THE HEPATIC CIRCULATION 



[427 



anesthesia in the experimental study of shock in- 

 troduces an additional variable. General anesthesia 

 with nitrous oxide, thiopental, or pentobarbital does 

 not seem to affect EHBF and SBV provided gas 

 exchange is carefully controlled (123, 124). Reactions 

 may differ with the agent employed [splenic volume 

 is increased, for example, by barbiturates and de- 

 creased by ether (132)] and more carefully controlled 

 studies are necessary to evaluate the effects of dif- 

 ferent dosage levels and anesthetic planes. Anesthetic 

 drugs also act like autonomic "blockers" to diminish 

 responsiveness so that data collected in experimental 

 studies may not be strictly relevant to the clinical 

 state. Studies in man have been helpful for this reason, 

 though complete control is impossible. The hepatic 

 circulatory changes of congestive heart failure have 

 been investigated only in man and, though the data 

 are of great value, reliable evaluation must wait upon 

 definitive studies of the condition produced experi- 

 mentally in laboratory animals. 



The effects of hemorrhage have been most ex- 

 tensively explored. In the anesthetized (pentobarbital) 

 dog and rat, splanchnic blood flow and volume de- 

 crease during and following blood loss (136, 137, 

 179, 243, 267). Blood flow appears to diminish in 

 proportion to the fall in arterial pressure. A transient 

 vasoconstriction may occur but the general tendency 

 appears to be rather in the direction of moderate 

 vasodilation, particularlv affecting the hepatic ar- 

 terioles. Mesenteric arteriolar constriction may de- 

 velop after prolonged hemorrhagic hypotension (96, 

 136) and may even be enhanced by the administra- 

 tion of norepinephrine, but there is no evidence that 

 it is effective in sustaining arterial pressure (193). 

 Portal venous pressure usually falls, too, presumably 

 as a result of both the shift in the balance between 

 input and output resistances (central venous pressure 

 also falls) and the drop in arterial pressure. Splanch- 

 nic blood volume decreases more than the total 

 blood volume (137, 243). The reduction in distend- 

 ing pressure is probably a major determinant of the 

 shift, but venoconstriction, demonstrable in isolated 

 preparations (6), must play a part also and un- 

 doubtedly accounts for the continued reduction in 

 splanchnic blood volume following restoration of 

 blood volume at a time when portal venous pressure 

 tends to rise. Certainly, splenic contraction occurs 

 in most species (132). The splanchnic venous reservoir 

 evidently participates as a whole in homeostatic 

 compensations by actively transferring blood into 

 the central veins and sustaining the "circulating blood 

 volume." This response continues to be detectable 



even in the terminal irreversible phase (137, 243). 

 How and to what extent anesthesia, adrenal medul- 

 lary discharge and neural activity contribute to or 

 modify hepatic vasomotor adjustments remains un- 

 settled. Studies of changes during hemorrhage in 

 human volunteers suggest that splanchnic vaso- 

 constriction may be more prominent in the absence 

 of anesthesia (28). 



A definite vasoconstrictive pattern is clearlv charac- 

 teristic of congestive heart failure in patients with 

 various cardiac diseases (236). In this situation, 

 EHBF has been found to be reduced to the same ex- 

 tent as cardiac output despite maintenance or even 

 elevation of the arterial blood pressure, indicating 

 vasoconstriction no greater than that elsewhere in 

 the body and certainly much less than that occurring 

 in the kidney. A uniform contraction of hepatic and 

 splanchnic arterioles probably occurs without much, 

 if any, change in postsinusoidal or portal venular 

 resistance, since wedged hepatic venous pressure did 

 not differ from the free hepatic venous pressure by 

 more than 2 mm Hg according to Rapaport and his 

 associates (236). Circulating splanchnic blood volume 

 is disproportionately increased by cardiac failure, 

 at least in those patients in whom atrial and wedged 

 hepatic venous pressure is elevated. There is no evi- 

 dence at present of either splanchnic venoconstriction 

 or venodilation and it is necessary to conclude, for 

 the moment, that the distention is passive. The se- 

 questration of a larger portion of the blood volume 

 in the splanchnic bed may effectively reduce the load 

 imposed upon the heart and, in so doing, serve as a 

 compensatory device. The large volume of blood 

 within the splanchnic veins is an ever-present hazard, 

 however, for exertion, violent respiratory movements, 

 or increased intra-abdominal pressure may displace a 

 large volume of blood from the abdomen and throw 

 an additional, and perhaps an overwhelming, burden 

 upon the heart at almost any time. More data are 

 needed to evaluate this possibility and to assess the 

 role of the hepatic vasculature in the pathogenesis 

 and therapy of congestive heart failure and other 

 cardiovascular disorders. 



Hepatosplatulmic Inter) elationships 



The interdependence of the liver and the gastro- 

 intestinal tract is self-evident. Digestion and absorp- 

 tion depend upon normal biliary secretion, while the 

 enterohepatic circulation of bile salts and the release of 

 secretin, in turn, determine bile flow and composition. 

 Water, electrolytes, and various organic compounds 



