Ammonia‐induced brain edema and intracranial hypertension in rats after portacaval anastomosis

• Published in: Hepatology (Baltimore, Md.) Md.), 1994-06, Vol.19 (6), p.1437-1444
• Main Authors: Blei, Andres T., Olafsson, Sigurdur, Therrien, Guy, Butterworth, Roger F.
• Format: Article
• Language: English
• Subjects: Ammonia - toxicity; Animals; Biological and medical sciences; Blood Pressure; Body Water; Brain Edema - etiology; Cerebral Cortex - chemistry; Cerebral Cortex - drug effects; Dose-Response Relationship, Drug; Glutamates - metabolism; Glutamine - biosynthesis; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Intracranial Pressure; Male; Medical sciences; Methionine Sulfoximine - pharmacology; Nervous system (semeiology, syndromes); Neurology; Portacaval Shunt, Surgical; Pseudotumor Cerebri - etiology; Rats; Rats, Sprague-Dawley
• ISSN: 0270-9139; 1527-3350
• DOI: 10.1002/hep.1840190619

Brain edema, leading to intracranial hypertension and brain herniation, is a major cause of death in fulminant liver failure. Astrocyte swelling is a prominent neuropathological feature in experimental fulminant liver failure. It has been postulated that the osmotic effects of glutamine, generated in astrocytes from ammonia and glutamate in a reaction catalyzed by glutamine synthetase, could mediate brain swelling. Normal rats and rats that received a portacaval anastomosis were infused with ammonium acetate or a sodium acetate control; brain water in cerebral cortex was measured with the gravimetry method, intracranial pressure by means of a cisterna magna catheter and cortical amino acids using high‐performance liquid chromatography. Although brain edema was detected in both groups receiving ammonia, it was of a greater magnitude in portacaval anastomosis rats (80.94%+0.17% vs. 80.24%+0.09%, p