.4 mm Hg increase from basal), which declined gradually to a steady state pressure of 13-3-15*1 mm Hg (4-0-5.0 mm Hg increase). There was no significant difference between pressure increases produced by microspheres of differing sizes. It is concluded that portal hypertension can be produced acutely by blocking portal radicles with microspheres. The maximum pressure achieved, however, is substantially less than that obtained by total portal vein occlusion (mean: 57 6 mm Hg). This suggests the existence of functional intrahepatic portal systemic shunts not previously described in the normal liver.
Diversion of portal blood away from the liver can be accomplished in the rat by two straightforward surgical procedures: subcutaneous transposition of the spleen followed later by portal vein ligation. This experimental model has great potential value in the study of liver cell transplants, porto-systemic shunts and hepatic porto-privation. Contrast medium radiology has been used to clarify and define the model further. Splenography, achieved by direct percutaneous puncture, demonstrated the developing spleno-subcutaneous vessels. Collaterals are seen as early as 3 days and appear extensive by 21 days after transposition. Almost all emanate from the convex outer surface of the spleen and course cranially and caudally in the subcutaneous tissues to drain into the subclavian and iliac veins. The appearance of these collaterals correlates well with survival after portal vein occlusion subsequent to splenic transposition. Direct portography demonstrates that, following portal vein ligation, contrast medium is diverted away from the liver into the splenic veins, through and around the spleen, before draining into the systemic circulation through spleno-subcutaneous collaterals. These radiological studies have demonstrated the changed circulatory pathways of this model of portal diversion and have confirmed that it is the splenic veins and the spleno-subcutaneous collaterals which are fundamental to its successful outcome.
Diversion of portal blood away from the liver has been accomplished, in the rat, by transposition of the scarified spleen, followed by later portal vein ligation. The resulting dynamic portal pressure changes have been measured. In 7 control (sham-transposed) rats, portal ligation produced a 7-fold sustained and fatal pressure increase. In 7 previously transposed rats, the increase was only 3-fold and was followed by a slow fall to a lower plateau pressure, with 100% 3 h survival; clamping the splenic pedicle converted the pressure trace to that of controls. These results support the view that splenosubcutaneous collaterals, stimulated by scarification, are essential for successful portal diversion.
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