Salt mixtures for purified-type diets. II. Effect of salts on the Maillard browning reaction.
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The following perfusion media for dissolving bile duct calculi were infused via a cutaneobiliary tube into the biliary tract of 12 mongrel dogs: 4.3% cholate solution, 0.34% chenodeoxycholate solution, Capmul, GMOC (special formulation of Capmul), BA-EDTA and 0.9% saline. Infusion lasted 50 h. Postmortem examination revealed hemorrhagic, partly phlegmonous cholangitis, acute duodenitis, necrosis and abscesses in the liver. The lesions were most pronounced after the cholate solution and with Capmul and GMOC, but were only detected to a slight extent after BA-EDTA and the chenodeoxycholate solution. 0.9% saline had no side effects. The investigations could demonstrate that it is the very irrigation media that today are recommended for treatment of bile duct stones in patients, that cause considerable morphologic side effects. The alternating administration of an EDTA solution with a Capmul preparation may diminish local toxicity of the latter.
The mechanisms of intracellular transport of bile acids from the sinusoidal pole to the canalicular pole of the hepatocyte are poorly understood. There is physiological and autoradiographic evidence for a vesicular pathway. The purpose of this study was to determine the localization of natural bile acids in the liver using antibodies against cholic acid conjugates and ursodeoxycholic acid. An indirect immunoperoxidase technique was used on rat liver sections fixed either with paraformaldehyde (PF) and saponin, a membrane-permeabilizing agent that allows penetration of antibodies into the cell, or with PF alone. Retention of taurocholate in the liver after tissue processing was 26 +/- SD 15% of the bile acid initially present. When sections fixed with PF and saponin were incubated with the antibody against cholic acid conjugates, a granular cytoplasmic staining was observed by light microscopy in all hepatocytes. By electron microscopy, strong electron-dense deposits were observed mostly on vesicles of the Golgi apparatus (GA) and, sometimes, in the smooth endoplasmic reticulum (SER). After taurocholate infusion, the intensity of the reaction increased. When the liver was fixed with PF alone, almost no reaction was visible on light microscopy, but on electron microscopy the label was localized on the hepatocyte plasma membrane, mainly on the bile canalicular domain and to a lesser extent on the sinusoidal domain. With the antibody against ursodeoxycholic acid, no staining was observed in three of four livers, and a slight staining was observed in one. However, after infusion of ursodeoxycholic acid, staining of GA and SER vesicles was observed when the liver was fixed with PF and saponin. With PF alone, the reaction was intense on the canalicular membrane. These results support the view that, within the limits of the method, vesicles from the GA and possibly vesicles of the SER are involved in the intracellular transport of bile acids before canalicular secretion.
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