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Between March 1976 and December 1992, 137 (57 per cent) of 239 patients with pancreatic duct cell cancer underwent resection; 79 (58 per cent) of the 137 had combined resection of the pancreas and portal vein. Sixty-three of the 79 patients underwent resection of the portal vein alone; six died (mortality rate 10 per cent). The mortality rate was the same as that in 58 patients with no resection of the portal vein. In the remaining 16 patients adjacent arteries were also resected, with seven deaths. Of patients with resection of the portal vein alone who underwent curative resection, four survived more than 5 years, accounting for nearly half of the nine 5-year survivors. Combined resection of the pancreas and portal vein is associated with both an increased resectability rate and improved long-term survival.

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The pressure-natriuresis relationships in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were characterized with or without intrarenal renin-angiotensin system (RAS) blockade. The pressure-natriuresis relationship in SHR was shifted toward higher pressure in comparison to WKY. The inhibition of intrarenal RAS by MK-422 (0.3 ug/kg/min) in SHR enabled to excrete more sodium at the same pressure (P less than 0.05), whereas no significant changes were observed in WKY. In SHR, during administration of Thi5,8, D-Phe7-bradykinin (50 micrograms/kg/min), the natriuretic responses to MK-422 were maintained. Intrarenal infusion of Sar1, Ile8-angiotensin (70 ng/kg/min) into SHR increased sodium excretion accompanied by an increase in renal plasma flow. Intrarenally administered angiotensin I (10 ng/kg/min) into WKY showed antinatriuretic effects with minimal changes in renal hemodynamics. These results indicate that alteration of intrarenal RAS in SHR might contribute to reset the pressure-natriuresis relationship.

No abstract