citrulline/hypoxia

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Prolonged hypoxia augments L-citrulline transport by system A in the newborn piglet pulmonary circulation.

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OBJECTIVE Pulmonary arterial endothelial cells (PAECs) express the enzymes needed for generation of l-arginine from intracellular l-citrulline but do not express the enzymes needed for de novo l-citrulline synthesis. Hence, l-citrulline levels in PAECs are dependent on l-citrulline transport. Once

Nitric oxide (no), citrulline - no cycle enzymes, glutamine synthetase and oxidative stress in anoxia (hypobaric hypoxia) and reperfusion in rat brain.

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Nitric oxide is postulated to be involved in the pathophysiology of neurological disorders due to hypoxia/ anoxia in brain due to increased release of glutamate and activation of N-methyl-D-aspartate receptors. Reactive oxygen species have been implicated in pathophysiology of many neurological

L-Citrulline ameliorates chronic hypoxia-induced pulmonary hypertension in newborn piglets.

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Newborn piglets develop pulmonary hypertension and have diminished pulmonary vascular nitric oxide (NO) production when exposed to chronic hypoxia. NO is produced by endothelial NO synthase (eNOS) in the pulmonary vascular endothelium using l-arginine as a substrate and producing l-citrulline as a

Combined L-citrulline and tetrahydrobiopterin therapy improves NO signaling and ameliorates chronic hypoxia-induced pulmonary hypertension in newborn pigs.

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Newborn pigs with chronic hypoxia-induced pulmonary hypertension (PH) have evidence of eNOS uncoupling. In this model, we showed that therapies that promote eNOS coupling, either tetrahydrobiopterin (BH₄), a NOS co-factor, or L-citrulline, a NO-L-arginine precursor, inhibit PH. We wanted

Arginine and citrulline protect intestinal cell monolayer tight junctions from hypoxia-induced injury in piglets.

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BACKGROUND Arginine (Arg) is deficient in the serum of the preterm neonate and is lower in those developing intestinal ischemia. We investigated whether Arg or its precursor, citrulline (Cit), protects intestinal tight junctions (TJs) from hypoxia (HX) and determined whether inducible nitric oxide

Rescue Treatment with L-Citrulline Inhibits Hypoxia-Induced Pulmonary Hypertension in Newborn Pigs.

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Infants with cardiopulmonary disorders associated with hypoxia develop pulmonary hypertension. We previously showed that initiation of oral L-citrulline before and continued throughout hypoxic exposure improves nitric oxide (NO) production and ameliorates pulmonary hypertension in newborn piglets.

Hypoxia inhibits L-arginine synthesis from L-citrulline in porcine pulmonary artery endothelial cells.

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Both non-arginine-depleted and arginine-depleted pulmonary artery endothelial cells (PAEC) actively convert citrulline into arginine. Exposure to hypoxia for 4-24 h inhibited arginine synthesis from citrulline in intact cells and in cell homogenates. The conversion of L-citrulline to

Prolonged mild fetal hypoxia up-regulates type I nitric oxide synthase expression in discrete areas of the late-gestation fetal sheep brain.

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OBJECTIVE Our purpose was to study the effects of prolonged mild hypoxemia on type I nitric oxide synthase (NOS) messenger RNA, protein, and enzymatic activity in the fetal sheep brain. METHODS Pregnant sheep were randomly allocated to receive maternal nitrogen (n = 8) or compressed air (controls, n

Nitric oxide kinetics during hypoxia in proximal tubules: effects of acidosis and glycine.

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In the present study, we directly monitored nitric oxide (NO) with an amperometric NO-sensor in suspensions of rat proximal tubules. Hypoxia-stimulated NO generation was characterized by an initial rise and a subsequent sustained increase which preceded cell membrane damage as assessed by lactic

Use of a microbial model for the determination of drug effects on cell metabolism and energetics: study of citrulline-malate.

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Euglena gracilis can be used as a microbial model to study the effect of drugs on lactate metabolism and gluconeogenetic synthesis. The cell growth and metabolism have been characterized in a 33 mM lactate medium, non-supplemented or supplemented by dl-malate or by l-citrulline alone or by the

L-Citrulline, but not L-arginine, prevents diabetes mellitus-induced glomerular hyperfiltration and proteinuria in rat.

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Diabetes mellitus–induced oxidative stress causes increased renal oxygen consumption and intrarenal tissue hypoxia. Nitric oxide is an important determinant of renal oxygen consumption and electrolyte transport efficiency. The present study investigates whether l-arginine or l-citrulline to promote

Profile of plasma amino Acid levels in rats exposed to acute hypoxic hypoxia.

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The effect of acute hypoxic hypoxia on the profile of plasma amino acids in rats was studied and compared to that resulting from acute liver injury induced by giving carbon tetrachloride. In hypoxic rats exposed to 45% air in N(2) for 5 h, the concentrations of branched chain amino acids, including

Chronic hypoxia inhibits contraction of fetal arteries by increased endothelium-derived nitric oxide and prostaglandin synthesis.

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OBJECTIVE Chronic hypoxia causes redistribution of fetal cardiac output by mechanisms poorly understood. We tested the hypothesis that chronic hypoxia alters vascular reactivity of arteries from near-term fetal guinea pigs. METHODS Pregnant guinea pigs (50 days, term = 65 days) were exposed to

L-citrulline treatment alters the structure of the pulmonary circulation in hypoxic newborn pigs

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Background: Dysregulated nitric oxide (NO) signaling contributes to chronic hypoxia (CH)-induced pulmonary hypertension (PH). NO signaling is improved and pulmonary vascular resistance (PVR) is reduced in CH piglets treated with the

Role of nitric oxide in hypoxia-induced colonic dysfunction in the neonatal rat.

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In addition to being an important mediator in the regulation of intestinal integrity, nitric oxide (NO), when produced in large quantities by the inducible isoform of NO synthase, can also be cytotoxic. The aim of this study was to examine the role of NO in hypoxia-induced colonic injury in neonatal

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