1408 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



the wedged hepatic venous-central venous pressure 

 differential gives proof to its operation while the 

 thick throttling musculature of the small hepatic 

 veins (in the dog, at least) suggests a mechanism for 

 its production. The musculature of the arterioles 

 also indicates an apparently adequate basis for 

 variation noted in intrahepatic or splanchnic re- 

 sistances and blood flows. Nevertheless, other factors 

 enter the equation and under certain circumstances 

 contribute effectively in changing the total vascular 

 cross section independently of vasomotor activity. 



Collapse of vessels secondary to changes in trans- 

 mural pressure may result in the redistribution of 

 resistances and in the reduction of the number and 

 diameter of the units perfused at any level. Much 

 work in recent years (149, 162, 226, 307) indicates 

 that perfusing pressure and blood flow are linearly 

 correlated only above 20 to 40 mm Hg in the maxi- 

 mally dilated vascular beds of the isolated hind limb 

 of the dog. At lower pressures the pressure-flow curve 

 is sigmoid with a positive intercept on the pressure 

 axis. Green and his associates (162) have suggested 

 that vascular compliance may produce the convexity 

 to the base and the positive pressure intercept at zero 

 flow, the perfused vessels decreasing in cross section 

 and number as the distending pressures are lowered 

 with increasing resistance in consequence. This phe- 

 nomenon has been extensively studied by Burton 

 and his associates (70-72) who attribute it to an 

 inherent vascular instability that develops as the 

 product of the intraluminal pressure and the radius 

 falls below the "tension" in the wall. At this point, 

 that of "critical closing pressure," collapse occurs and 

 the vessel "shuts down." The mural tension is at- 

 tributed to the interplay of elastic tension or tissue 

 resistance to stretch, active tension generated by 

 muscular contraction, and interfacial tension arising 

 from the surface forces between blood and the "un- 

 wettable" intima. A significant correlation noted 

 between critical closing pressure and resistance to 

 flow in various preparations (including the perfused 

 ear of the rabbit, intact dogs with extracorporeal 

 circulation, the human hand during changes in 

 transmural pressure) has been interpreted as evidence 

 that the arterioles are chiefly concerned. The linear 

 relationship between high pressures and flows ob- 

 served by Whittaker & Winton (307), Pappenheimer 

 & Maes (226), and others (70, 71) indicates non- 

 distensibility of the resistance vessels and appears to 

 be a result of maximal dilatation in their experiments. 

 Levy (194), Folkow & Lofving (131), and others 

 (166) have shown that the resistance vessels are freely 



distensible over a wide range of pressures produced by- 

 equal increments in both arterial and venous pressures, 

 less so when arterial pressure alone is raised and more 

 obviously with a rise in venous pressure alone; pro- 

 vided the bed is denervated and before local adjust- 

 ments obtrude. Thus resistance to flow through an 

 extremity may be diminished by raising the in- 

 travascular pressure and increased by lowering it. 



Studies by Brauer el al. (57), Trapold (292), and 

 Selkurt it al. (269) indicate that critical closing pres- 

 sures may also be defined for the vasculatures of the 

 liver and intestines. All have used isolated denervated 

 tissues perfused in vitro over a wide range of pressures. 

 Brauer el al. (57) obtained a sigmoid relationship 

 between perfusion pressure and flow through the 

 isolated rat liver perfused via the portal vein alone. 

 They found an increment in resistance below pressures 

 of 5 to 10 mm Hg apparently attributable to closure 

 of a significant proportion of vessels that occurred in 

 association with impairment in bile formation. Pres- 

 sure-flow relationships were evaluated by Trapold 

 (292) and Selkurt et al. (269) in the vessels of isolated 

 loops of small intestine. Both observed linearity 

 between 60 and 1 50 mm Hg, convexity to the pressure 

 axis at about 60 mm Hg or lower, and a tendency for 

 flattening at higher pressures. The zero flow in- 

 tercept on the pressure axis was 16 mm Hg. They 

 interpreted these findings as evidence of "critical 

 closing" at low pressures and of distension with 

 diminishing resistance as pressure was increased. All 

 three groups noted the changes in critical closing 

 pressure (rising with vasoconstriction and falling with 

 dilatation) observed by Burton and his co-workers 

 (70-72) during vasomotor activity produced by 

 drugs and anoxia, and attributed by them to a 

 change in "active tension." In normally innervated 

 beds or in carefully prepared tissues, however, the 

 correlation between critical closing pressure and the 

 level of vasomotor tone did not appear to be readily 

 demonstrable and free distensibility was not ap- 

 parent (250). Indeed, additional evidence suggests 

 that stretch of the vessel wall by a rise in intravascular 

 or transmural pressure may actually elicit a reactive 

 contraction of the smooth muscle, that prevents dis- 

 tension and that may even reduce cross section. 



The possibility that intraluminal tension might 

 determine vascular tone in this manner was raised 

 by W. M. Bayliss in 1902 as an explanation for his 

 observations that transient occlusion of the femoral 

 artery was followed immediately in the denervated 

 limb by hyperemia, and that a sharp rise in intra- 

 luminal pressure elicited an increase in "tone" of 



