Epr analysis reveals three tissues responding to endotoxin by increased formation of reactive oxygen and nitrogen species

Kozlov, Andrey V.; Szalay, L.; Umar, F.; Fink, Bruno; Kropik, K.; Nohl, Hans; Redl, Heinz; Bahrami, Soheyl

doi:10.1016/s0891-5849(03)00179-5

Cited by 68 publications

(40 citation statements)

References 28 publications

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“…The likelihood of NO responses from different organs after various stimuli is debated in the literature (Suzuki et al, 1998;Dambrova et al, 2003;Kozlov et al, 2003;Plonka et al, 2003;Hayashi et al, 2005). In contrast to our results, Kozlov et al (2003) reported that in septic shock the brain and kidneys do not always respond.…”

Section: Discussioncontrasting

confidence: 85%

“…Nitric oxide has been detected previously in normal animals (Dambrova et al, 2003;Kozlov et al, 2003) and may represent NO production from constitutive NOS isoforms or non-enzymatic NO production (Berliner and Fujii, 2004) but could also be from pre-existing disease. In contrast, iNOS activity stimulated by endotoxin exposure typically produces significant (micromolar) concentrations of NO.…”

Section: Discussionmentioning

confidence: 89%

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Single oral inoculation with Escherichia coli (ATCC 25922) stimulates generalised production of nitric oxide in mice

Nemec

Pavlica

Crossley

et al. 2009

Acta Veterinaria Hungarica

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Nitric oxide (NO) production was investigated in the lungs, thoracic aorta, heart, liver, spleen, kidneys and brain of mice inoculated orally with Escherichia coli ATCC 25922. Detection of NO was performed by electron paramagnetic resonance (EPR) using diethyldithiocarbamate (DETC) spin trap. Nitric oxide synthase (NOS) inhibitors [nonselective: L-NAME and inducible NOS (iNOS) selective: 1400W] were used to determine the source of NO. Spin-trap only and untreated mice were included as controls. Within 2.5 hours (h) of a single oral inoculation with E. coli half of the animals had increased NO levels in all investigated organs. Thereafter the signals dropped before increasing again to reach maximal median values by 25 h in all organs of all inoculated mice. The most intense response occurred in livers, followed by aorta and lungs. Early (2.5 h) inhibition of the signal was achieved using both NOS inhibitors. L-NAME was also effective at 25 h, while 1400W-treated mice had increased NO levels beyond 7 h. The generalised increase in NO production in the short and longer term indicates a host response to E. coli administered by the oral route of infection.

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Section: Discussioncontrasting

confidence: 85%

Section: Discussionmentioning

confidence: 89%

Single oral inoculation with Escherichia coli (ATCC 25922) stimulates generalised production of nitric oxide in mice

Nemec

Pavlica

Crossley

et al. 2009

Acta Veterinaria Hungarica

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“…In addition, LPS-induced iNOS/NO production may favor excessive generation of ROS and nitrogen species in liver, heart, lung, and blood. In contrast, ROS levels seem to be unchanged in rat kidney 4 h after LPS injection (37). Endothelium-dependent vasorelaxation was tested with acetylcholine in preconstricted isolated vessels.…”

Section: Discussionmentioning

confidence: 99%

Maintenance of Renal Vascular Reactivity Contributes to Acute Renal Failure during Endotoxemic Shock

Boffa

Arendshorst

2005

Journal of the American Society of Nephrology

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Septic shock is characterized by hypotension and decreased systemic vascular resistance and impaired vascular reactivity. Renal vasoconstriction markedly contrasts with sepsis-induced generalized systemic vasodilation, which is strongly dependent on nitric oxide. Whether maintained renal vascular reactivity to vasoconstrictors contributes to the decrease in renal blood flow (RBF) and GFR observed during LPS-induced sepsis was tested by assessment of the acute effects of pressor agents on mean arterial pressure (MAP) and renal hemodynamics in endotoxemic and control mice. LPS-injected mice displayed lower MAP, RBF, and GFR than controls (P < 0.001). Despite a lower MAP, basal renal vascular resistance (RVR) was higher during endotoxemia (P < 0.02). Angiotensin II infusion produced a weaker MAP response in septic mice (24 versus 37%; P < 0.005), suggesting impaired vasoconstriction and hyporeactivity. A similar MAP increase was observed between groups during norepinephrine (NE) infusion. The MAP increase to nitric oxide synthase inhibition by N G -nitro-L-arginine methyl ester (L-NAME) was much greater in LPS-treated mice (41 versus 15%, P ‫؍‬ 0.01), indicating a strong influence of nitric oxide in sepsis. In contrast, the RBF and RVR responses to angiotensin II, NE, or L-NAME were similar in both groups. Moreover, vasopressin produced greater changes in MAP, RBF, and RVR in septic mice than in controls. Among the vasoconstrictor challenges, only NE ameliorated the decrease in GFR 14 h after LPS injection. The in vivo results demonstrate that the renal microvasculature displays a normal or enhanced reactivity to constrictor agents as compared with nonrenal circulatory beds. Such responsiveness may contribute to reduced RBF and GFR during endotoxemia.

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“…The rates of ROS generation in mitochondria isolated from control-and LPS-treated rats were detected in the presence of 250 lM of 1-hydroxy-3-carboxy-pyrrolidine, using electron spin resonance spectroscopy as described previously [11,12]. As substrates we used either glutamate/malate or succinate as previously described.…”

Section: Detection Of Rosmentioning

confidence: 99%

Proteome analysis of rat liver mitochondria reveals a possible compensatory response to endotoxic shock

Miller¹,

Gemeiner²,

Gesslbauer³

et al. 2006

FEBS Letters

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Organ failure induced by endotoxic shock has recently been associated with affected mitochondrial function. In this study, effects of in vivo lipopolysaccharide-challenge on protein patterns of rat liver mitochondria in treated animals versus controls were studied by two-dimensional electrophoresis (differential image gel electrophoresis). Significant upregulation was found for ATP-synthase a chain and superoxide dismutase [Mn]. Our data suggest that endotoxic shock mediated changes in the mitochondrial proteome contribute to a compensatory reaction (adaptation to endotoxic shock) rather than to a mechanism of cell damage.

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Epr analysis reveals three tissues responding to endotoxin by increased formation of reactive oxygen and nitrogen species

Cited by 68 publications

References 28 publications

Single oral inoculation with Escherichia coli (ATCC 25922) stimulates generalised production of nitric oxide in mice

Single oral inoculation with Escherichia coli (ATCC 25922) stimulates generalised production of nitric oxide in mice

Maintenance of Renal Vascular Reactivity Contributes to Acute Renal Failure during Endotoxemic Shock

Proteome analysis of rat liver mitochondria reveals a possible compensatory response to endotoxic shock

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