1406 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



fig. I. The hepatic and splanchnic cir- 

 cuits. The vascular resistances in the splanch- 

 nic bed (A) are shown here in diagrammatic 

 form (B). The resistances indicated are the 

 determinants of sinusoidal and portal venous 

 pressures and of flows through the portal 

 vein and hepatic artery. In addition to the 

 hepatic arteriolar resistance {R\), colic, 

 mesenteric, pancreatic, gastric, and splenic 

 arteriolar (/?;), portal venular (/?,) and post- 

 sinusoidal (R,) resistances, a fifth resistance 

 lying in direct communication between the 

 portal vein and inferior vena cava (the col- 

 lateral resistance) is shown as a dotted line. 

 It may be seen that the resistance pattern 

 resembles that of the Wheatstone bridge, 

 though the electrical analogy must not be 

 taken too literally. The total splanchnic 

 resistance (R T ) may be expressed (44) in 

 terms of its constituent resistances as follows 

 (omitting the collateral resistance) : 



R I R Z 



R , R 3 



+ R. 



R,+R 2 +R 3 



[Reprinted from (43) with permission of the 

 publishers.] 



Inf V.C. 



*2 



Splanchnic 

 arter: 'i- 

 PORTAL V resist 



AORTA 



gradient alone is fraught with the danger of serious 

 error. If the values above are correct, it is evident 

 that the resistance to outflow from the liver and the 

 portal venous bed is a fraction of inflow resistance. 

 It may be inferred therefrom that relatively small 

 absolute changes in R f and R* would influence portal 

 venous and sinusoidal pressure markedly, and in 

 doing so, affect the volume of blood distending the 

 portal and hepatic vasculature. 



Splanchnic Blood Volume 



The balance between input and outlet resistances 

 and the "capacity" of the vasculature together 

 presumably determine splanchnic blood volume and 

 the pressures under which the vessels are distended. 

 The relative contribution of each is difficult to assess 

 not only during change but also in the basal reference 

 state. The total circulating splanchnic blood volume 

 (regional dilution method) in both dog and man at 

 rest amounts to approximately 20 per cent of the 

 total blood volume, within a wide range attributable 

 both to technical and physiologic factors (43, 44, 50, 

 106, 175, 181). Of this, the bulk appears to be held 

 within the large veins (for details see below), though 

 an important moiety is lodged within the sinusoids of 

 the liver and the spleen. The intrinsic capacity of 

 this variegated system at any pressure thus depends 

 upon the elasticity of muscular veins and the counter- 



forces operating to compress or distend the intra- 

 abdominal viscera and their vasculatures. 



Muscular contraction may quickly modify the 

 former, whereas the introduction of food, water, and 

 air into the gastrointestinal tract and the movement 

 of fluid across the cell walls may change the latter 

 very slowly. It is difficult, under the circumstances, 

 to establish satisfactory reproducible control values. 

 Moreover, the pressures acting in the different parts 

 of the bed are effective in proportion to diameter, 

 in accord with Laplace's law (70) so that a much 

 greater pressure rise is necessary to increase sinusoidal 

 volume than to produce the same increment in 

 venous volume. Insufficient data are available to 

 permit quantitative evaluation of this factor in dif- 

 ferent regions and to give proper importance to 

 venous and capillary pressure levels. 



The cross-sectional distribution of the vessels, 

 containing the blood, figures importantly not only 

 in determining the average distensibility but also in 

 fixing the average hematocrit and the composition 

 of the splanchnic blood volume. Lamination of 

 flowing blood results in a lower hematocrit in 

 capillaries than in large vessels, owing to the relatively 

 large volume of plasma in the layer immediately 

 adjacent to the vessel wall. Sequestration of blood 

 with sluggish turnover may lead to accumulation of 

 red cells, however, and to a higher hematocrit than 

 in the large vessels. The hematocrit of the circulating 



