To determine the relationship of splanchnic blood flow and portal venous resistance to elevated portal pressure, in situ perfusion of the splanchnic circuit was carried out in 12 freshly killed dogs at varying perfusion rates and degrees of acute and chronic chronic portal vein constriction. In six normal dogs before being killed, portal pressure averaged 8.8 ± 1.2 mmHg and portal flow 658 ± 81 ml/min. In the absence of portal vein constriction, increasing splanchnic perfusion to 1800 ml/min, minimally raised portal pressure (12.8 ± 1.5 mmHg). With progressive acute constriction of the portal vein, however, comparable perfusion rates lead to progressively higher portal pressure levels and with >90% constriction, portal pressure was >30 mm Hg with minimal elevation in splanchnic flow rate. In six other dogs before being killed but alive nine weeks after placement of an ameroid constrictor on the portal vein, portal pressure averaged 13.6 ± 1.4 mmHg or slightly higher than in normal dogs (P>0.02). Mesenteric venography and necropsy findings uniformly demonstrated 90% occlusion of the portal vein with extensive portasystemic collateralization. With increased perfusion of the splanchnic bed, portal pressure rose rapidly to 35 mmHg with a flow rate of 1800 ml/min. These data suggest that, in disorders where resistance to transhepatic portal flow is marked, a small increment in splanchnic blood flow, which normally exerts little or no influence on portal pressure, promotes profound portal hypertension and may account for spontaneous 'rupture' of oesophageal varices. On the other hand, where resistance to transhepatic portal flow is mild but splanchnic blood flow is markedly hyperdynamic, reducing inflow may be sufficient to ameliorate extreme portal hypertension and its sequelae.
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