Plasma nitric oxide levels in newborn infants with sepsis

Shi, Yuan; Li, Huaqiang; Shen, Chengcheng; Wang, Jianghuai; Qin, Shiwen; Liu, Ren; Pan, Jie

doi:10.1016/s0022-3476(05)81753-6

Cited by 127 publications

(55 citation statements)

References 18 publications

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“…On the other hand, enhanced NO levels mediate beneficial hemodynamic effects in GBS infection by reducing pulmonary hypertension (2) and cerebral ischemia (15). The role of NO in septic shock and pulmonary hypertension in GBS infections of humans is controversial (5,27).…”

Section: Discussionmentioning

confidence: 99%

Cytokine Responses to Group B Streptococci Induce Nitric Oxide Production in Respiratory Epithelial Cells

Goodrum

Poulson-Dunlap

2002

Infect Immun

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Streptococcus agalactiae (group B streptococcus [GBS]) is a leading cause of neonatal pneumonia, sepsis, and meningitis. Early-onset GBS pneumonia is characterized by marked pulmonary epithelial and endothelial cell injury. Innate proinflammatory responses to GBS infection that may contribute to the respiratory pathology include the synthesis and release of cytokines, prostaglandins, and nitric oxide (NO). The hypothesis that NO is directly induced in lung epithelial cells by invading GBS or indirectly induced by cytokines released by GBS-infected mononuclear cells was tested. A549 transformed human respiratory epithelial cells were directly cultured with GBS, cocultured with GBS-infected human mononuclear cells or purified macrophages, or exposed to conditioned culture medium from human mononuclear cells infected by GBS. The culture medium of A549 cultures was assayed for NO secretion, and the cell lysates were tested for presence of inducible nitric oxide synthase (iNOS) mRNA by reverse transcriptase PCR (RT-PCR). GBS-treated A549 cells neither secreted detectable NO nor expressed iNOS mRNA. GBS interaction with human mononuclear cells, however, stimulated release of soluble factors that readily induced iNOS mRNA expression and NO secretion by A549 cells. Inflammatory mediator-induced nitric oxide (NO) production by alveolar epithelium may exceed that of other lung cell types such as macrophages, and induction during GBS infection may play a significant role in pulmonary defense or free-radical-mediated lung injury. Streptococcus agalactiae (group B streptococcus [GBS]) is a leading cause of neonatal pneumonia, sepsis, and meningitis (26). GBS is also an important pathogen in maternal infections and in infections of nonpregnant adults with risk factors such as older age and underlying disorders (25). Early-onset GBS pneumonia is characterized by presence of numerous bacteria, an inflammatory exudate, and marked pulmonary epithelial and endothelial cell injury (1, 10). Innate proinflammatory responses to GBS infection which may contribute to the respiratory pathology include the synthesis and release of cytokines (12,22), prostaglandins (16), and nitric oxide (NO) (6, 15).In the lung, alveolar macrophages, airway epithelial cells, endothelial cells, and inflammatory cells may be sources for NO (24). Though GBS, with or without cytokines, has been shown to induce NO production in cultured murine macrophages (3,6,20), human macrophages produce far less NO (5-to 100-fold less) in response to cytokine or microbial stimuli than do murine macrophages (31). An alternate source of alveolar NO are human lung epithelial cells, which possess a nitric oxide synthase (iNOS, NOS2) that is inducible by a mixture of cytokines (21) that should, based on in vitro data, be released locally by GBS-infected alveolar macrophages and mononuclear cells (12). Alternatively, direct GBS invasion of respiratory epithelial cells (23) might also induce NO production.In this report, human respiratory epithelial cells were directly cultured w...

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Section: Discussionmentioning

confidence: 99%

Cytokine Responses to Group B Streptococci Induce Nitric Oxide Production in Respiratory Epithelial Cells

Goodrum

Poulson-Dunlap

2002

Infect Immun

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“…Hypotensive adults with septic shock have responded to NO synthase (NOS) inhibitors with increased blood pressure [11], implicating NO as a contributor to the hemodynamic response. In another clinical setting, Shi et al [8] demonstrated increased nitrite and nitrate levels in the urine of septic newborns, supporting NO as a potential mediator of the cardiovascular responses observed in these neonates. More recently, methylene blue, a soluble guanylate cyclase inhibitor, has been shown to increase blood pressure in neonates with hypotension, presumably secondary to infection, unresponsive to colloids, inotropic agents, and corticosteroids [9].…”

Section: Introductionmentioning

confidence: 93%

“…Their death is usually characterized by cardiovascular collapse, presumably mediated by endotoxins. The cardiovascular responses to endotoxin which have been studied extensively in both adult humans and animal models [3][4][5][6][7] have been less well characterized in the newborn [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Role of Nitric Oxide in Cardiovascular Responses to Endotoxemia in Neonatal Lambs

et al. 1999

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To determine whether systemic cardiovascular responses to gram-negative endotoxemia are mediated by nitric oxide, we evaluated time-dependent changes in contractility and hemodynamics in a neonatal sheep model subjected to nitric oxide synthesis inhibition with L-Name (N^ω-nitro-L-arginine methyl ester). Four groups were studied: control (C), endotoxin (E), endotoxin L-Name where the nitric oxide synthase inhibitor was given prior to endotoxin (ELN), and a control L-Name group pretreated with L-Name (CLN). The contractility, measured as end-systolic elastance (Ees), increased transiently in the E group and then returned to baseline. In contrast, Ees declined over time in the ELN group. In terms of peripheral hemodynamics, both the E and ELN groups demonstrated significant progressive decreases in blood pressure and vascular resistance. The results of this study suggest that nitric oxide contributes to the newborn contractile response of the heart to endotoxin, but does not appear to mediate the systemic vascular relaxation response.

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“…'The supernatants were subsequently assayed for N0 2 ' + N0 3 -content. Nitrite was measured by the Griess assay (3,4,11,12). Briefly, 100 IJ-L Griess reagent (1% sulfanilamide/0.1 % naphthylethylenediamine dihydrochloridel2.5% H 3P04; Sigma Chemical, St. Louis, MO, USA) were added to 100 IJ-L of each of the above supernatants.…”

mentioning

confidence: 99%

“…High-output NO production by cells or its accumulation in biological solutions has been assayed in various ways (1-5,7-9,11). The simplest assay methods for relatively large amounts of NO in biological fluids have relied on the reaction of NO in aqueous solutions to form nitrite (N0 2 -) and nitrate (N0 3 -) (1,3,4,9,11). In urine and plasma, NO is found primarily as N0 3 -, but N0 2 -can be assayed more easily by colorimetric diazotization (Griess reaction; References 1, 3, 4 and 11).…”

mentioning

confidence: 99%

Modified Microassay for Serum Nitrite and Nitrate

Vodovotz

1996

BioTechniques

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BenchmarksFigure 1. Recovery of N0 2 ' after deproteination of serum. 190 IJ.L of the indicated concentrations of NaN0 2 in water (0, 1.56,3.13,6.25, 12.5,25,50 and 100 IJ.M) were incubated with 10 IJ.L of normal rabbit serum and then deproteinated (filled circles , solid line). Control samples contained the same concentrations of NaN0 2 and ZnS04, but did not contain serum and were not deproteinated (open squares, dashed line) . After centrifugation of all the samples, the supernatants wer e assayed for N0 2 ' by the Gries s assay. Each point represents the mean ±standard error of three separate experiments. Lines represent a linear regression analy sis of recovered N0 2 ' vs. input N0 2 ' either with or without added serum.

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Plasma nitric oxide levels in newborn infants with sepsis

Cited by 127 publications

References 18 publications

Cytokine Responses to Group B Streptococci Induce Nitric Oxide Production in Respiratory Epithelial Cells

Cytokine Responses to Group B Streptococci Induce Nitric Oxide Production in Respiratory Epithelial Cells

Role of Nitric Oxide in Cardiovascular Responses to Endotoxemia in Neonatal Lambs

Modified Microassay for Serum Nitrite and Nitrate

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