Abstract
Ammonia intoxication, a complication of advanced liver disease, is believed responsible for part of the clinical syndrome of hepatic coma. When massive hemorrhage occurs from gastroesophageal varices, intestinal microorganisms break down blood proteins to ammonia. Portal-systemic venous collateral channels permit portal blood with high ammonia content to bypass the liver and enter the systemic circulation, thereby avoiding conversion to urea. Elevated levels of blood ammonia in the systemic circulation act on the central nervous system, and are thought to contribute to confusion, irritability and stupor.
Ammonia intoxication may be produced experimentally in dogs by oral administration of blood or protein substances to Eck-fistula animals. Certain cation exchange resins are known to have an affinity for ammonium ions. Oral administration of such resins following administration of the challenging dose of blood would place the resin at the site of ammonia formation within the intestines. This should permit the resin to act with maximal efficiency, and prevent intestinal absorption of ammonia.
This report presents our laboratory experience with a sodium cycle sulphonic polystyrene resin,‡ which exchanges sodium ions for ammonium and potassium ions. It is available in particles of small size (5-10 μ diameter), thereby providing large surface area for interaction and exchange.
These experiments tested the ability of this cation exchange resin to prevent development of ammonia intoxication in Eck fistula dogs given a challenging dose of blood by gastric tube.
Methods. Eight healthy, mongrel dogs weighing 9 to 15 kg were selected and end-to-side portacaval shunts were constructed under intravenous pentobarbital sodium anesthesia (30 mg/kg). The dogs were allowed 5 to 7 days to recover from the operation before the specific experiments were performed.
The first experiment consisted of obtaining baseline ammonia response curves to a standard dose of blood.
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