The source of internal ammonia and _ general knowledge of the outlet at the time of liver cirrhosis
(1)The source of ammonia: Mainly there are two sources of inner ammonia of human body: What the catabolism of amino acid is produced (such as various deamination ): This is a main source of internal ammonia, are called endogenous ammonia; The ones that are absorbed by the intestine: Ammonia that produce the digestive tract was mainly decomposed, included nitrogen compound to emerge by intestinal bacterium, called other source ammonia. So, when eating protein more, the endogenous and other source increases. (2)The outlet of ammonia: Ammonia is a poisonous material, the content is very low in the normal people's blood, generally less than 0.1mg%. It is obvious ammonia produce constantly, turn into, have toxicity suck nitrogen material while being other rapidly constantly in body. Its main outlet is as follows, Formate the urea: This is a main outlet of ammonia, formate the nonpoisonous urea, pass the kidney, discharge with the urine outside the body. The raw materials formated: Besides ammonia, there is CO2. The route to formate: Urea is synthetic, not it is direct compound that take shape, pass a complicated organization, called ornithine to circulate. This cycle includes three key steps: The first step is that ornithine binds with a molecule ammonia and a molecule carbon dioxide and forms the citrulline first; The second step is that the citrulline reacts, produces arginine with another molecule ammonia again; The third step is that arginine is hydrolyzed by arginase, produced a molecule urea and a molecule ornithine. Ornithine can repeat the first step and react again. Circulate once like this, can impel two molecule ammonia and a molecule CO2 to formate a molecule urea. The synthetic place of urea: Mainly in the liver. Because the above-mentioned every step reflects necessary enzyme, especially arginine is stored in the liver. The urea is mainly discharged from kidney, when the renal function is bad, the urea is discharged and reduced, urea nitrogen (BUN) in the blood The content obviously rises. Check this index, can be regarded as a method of the renal function. Formate glutamine: Internal ammonia is besides using mainly for formating the urea, there is a part that can be bound with glutaminic acid, produce glutamine. Glutamine have toxicity, transport kidney to by blood circulation, hydrolyze in leather cells by glutaninase on the renal tubule, regeneration becomes ammonia and glutaminic acid. Leather cells secrete ammonia ammonia on function, can drain into the urine directly at ammonia namely renal tubule turned into. In addition, ammonia can with sour, in order to become another - amino acid again, this is a synthetic route of non- essential amino acid in body. Ammonia can also formate, include nitrogen compound while being other, the intersection of purine and alkali and the intersection of pyrimidine and alkali,etc.. As stated above, ammonia has very strong toxicity, animal's experiment proves, when ammonia content of blood reaches 5mg%, can cause the death of the rabbit. Ammonia formates an important outlet that the urea is ammonia in the liver, when liver function is severed, urea formate take place obstacle, blood ammonia increase, ammonia enter brain organize and influence the intersection of energy and supersession (if three the intersection of carboxyl and acid circulate) ,Can cause and go into a coma, is called the hepatic coma. On the basis of the source of ammonia and reason of the outlet, if is the hepatic coma caused because ammonia of blood increases, it should reduce the source, increase the outlet to treat the principle. If eat protein (reduce endogenous ammonia) few ,Enema, reduce the excrement and urine and stay in the intestines, kill the intestinal bacterium (reduce other source ammonia) with antibiotic of wide table ; Treating with arginine or glutaminic acid, the former promotes ornithine to circulate and formate the urea, the latter makes glutaminic acid bind with ammonia and turn into glutamine, increase the outlet of ammonia.
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