ArticleIntensive care medicine2007
The effect of iNOS deletion on hepatic gluconeogenesis in hyperdynamic murine septic shock.
Article in Intensive care medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- Metabolic Effects of Sodium Thiosulfate During Resuscitation from Trauma and Hemorrhage in Cigarette-Smoke-Exposed Cystathionine-γ-Lyase Knockout Mice.Biomedicines · 2024Article
- Effects of Sodium Thiosulfate During Resuscitation From Trauma-and-Hemorrhage in Cystathionine-γ-Lyase Knockout Mice With Diabetes Type 1.Frontiers in medicine · 2022Article
- Part II: Minimum Quality Threshold in Preclinical Sepsis Studies (MQTiPSS) for Types of Infections and Organ Dysfunction Endpoints.Shock (Augusta, Ga.) · 2019Review
- Article
- Lipopolysaccharide inhibits hepatic gluconeogenesis in rats: The role of immune cells.Journal of diabetes investigation · 2017Article
- The effects of acute renal denervation on kidney perfusion and metabolism in experimental septic shock.BMC nephrology · 2017Article
- Adrenomedullin binding improves catecholamine responsiveness and kidney function in resuscitated murine septic shock.Intensive care medicine experimental · 2013Article
- A novel antihypoglycemic role of inducible nitric oxide synthase in liver inflammatory response induced by dietary cholesterol and endotoxemia.Antioxidants & redox signaling · 2013Article
- Year in review in Intensive Care Medicine, 2007. I. Experimental studies. Clinical studies: brain injury and neurology, renal failure and endocrinology.Intensive care medicine · 2008Review
- Neuronal nitric oxide synthase deficiency decreases survival in bacterial peritonitis and sepsis.Intensive care medicine · 2007Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the role of the inducible nitric oxide synthase activation-induced excess nitric oxide formation on the rate of hepatic glucose production during fully resuscitated murine septic shock.
designProspective, controlled, randomized animal study.
settingUniversity animal research laboratory. SUBJECTS: Male C57Bl/6 and B6.129P2-Nos2(tm1Lau)/J (iNOS-/-) mice.
interventionsFifteen hours after cecal ligation and puncture, anesthetized, mechanically ventilated and instrumented mice (wild-type controls, n = 13; iNOS-/-, n = 12; wild-type mice receiving 5 mg.kg(-1) i.p. of the selective iNOS inhibitor GW274150 immediately after cecal ligation and puncture, n =8) received continuous i.v. hydroxyethylstarch and norepinephrine to achieve normotensive and hyperdynamic hemodynamics. MEASUREMENTS AND
resultsMeasurements were recorded 18, 21 and 24 h after cecal ligation and puncture. Liver microcirculatory perfusion and capillary hemoglobin O2 saturation (laser Doppler flowmetry and remission spectrophotometry) were well maintained in all groups. Despite significantly lower norepinephrine doses required to achieve the hemodynamic targets, the rate of hepatic glucose production (gas chromatography--mass spectrometry measurements of tissue isotope enrichment during continuous i.v. 1,2,3,4,5,6-13C6-glucose infusion) at 24 h after cecal ligation and puncture was significantly higher in both iNOS-/- and GW274150-treated mice, which was concomitant with a significantly higher hepatic phosphoenolpyruvate carboxykinase activity (spectrophotometry) in these animals.
conclusionsIn normotensive, hyperdynamic septic shock, both pharmacologic and genetic deletion of the inducible nitric oxide synthase allowed maintenance of hepatic glucose production, most likely due to maintained activity of the key regulatory enzyme of gluconeogenesis, phosphoenolpyruvate carboxykinase.
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