{"title":"[Experiences with L-carnitine in the post-stress phase].","authors":"D Balogh, J M Hackl, E Legenstein, H E Musil","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>A prospective randomized double blind investigation was made in 24 multiple injured patients. All patients were treated with a combined parenteral-enteral nutrition during 7 days. A group of 11 patients received as a continuous infusion over 16 h 60 mg/kg BW carnitine daily. Beside carnitine and acetylcarnitine levels in plasma and urine the following parameters were determinated to evaluate the effect of carnitine: for the metabolism of fatty acids: triglycerides, free fatty acids (FFA), alpha-hydroxy-butyrate for the metabolism of carbohydrates: glucose, insulin and lactate in plasma. Finally for amino acid metabolism: urea, creatinine, cholinesterase and kolloid osmotic pressure in plasma as well as ureanitrogen and alpha-aminonitrogen excretion in urine. In the patients receiving carnitine especially acetyl-carnitine in plasma and acetyl-carnitine excretion in urine increased, proving that the administered carnitine can pass through the mitochondrial membrane. In these patients the plasma level of FFA was markedly lower than in the group without carnitine. Simultaneously the level of the alpha-hydroxybutyrate was elevated, equivalent to an increased oxydation of fatty acids. There was no difference between the two groups in the metabolism of carbohydrates. Administration of carnitine caused a slight increase of the production of urea (PU), catabolism could not be reduced. The excretion of alpha-aminonitrogen in urine augmented after carnitine infusion. Carnitine is an AA itself and so the amount of excreted alpha-amino nitrogen will increase; additionally the reabsorption of AA in the proximal renal tubulus may be inhibited by carnitine.</p>","PeriodicalId":75931,"journal":{"name":"Infusionstherapie und klinische Ernahrung","volume":"13 5","pages":"204-8"},"PeriodicalIF":0.0000,"publicationDate":"1986-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infusionstherapie und klinische Ernahrung","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
A prospective randomized double blind investigation was made in 24 multiple injured patients. All patients were treated with a combined parenteral-enteral nutrition during 7 days. A group of 11 patients received as a continuous infusion over 16 h 60 mg/kg BW carnitine daily. Beside carnitine and acetylcarnitine levels in plasma and urine the following parameters were determinated to evaluate the effect of carnitine: for the metabolism of fatty acids: triglycerides, free fatty acids (FFA), alpha-hydroxy-butyrate for the metabolism of carbohydrates: glucose, insulin and lactate in plasma. Finally for amino acid metabolism: urea, creatinine, cholinesterase and kolloid osmotic pressure in plasma as well as ureanitrogen and alpha-aminonitrogen excretion in urine. In the patients receiving carnitine especially acetyl-carnitine in plasma and acetyl-carnitine excretion in urine increased, proving that the administered carnitine can pass through the mitochondrial membrane. In these patients the plasma level of FFA was markedly lower than in the group without carnitine. Simultaneously the level of the alpha-hydroxybutyrate was elevated, equivalent to an increased oxydation of fatty acids. There was no difference between the two groups in the metabolism of carbohydrates. Administration of carnitine caused a slight increase of the production of urea (PU), catabolism could not be reduced. The excretion of alpha-aminonitrogen in urine augmented after carnitine infusion. Carnitine is an AA itself and so the amount of excreted alpha-amino nitrogen will increase; additionally the reabsorption of AA in the proximal renal tubulus may be inhibited by carnitine.