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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



ported that glass spheres up to 180 n in diameter 

 may be recovered from hepatic venous effluent fol- 

 lowing injection into the portal vein. In contrast, 

 Gordon et al. (150) obtained much smaller values with 

 a method based upon the established relationship 

 between perfusate surface tension, minimal perfusing 

 pressures, and the largest radius in a system of tubes. 

 They found that portal to hepatic vein "anastomoses" 

 did not exceed 24 n in diameter and hepatic A-V 

 anastomosis ranged from 18 to 26 ii in the rat and 

 rabbit. The former are probably the hepatic sinusoids 

 proper; the latter, the A-V anastomosis reported by 

 Wakim & Mann (299) and Seneviratne (270). With 

 respect to the data obtained with glass beads, they 

 note that the method "yields remarkable results in 

 that every organ investigated by this means has been 

 shown to have very large A-V anastomoses." What- 

 ever the merits of this dispute, vascular anastomoses 

 do not seem to play a large part in determining 

 hepatic hemodynamics. Possibly they operate in 

 establishing distributional patterns of flow but even 

 here cross section and path length per se appear to 

 be more important. 



The characteristic patterns of the pathways by 

 which blood travels through the capillary beds within 

 the hepatic and splanchnic vasculature are imperfectly- 

 understood. There is now fairly general agreement 

 that capillaries themselves possess no intrinsic capacity 

 for contractility or for autoregulation of flow and 

 volume within them. Chambers & Zweifach (82) 

 claim that capillary nets are characterized by con- 

 tinuously active and well-marked "thoroughfare chan- 

 nels" or "A-V capillaries," which pass more or less 

 directly from the arterioles to the draining veins and 

 from which the bulk of the capillaries take origin. 

 According to these workers, the proximal portion of 

 the central channel is encircled by muscle cells and 

 is to be regarded as a junctional arteriole or "met- 

 arteriole" which gives rise to even less well-muscled 

 "precapillary" vessels or "precapillary sphincters" 

 controlling inflow cross section. This arrangement 

 has been described with what seems complete validity 

 in the mesenteries (82, 317) but does not seem to be 

 typical of capillary nets in other tissues (154) [see 

 also Chapter 27 of this volume]. Active, more or 

 less rhythmic, alternating dilatation and contraction 

 or so-called "vasomotion" has also been observed in 

 the terminal arterioles by time-lapse photography. 

 Xot all workers have been successful in convincing 

 themselves of the validity of vasomotion but all 

 seem in agreement regarding the phenomenon of 

 "intermittency" or transient nonperfusion of a frac- 



tion of any given capillary bed. Flow ceases or capil- 

 laries empty completely and remain so for a time, 

 then flow resumes without apparent cause. During 

 hyperemia nearly every capillary visualized will be 

 active. Ischemia seems to reduce the number of 

 active capillaries as well as to diminish flow through 

 those remaining in function. This phenomenon has 

 been repeatedly observed (185, 225, 270, 299, 317) 

 in the hepatic sinusoidal system as well as in the 

 capillary beds of the mesenteric distribution, the 

 pancreas, and the spleen. Of course, the capillaries 

 accessible to direct visualization are an infinitesimal 

 fraction of the total and probably not a representative 

 or random sampling. Intermittency probably occurs 

 during normal life and may be involved in altering 

 actively the total resistance to flow, but it seems not 

 unlikely that it is an expression of capillary instability 

 resulting from a critical reduction in distending pres- 

 sures by "path-length resistance." 



Innumerable routes of various lengths may be 

 followed by the blood from the aorta to the hepatic 

 vein. On the arterial side, the gastric, mesenteric, and 

 colic vessels are particularly long and variable with 

 interconnection by arcades that may serve to equalize 

 input pressures and flows. The hepatic and splenic 

 arteries are shorter and more direct but path length 

 varies nonetheless because hilar entry results in short 

 routes in the more central regions and longer ones 

 by way of the parenchymal tissues situated at the 

 periphery. The same configuration applies to the 

 hepatic portal inflow tract but here the low pressure 

 head and the minimal cross-sectional resistance ap- 

 pear to confer greater importance upon path length 

 as a determinant of energy loss. Daniel & Prichard 

 (10 1, 102) claim that portal blood does not always 

 perfuse the entire liver for this reason. They used 

 rapid serial angiography as a means of assessing 

 distribution of flow following injection of Thorotrast 

 into a mesenteric vein in cats, rabbits, guinea pigs, 

 pigs, and goats. The contrast medium was usually 

 found to move freely into the portal vein and its 

 branches, then into the sinusoids, opacifying the 

 organ diffusely with sharp definition of its profile, 

 and finally into the hepatic veins and inferior vena 

 cava. In a few rats and kittens, a "restricted intra- 

 hepatic circulation" was demonstrable with failure of 

 the Thorotrast to fill the outermost ramifications of 

 the portal vein, with an irregular and patchy opacifi- 

 cation limited to the central tissues and with filling 

 of only those segments of the hepatic veins which lie 

 relatively near the hilum. This phenomenon could be 

 induced by stimulation of the hepatic nerves and by 



