Glutathione and Nitric Oxide Concentrations in Glutamine-Infused Rabbits with Intestinal Ischaemia/Reperfusion

Başoğlu, Mahmut; Yildirgan, İlhan; Akçay, Fatih; Kızıltunç, Ahmet; Kavak, İbrahim; Ören, Durkaya

doi:10.1515/cclm.1997.35.6.415

Cited by 14 publications

(10 citation statements)

References 26 publications

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“…This could point to a reduction in the rate of muscle glutamine de novo synthesis. However, if, similar to other studies, glutamine efflux from muscle would have been increased 48 hours after surgery, then the unchanged plasma glutamine Ra observed in this most recent study could only be explained by the fact that the increased release from muscle is offset by a decreased release from sources other than muscle such as liver. We previously showed that in pigs the liver switches from glutamine production in the preoperative setting to glutamine consumption after operation.24 Changes in the flow of glutamine between organs apparently may occur without the whole-body plasma glutamine Ra being altered.…”

Section: Kinetics Of Glutaminesupporting

confidence: 82%

Glutamine: The Pivot of Our Nitrogen Economy?

Acker

Meyenfeldt

Hulst

et al. 1999

J Parenter Enteral Nutr

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Glutamine serves as a shuttle of useful nontoxic nitrogen, supplying nitrogen from glutamine-producing (eg, muscle) to glutamine-consuming tissues. True production rates of glutamine are difficult to measure, but probably are less than 60 to 100 g/d for a 70-kg man. During catabolic stress increased amounts of glutamine are released from muscle, consisting of protein derived glutamine, newly synthesized glutamine, and glutamine losses from the intramuscular free pool. The large and rapid losses of free muscle glutamine are difficult to restore, presumably as a result of disturbances in the Na+ electrochemical gradient across the cell membrane. Whereas increased amounts of glutamine are released from muscle, glutamine consumption by the immune system (liver, spleen) also is enhanced. Thus, during catabolic stress changes occur in the flow of glutamine between organs. These changes are not necessarily reflected by alterations in the whole-body appearance rate of glutamine. In contrast with the gut, where glutamine is taken up in a concentration dependent manner, the immune system actively takes up glutamine despite decreased plasma concentrations. Supplementation with glutamine influences uptake by both the gut and the immune system, as evidenced by increased mucosal glutamine concentrations and gut glutathione production. There is evidence suggesting that this improves gut barrier function. Although the benefit of glutamine supplementation is most evident from experimental studies, clinical studies on the effect of glutamine do exist and suggest that glutamine supplementation has beneficial effects with regard to patient outcome.

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Section: Kinetics Of Glutaminesupporting

confidence: 82%

Glutamine: The Pivot of Our Nitrogen Economy?

Acker

Meyenfeldt

Hulst

et al. 1999

J Parenter Enteral Nutr

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“…Indeed, Cit-Arg cycling was upregulated in endotoxemic rats (16), supporting regulation of NO production by Gln. On the other hand, it has also been suggested that Gln supplementation inhibits NO production (1,14). In our study, Gln net consumption in the gut appeared to have a stimulating effect on NO production.…”

Section: Discussionsupporting

confidence: 56%

NOS2 deficiency increases intestinal metabolism both in nonstimulated and endotoxemic mice

Vissers¹,

Hallemeesch²,

Soeters³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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Animal studies have suggested that nitric oxide (NO) synthases (NOS) play a role in the regulation of protein metabolism in endotoxemia. We therefore investigated the role of inducible NOS (NOS2) on intestinal protein and neuronal NOS (NOS1) and endothelial NOS (NOS3) on amino acid metabolism. Three groups of mice were studied: 1) wild-type (WT), 2) NOS2 knockout (NOS2-KO), and 3) NOS2-KO + N(omega)-nitro-l-arginine methyl ester (NOS2-KO + l-NAME), both in nonstimulated and LPS-treated conditions. By infusion of the stable isotopes l-[phenyl-(2)H(5)]Phe, l-[phenyl-(2)H(2)]Tyr, l-[guanidino-(15)N(2)]Arg, and l-[ureido-(13)C; (2)H(2)]citrulline (Cit), intestinal protein, amino acid, and Arg/NO metabolism were studied on the whole body level and across intestine. In nonstimulated situations, NOS2 deficiency increased whole body protein turnover and intestinal Gln uptake and Cit production. In NOS2-KO + l-NAME, the above-mentioned changes were reversed. After LPS in WT, whole body NO and Cit production increased. In contrast to this, LPS decreased net intestinal Gln uptake, whole body NO, and Cit production in NOS2-KO mice. Treatment of NOS2-KO + l-NAME with LPS was lethal in eight of eleven mice (73%). The surviving mice in this group showed a major drop in intestinal protein breakdown and synthesis to almost zero. Thus both in baseline conditions and during endotoxemia, the absence of NOS2 upregulated NOS1 and/or NOS3, which increased intestinal metabolism. The drop in intestinal protein metabolism in the endotoxemic NOS2-KO + l-NAME group might play a role in mortality in that group.

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“…Ischaemia–reperfusion (I/R) injury is the underlying cause of morbidity and mortality in several diseases, including stroke, myocardial infarction and acute renal tubular necrosis 1 . Ischaemia causes a depletion of ATP and an accumulation of toxic metabolites, whereas the subsequent reperfusion injury stimulates the production of reactive oxygen intermediates 2 . The pathogenic mechanisms that underlie coronary atherosclerotic heart disease are undefined at present 3…”

Section: Introductionmentioning

confidence: 99%

Increased expression of calcium‐sensing receptors induced by ox‐LDL amplifies apoptosis of cardiomyocytes during simulated ischaemia–reperfusion

Guo

Li²,

Zhang

et al. 2010

Clin Exp Pharma Physio

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1. Acute myocardial infarction (AMI) is strongly associated with atherosclerosis, and is responsible for significant morbidity and mortality worldwide. The pathogenic mechanisms that underlie atherosclerosis and AMI are undefined at present. The calcium-sensing receptor (CaSR) is a member of the superfamily of G-protein coupled receptors. It has been demonstrated previously that the expression of CaSR is increased in atherosclerotic cardiac tissue of rats. It has also been suggested that CaSR has a crucial role in cardiac ischaemia-reperfusion injury, apoptosis and hypertrophy. However, it remains to be determined whether an increase in the expression of CaSR influences the sensitivity of cardiomyocytes to AMI. 2. The present study used cultured ventricular cardiomyocytes from neonatal rats to investigate the effect of oxidized low-density lipoprotein (ox-LDL), ischaemia-reperfusion, GdCl(3) (an agonist of CaSR) and NPS-2390 (an antagonist of CaSR) on the expression of CaSR. The amount of apoptosis, alterations in the morphology of the cells, the intracellular calcium concentration ([Ca(2+)](i)) and components of critical mitochondrial pathways were also analysed. 3. Cardiomyocytes treated with ox-LDL showed upregulated expression of CaSR, cytochrome c (cyt-c), Bax and activated caspase 3 (17 kD) and downregulated expression of Bcl-2, as well as elevated [Ca(2+)](i) and apoptosis. Application of GdCl(3) augmented these effects, and NPS-2390 decreased the expression of CaSR and reduced apoptosis. 4. In conclusion, ox-LDL was found to increase the expression of CaSR in a manner that was dependent on time and dose. It also augmented apoptosis during simulated ischaemia-reperfusion in cultured ventricular cardiomyocytes from neonatal rats.

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Glutathione and Nitric Oxide Concentrations in Glutamine-Infused Rabbits with Intestinal Ischaemia/Reperfusion

Cited by 14 publications

References 26 publications

Glutamine: The Pivot of Our Nitrogen Economy?

Glutamine: The Pivot of Our Nitrogen Economy?

NOS2 deficiency increases intestinal metabolism both in nonstimulated and endotoxemic mice

Increased expression of calcium‐sensing receptors induced by ox‐LDL amplifies apoptosis of cardiomyocytes during simulated ischaemia–reperfusion

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