it betrays itself in changes in the dynamical conditions of the portal system. They were performed upon dogs during ether narcosis. The chest having been opened and artificial respiration instituted, a glass cannula was inserted in the pericardial sac. The stromuhr was then connected with the portal vein. The venous pressure was registered by a membrane manometer connected with the distal cannula of this instrument, and the arterial pressure by a mercury manometer connected with the carotid artery. The procedure consisted in all cases in obtaining these different records under normal conditions as well as during periods of increased intrapericardial presThe latter end was attained by permitting air from a pressurebottle to flow into the pericardial sac until a very moderate degree of inflation had been established. The height of this pressure was recorded by a water-manometer.

sure.

As the results are perfectly uniform, a brief discussion of figure 2 will no doubt suffice to show their character. In the present animal, a dog weighing 14 kilos, the flow in the portal vein, S, amounted to 3.69 cc. in a second. The inflation of the pericardial sac was begun at A. It was continued during a period of about twenty seconds, i.e., to point B, reaching a maximal value of 4 mm. Hg. It is evident in the record that the flow decreases very markedly at A and continues small for some time after the cessation of the inflation, i.e., to about point C. The average flow during this period is only 1.81 cc. in a second, a reduction of 50 per cent.

Fig. 2. Portal bloodflow on increasing intrapericardial pressure. A to B (Red. to original).

If we now observe the records of the pressures, it is apparent that this period of decreased flow coincides with a fall in the arterial pressure, CA, and a rise in the venous pressure, PV. These phenomena of low arterial driving force and venous stagnation disappear soon after the cessation of the inflation. It need scarcely be mentioned that greater increases in pressure do not alter the character of these changes but merely tend to render them more conspicuous.

BLOODFLOW

The method employed to reproduce the clinical picture of tricuspid regurgitation as it betrays itself in changes in the portal system was