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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



crease because of the operation of Laplace's law. 

 After a period of time at high pressures the stretched 

 vein does not return at once to the control volume 

 when distending pressures are lowered to the control 

 but assumes temporarily a new larger "zero volume." 

 The viscous element which is responsible for this 

 phenomenon is particularly difficult to explain. To 

 some extent it may be referred to architectural ad- 

 justments such as slippage or uncoiling of intertwined 

 elements, but all tissues in the wall, under sufficiently 

 prolonged stress, are subject to a kind of viscous flow. 

 Alexander (4, 5, 7) has encountered the same prob- 

 lem in a somewhat different form in the course of a 

 study of splanchnic venous distensibility in anesthe- 

 tized dogs. Volumes of blood were injected by a motor- 

 driven syringe at constant rates (10 — 250 ml min) 

 into the vein draining a loop of ileum isolated with 

 all collateral vessels and nerves ligated and cut. 

 Simultaneous arterial and venous pressure measure- 

 ments permitted direct determination of pressure- 

 volume relationships. By this means two types of 

 distensibility were evident; /) rapid elastic expansion 

 yielding the expected sigmoid pressure-volume curve 

 during the injection of relatively small volumes of 

 blood and, 2) an additional, more slowly developing 

 distention increasingly apparent at slower injection 

 speeds. Alexander attributes the latter phenomenon 

 to viscous creep and refers to it as "delayed com- 

 pliance." Apparently, it is a continuously changing 

 factor, possibly arising from the operation of multiple 

 viscoelastic units arranged in series with the other 

 components. Whatever the mechanism, delayed 

 compliance may be of major importance in deter- 

 mining splanchnic vascular pooling at any distending 

 portal venous pressure. 



SECONDARY DETERMINANTS OF HEPATIC 

 HEMODYNAMIC ADJUSTMENTS 



Although the dimensions and the physical proper- 

 ties of all parts of the splanchnic vascular bed are 

 primarily responsible for its over-all hemodynamic 

 character, both circulatory stability and rearrange- 

 ment are mediated by essential secondary mecha- 

 nisms. Neural, humoral, and physical agents are 

 demonstrably involved in the maintenance of the 

 "reference" state and in the production of appropriate 

 patterns of response. Change in any one of these 

 factors elicits adjustments in all the others that must 

 also be taken into account. A rich innervation assures 

 integration and spread of vascular adjustments. 



Whether neural activity is also responsible for the 

 tone of vascular smooth muscle remains uncertain. 

 Xo matter how defined, tone is not clearly dependent 

 upon a continuous release of neural impulses. A very 

 slow and indetectable discharge rate might be in- 

 volved, but local factors, chemical and physical, still 

 seem to take precedence over and replace neural 

 regulation under certain circumstances. Neurohu- 

 moral transmitters, such as epinephrine, norepineph- 

 rine, and acetylcholine may also have considerable 

 importance, contributing by local release in the 

 maintenance of tone observed following denervation, 

 for example, or by release into the circulation, in 

 systemic integrations. Other local biochemical factors 

 that must be considered to participate include oxygen, 

 carbon dioxide, hydrogen ion, and metabolites like 

 histamine or serotonin. Among the physical deter- 

 minants are to be numbered intra-abdominal pres- 

 sure, gravity, intestinal motility, and the changes 

 associated with respiration and body movements. 



Neural Determinants 



The nerves of the liver, gall bladder, and bile ducts 

 form a plexiform structure made up of numerous 

 small ganglia with a) the anterior hepatic plexus 

 (derived from the left portion of celiac plexus and the 

 right abdominal branch of the left vagus) immeshing 

 the hepatic artery, and b) the posterior hepatic plexus 

 (derived from the right portion of the celiac plexus 

 and the branches of the right vagus that traverse the 

 celiac plexus) investing the portal vein and bile duct 

 (8, 190, 253). Ganglia required for parasympathetic 

 synapses are not present. The spleen receives its supply 

 almost entirely from the celiac plexus possibly with 

 some contribution by the left phrenic nerve. Like the 

 liver, the spleen receives no parasympathetic com- 

 ponent (53, 294). Throughout the splanchnic bed 

 bundles of nerves accompany blood vessels in their 

 distribution to the tissues. Within the walls of the 

 larger arteries subsidiary plexuses are arranged in a 

 more or less orderly manner. An outer plexus in the 

 adventitia, a deeper plexus between adventitia and 

 media, and a plexus within the muscular media have 

 been recognized. The complexity of these networks 

 becomes progressively less marked in the vessel walls 

 as caliber diminishes until at the capillars' level it i^ 

 difficult or impossible to find any evidence of specific 

 innervation. The close association of vagal and sym- 

 pathetic fibers in many regions does not imply an 

 association in controlling vascular smooth muscle. 

 Indeed the reverse seems to be true for vagal fibers 



