Artificial Liver Support by Hans Popper (auth.), Professor Dr. Gorig Brunner, Professor

By Hans Popper (auth.), Professor Dr. Gorig Brunner, Professor Dr. Friedrich Werner Schmidt (eds.)

The regenerative capability of the liver telephone is sort of limitless. as a result after acute liver harm, be it viral, poisonous, hypoxic, or surgical in starting place, restitutio advert integrum is the standard final result. In types of liver ailment, in spite of the fact that, this isn't the case: in fulmi­ nant hepatic failure, liver regeneration usually isn't really quickly adequate to maintain the organism alive; in end-stage cirrhosis, regeneration is dis­ turbed by way of a hypertrophic structure of fibrotic tissue. For those severe sorts of liver sickness and for severe events prior to and after liver surgical procedure, synthetic liver aid is required. This e-book includes the newest leads to this region of study pre­ sented via scientists from allover the area at a world symposium held in Celle, Germany, June 2-4, 1980. fascinating new equipment like non-stop membrane plasma sepa­ ration and liver telephone transplantation into the spleen were de­ veloped. The older equipment of hemoperfusion and dialysis were enhanced. Enzymological tools and liver transplantation have made reliable development. we are hoping that this quantity may also help the clinician in his decision-making and stimulate inventive new re­ look for the good thing about our liver patients.

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10 mmol/kg phenol was needed to produce coma in the rabbit. '" "0 E E 5 4 3 2 Fig. 2. Molar coma doses in the rabbit for phenol, hexanoate and ammonium acetate .. Ammonia" .. Fattyacid" Phenol Synergism While in the rabbit synergism between ammonium acetate and hexanoate was only minor, a significant synergism could be observed between phenol and hexanoate and between phenol and ammonium acetate. 02). 1 O)(Fig. 3). Discussion The results clearly demonstrate that phenols cannot be overlooked as toxins in severe hepatic disease.

A prime example is phenol, which can be glucuronidated or sulphated. The precise reason for the necessity or desirability of this duplicity, or in some cases, multiplicity of metabolic pathways is not clear, although the different locations of the enzyme systems may be essential to provide comprehensive protection throughout the intracellular space. Intoxication can be viewed as a failure in the detoxification processes, and can arise from two metabolic limitations. The most obvious weakness in the system may come about from the kinetic inferiority of the detoxification mechanism with respect to the rate of toxic action of the substance.

Hibition studies was carried out by the method described by Stott (1968). Glucuronidation of phenols in serum was undertaken as previously described (Brunner et al. 1979). Enzyme determination in brain and liver tissue homogenates was carried out by standard methods (Bergmeyer 1970) and mitochondrial respiration was determined as described by Hagihara (1961). From the large number of phenolic subtances found by this method in the serum of liver disease patients, we chose phenol itself as a substance which cannot easily be excreted but has to be conjugated for excretion.

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