ABSTRACT
Experimental studies have made use of several methods for simulating hyperammonia states. Injections of ammonium salts provide an increase in the ammonia load. Portasystemic shunts have simulated bypass of the liver, and hepatectomy or hepatic necrosis by various toxins and manipulations have simulated clinical hepatic failure. The changes in various tissues accompanying hyperammonia states produced by each of the models will be considered, along with the changes observed in human diseases. Conditions resulting in long-term exposure of the brain to hyperammonia alone produced typical pathologic changes in the astrocytes like those seen in hepatic coma. Ammonia is an important constituent in the synthesis of urea, glutamine, aspartate, or glutamate by the liver. Most of the ammonia presented to the cat liver was metabolized to urea. The intestine accounts for much of the ammonia produced in the body. The kidney produces ammonia from glutamine and transports it into the renal tubule by several processes.
