PORTAL PRESSURE GRADIENTS UNDER EXPERIMENTAL CONDITIONS, INCLUDING HEMORRHAGIC SHOCK

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Abstract
In dogs anesthetized with morphine and Na barbital, pressures were recorded in the aorta, portal vein, and inferior vena cava (near the entry of the hepatic vein) by calibrated optical manometers of adequate frequency and sensitivity. Mean pressure values having dynamic significance were detd. by integrating pressure variations during expiratory pauses. By evaluating directional changes in flow based on a priori considerations or by deducing such changes from estimates of cardiac output in similar previous expts., conclusions could often be drawn from changes of pressure gradients regarding directional changes of resistance in mesenteric tributaries and in portal outflow channels. In addition, relative resistances in the mesenteric and portal vessels could often be inferred by comparing the aortic-portal and portal-caval gradients as a quotient (Rm/Ri) at moments when portal inflow and outflow were obviously the same. The mean pressure in the portal vein averaged around 12 mm. Hg; that in the inferior vena cava about 6 mm. Hg. Hepatic resistance to portal flow is very low; it averages about 1/8th that in the mesenteric tributaries to the portal system. In consequence, large changes in portal flow can occur with only 2 mm. Hg difference in P-V pressure gradients. The reliability of the procedures was tested by using nerve stimulations and drugs with known actions. Thus, analyses indicated that epinephrine in small doses causes a primary dominant increase in mesenteric resistance, followed[long dash]as the pressor effect wanes[long dash]by dominant increase in hepatic resistance, that pitressin causes solely a tremendous augmentation of mesenteric resistance, and that histamine induces both a reduction in mesenteric and an increase in hepatic resistance. Hemorrhagic hypotension was produced at 50 mm. and 30 mm. Hg levels by standard bleeding as previously described. Hemorrhagic shock followed several hrs. after reinfusion of the withdrawn blood (heparinized). Portal pressure after a temporary decline tended to return to or toward control values during the period of 50 mm. Hg hypotension; it declined during the 30 mm. Hg period; increased far above control values after reinfusion and remained definitely above control levels until arterial pressures had fallen essentially to shock levels (50-60 mm. Hg). Analysis of pressure gradients during the periods of hemor-rhagic hypotension and shock strongly suggests that portal flow through the liver is reduced to a greater extent than suggested by changes in systemic and portal pressures; it is reduced in addition by relative increase in portal over mesen-teric resistance.

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