Blood Oxygen Transport in Rats under Hypothermia Combined with Modification of the l-Arginine–NO Pathway

Зинчук, В. В.; Dorokhina, L.V.

doi:10.1006/niox.2001.0377

Cited by 13 publications

(11 citation statements)

References 24 publications

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“…In the presence of RBCs and nitrite, a further inhibition of respiration was observed. Importantly, the onset of inhibition occurred at oxygen tensions lower than the rat RBC P 50 (35-40 mmHg 33,34 ), consistent with the data presented in Figure 3. For personal use only.…”

Section: Nitrite-dependent Hypoxic Vasodilation By Rbcs Is No Dependentsupporting

confidence: 87%

Hypoxia, red blood cells, and nitrite regulate NO-dependent hypoxic vasodilation

Crawford

Isbell

Huang

et al. 2006

Blood

446

467

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Local vasodilation in response to hypoxia is a fundamental physiologic response ensuring oxygen delivery to tissues under metabolic stress. Recent studies identify a role for the red blood cell (RBC), with hemoglobin the hypoxic sensor. Herein, we investigate the mechanisms regulating this process and explore the relative roles of adenosine triphosphate, S-nitrosohemoglobin, and nitrite as effectors. We provide evidence that hypoxic RBCs mediate vasodilation by reducing nitrite to nitric oxide (NO) and ATP release. NO dependence for nitrite-mediated vasodilation was evidenced by NO gas formation, stimulation of cGMP production, and inhibition of mitochondrial respiration in a process sensitive to the NO scavenger C-PTIO. The nitrite reductase activity of hemoglobin is modulated by heme deoxygenation and heme redox potential, with maximal activity observed at 50% hemoglobin oxygenation (P 50 ). Concomitantly, vasodilation is initiated at the P 50 , suggesting that oxygen sensing by hemoglobin is mechanistically linked to nitrite reduction and stimulation of vasodilation. Mutation of the conserved ␤93cys residue decreases the heme redox potential (ie, decreases E 1/2 ), an effect that increases nitrite reductase activity and vasodilation at any given hemoglobin saturation. These data support a function for RBC hemoglobin as an allosterically and redox-regulated nitrite reductase whose "enzyme activity" couples hypoxia to increased NO-dependent blood flow. (Blood. 2006;107:566-574)

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Section: Nitrite-dependent Hypoxic Vasodilation By Rbcs Is No Dependentsupporting

confidence: 87%

Hypoxia, red blood cells, and nitrite regulate NO-dependent hypoxic vasodilation

Crawford

Isbell

Huang

et al. 2006

Blood

446

467

View full text Add to dashboard Cite

show abstract

“…NO has function of a radical-trapping compound and modifies O 2 -binding properties of the blood. It is necessary to take into account that the pathogenesis of hepatic reperfusion injury is mediated by the O 2 -dependent mechanism [10].…”

Section: Resultsmentioning

confidence: 99%

“…Liver ischemia/reperfusion was induced in group 1 rabbits (n=10). Group 2 animals (n=8) with hepatic ischemia/reperfusion received intravenous infusion of NG (1.5 µg/kg) 5 min before the reperfusion period [10]. The total concentration of nitrites and nitrates in blood plasma was measured using Griess reagent [6].…”

Section: Methodsmentioning

confidence: 99%

Effect of nitroglycerine on some parameters of the prooxidant-antioxidant balance and functional state of the liver during ischemia/reperfusion

Ходосовский¹,

Зинчук²

2006

Bull Exp Biol Med

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The effect of nitroglycerine on some parameters of the prooxidant-antioxidant balance and functional state of the liver under conditions of ischemia/reperfusion was studied on rabbits. Hepatic ischemia/reperfusion was accompanied by accumulation of LPO products, depletion of the antioxidant defense system, and increase in blood transaminase activity. Nitroglycerine infusion before the reperfusion period decreased the concentration of LPO products, increased activity of the antioxidant system, and improved liver function.

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Section: Methodsmentioning

confidence: 97%

“…Tissue samples were taken from the heart, lungs, liver, kidneys, and muscles 180 min after LPS administration. The doses and route of treatment with the test preparations provided appreciable correction of NO synthesis in the organism [6,9].The concentration of conjugated dienes (CD) was estimated by measuring the amount of conjugated diene structures in hydroperoxides of polyunsaturated fatty acids [7]. The concentration of Schiff bases was determined by fluorescence of a chloroform extract at excitation and emission wavelengths of 344 and 440 nm, respectively.…”

mentioning

confidence: 99%

Prooxidant-antioxidant state of the organism during oxidative stress and correction of the L-arginine-NO system

Glebov

Зинчук

2006

Bull Exp Biol Med

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The prooxidant-antioxidant balance in rats with oxidative stress was studied during correction of the L-arginine-NO system. Oxidative stress was induced by intravenous injection of E. coli lipopolysaccharide. Under conditions of oxidative stress the prooxidant-antioxidant imbalance was least pronounced during selective correction of the L-arginine-NO system. L-Arginine and nonselective NO synthase inhibitor had little protective effect.

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Blood Oxygen Transport in Rats under Hypothermia Combined with Modification of the l-Arginine–NO Pathway

Cited by 13 publications

References 24 publications

Hypoxia, red blood cells, and nitrite regulate NO-dependent hypoxic vasodilation

Hypoxia, red blood cells, and nitrite regulate NO-dependent hypoxic vasodilation

Effect of nitroglycerine on some parameters of the prooxidant-antioxidant balance and functional state of the liver during ischemia/reperfusion

Prooxidant-antioxidant state of the organism during oxidative stress and correction of the L-arginine-NO system

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