Effects of sodium nitrite on ischemia-reperfusion injury in the rat kidney.
ABSTRACT Reactive oxygen and nitrogen species play a key role in the pathophysiology of renal ischemia-reperfusion (I/R) injury. Recent studies have shown that nitrite (NO(2)(-)) serves as an endogenous source of nitric oxide (NO), particularly in the presence of hypoxia and acidosis. Nanomolar concentrations of NO(2)(-) reduce injury following I/R in the liver and heart in vivo. The purpose of this study was to evaluate the role of NO(2)(-) in renal I/R injury. Male Sprague-Dawley rats underwent a unilateral nephrectomy followed by 45 min of ischemia of the contralateral kidney or sham surgery under isoflurane anesthesia. Animals received normal saline, sodium NO(2)(-), or sodium nitrate (NO(3)(-); 1.2 nmol/g body wt ip) at 22.5 min after induction of ischemia or 15 min before ischemia. A separate set of animals received saline, NO(2)(-), or NO(3)(-) (0.12, 1.2, or 12 nmol/g body wt iv) 45 min before ischemia. Serum creatinine and blood urea nitrogen were increased following I/R injury but were not significantly different among treatment groups at 24 and 48 h after acute renal injury. Interestingly, NO(3)(-) administration appeared to worsen renal injury. Histological scoring for loss of brush border, tubular necrosis, and red blood cell extravasation showed no significant differences among the treatment groups. The results indicate that, contrary to the protective effects of NO(2)(-) in I/R injury of the liver and heart, NO(2)(-) does not provide protection in renal I/R injury and suggest a unique metabolism of NO(2)(-) in the kidney.
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ABSTRACT: BACKGROUND: Glycine, pyruvate, resveratrol, and nitrite are well-known protective compounds among others in ischemic tissue injury. Here, we compared their effects in acute lipopolysaccharide (LPS)-induced shock in rats to assess whether inhibition of the proinflammatory cytokine response is a prerequisite for their protective actions. MATERIALS AND METHODS: Rats (six or eight per group) were anesthetized, received LPS as an intravenous bolus (2.5 mg/kg), and were observed for 5 h. Glycine, sodium pyruvate, resveratrol, and sodium nitrite were continuously infused starting 30 min before LPS administration. Parameters included histopathologic changes, organ-specific cytokine levels, plasma nitrite and nitrate concentrations, and time courses of biomonitoring parameters, marker enzyme activities, and plasma cytokine concentrations. RESULTS: Glycine, pyruvate, resveratrol, and nitrite enhanced arterial blood pressure after LPS-induced shock. Also, parameters reflecting tissue ischemia were significantly improved and plasma markers of organ injury ameliorated by all substances. Of the plasma cytokine concentrations increased by LPS, some were differently decreased or even further increased by the substances. None of them reduced the elevated plasma nitrite and nitrate concentration. Glycine diminished the increases in tissue cytokine levels organ specifically, pyruvate decreased some cytokine concentrations in all organs, and nitrite significantly affected only a few cytokine concentrations in some organs, whereas the levels of many cytokines were raised by resveratrol. All substances except resveratrol decreased granulocyte infiltrates in the liver. CONCLUSIONS: The present results demonstrate that glycine, pyruvate, resveratrol, and nitrite protect against LPS-induced shock and tissue injury (cell death) in rats and suggest that inhibition of the proinflammatory cytokine response is not mandatory for their protective actions.Journal of Surgical Research 02/2013; · 2.02 Impact Factor
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ABSTRACT: We have been studying the occurrence of low velocity detonations (LVI) in several liquid explosives. A hypothesis based on shock wave interactions and Mach reflections was proposed to explain the initiation and propagation of LVD. Using the card gap test we found general experimental agreement with this hypothesis. However, certain anomalous effects were noted. In addition, we developed a method to study the internal wave structure of a shocked liquid. This technique was applied to a liquid that sustains LVD and to one that does not. A comparison of these liquids shows that the reaction zone in a liquid explosive undergoing LVD is consistent with the Mach zone hypothesis. The anomalous effects noted during gap testing were subjected to a photographic study using a high speed framing camera. The results of this study showed that mechanisms other than that explainable by the Mach zone hypothesis were also responsible for LVD initiation. These were wave reflections from witness plates for high sound speed-high strength confinement and donor air shock initiation for lead (low sound speed-low strength) confinement. We conclude that there appears to be no unique mechanism for LVD and that each mechanism proposed so far explains some of the observations.Symposium (International) on Combustion 01/1969; 12(1):731–742.
Article: Nitrite in Organ Protection.[Show abstract] [Hide abstract]
ABSTRACT: In the last decade, the nitrate-nitrite-nitric oxide (NO) pathway has emerged to therapeutical importance. Modulation of endogenous nitrate and nitrite levels with the subsequent S-nitros(yl)ation of the downstream signalling cascade open the way for novel cytoprotective strategies. In the following we summarize the actual literature and give a short overview on the potential of nitrite in organ protection.British Journal of Pharmacology 07/2013; · 5.07 Impact Factor