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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The experiments on rats have shown that intraperitoneal administration of silver nitrate solution induces peritonitis while subplantar histamine, serotonin and prostaglandin E2 administration leads to an acute paw edema. Preliminary subcutaneous injection of lithium hydroxybutyrate prevents the development of inflammation.
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PMID:[Indices of acute inflammation against a background of lithium oxybutyrate action]. 381 1

It was shown in experiments on rats that intraabdominal administration of silver nitrate solution induces peritonitis and the subplantar administration of histamine, serotonin and prostaglandin E2 leads to an acute paw edema. Preliminary subcutaneous administration of esculamine or rutin inhibited the development of the inflammation. Esculamine proved more active here.
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PMID:[Effect of rutin and esculamine on models of aseptic inflammation]. 394 95

The article deals with a new method for determining the degree of intoxication in patients with peritonitis of various etiology. Bull sperm cells were used as the test-object. The degree of intoxication is judged according to the ratio of the mean life time of the spermatozoa in the studied filtrate, obtained from the blood serum of patients with peritonitis by filtration through polysulfone membranes with a pass band of up to 70,000 daltons, to the life time in a control glucose-nitrate solution. The authors called this ratio as the spermatic index of toxicity. It was 80.1 +/- 18.7% in the donors. The spermatic index of toxicity was 35.0 +/- 9.0% in the first day after the operation, 44.6 +/- 16.7% on the fifth day, and 70.8 +/- 27.7% before discharge from the hospital. The method is automatic, which excludes subjective a appraisal of the results, and may be suggested for use in clinical practice.
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PMID:[Spermatic index of intoxication, a method of the assessment of blood toxicity]. 783 45

During continuous ambulatory peritoneal dialysis (CAPD) peritoneal vessels are dilated. Nitric oxide (NO) causes vasodilation in many organs. Nitrate, a stable metabolite of NO, was measured in plasma and dialysate. In 6 stable CAPD patients standard peritoneal analyses were performed. The mass transfer area coefficient (MTAC) of nitrate was 11.5 mL/min (10.0-17.0 mL/min) (median and range). The MTAC of creatinine was of the same order of magnitude: 10.7 mL/min (8.0-14.2 mL/min), although the molecular weight of nitrate is lower (62 vs 113 dalton). The correlation between the MTAC of nitrate and the MTAC of creatinine indicated diffusion from the circulation and not local production of NO (r = 0.71; p = 0.11). Peritoneal permeability is increased in the acute phase of peritonitis, partly caused by extensive vasodilation. The potential role of NO during peritonitis was investigated in 8 CAPD patients with 11 peritonitis episodes in the acute phase and after recovery. The median dialysate/plasma (D/P) ratio of nitrate in the acute phase was 1.47 (range 0.96-2.55), which was higher than after recovery: 1.07 (0.99-1.75), p < 0.05. No relation was found between the D/P ratio of nitrate and the D/P ratio of TNF alpha (tumor necrosis factor). In conclusion, dialysate nitrate levels in stable CAPD patients are likely to be determined by diffusion from the circulation. D/P ratios exceeding 1.0 during the acute phase of peritonitis are probably the result of local NO production. This may contribute to the marked vasodilation during peritonitis.
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PMID:Nitrate in stable CAPD patients and during peritonitis. 853 33

Nitric oxide plays an important role in mediating the inflammatory process. The aim of this study was to evaluate if nitric oxide production was increased during peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD), and the association with the prognosis. The study population comprised 21 patients with 22 episodes of peritonitis. Fifteen patients without peritonitis were controls. Nitrate was measured by HPLC and nitrite by the Griess method, to reflect nitric oxide production. Peritoneal dialysate effluent and plasma were collected from six patients during peritonitis and 1 week after treatment to study changes in dialysate:plasma ratio. In 15 patients, nitrite was measured during peritonitis and every 3 days for 2 weeks or until normalized for evolutional changes. The dialysate:plasma ratios of nitrate and nitrite during peritonitis were reduced 26% and 41.5%, respectively, after 1 week of treatment, indicating the peritoneal production of nitric oxide during peritonitis. In the evolutional study, a 5.1-fold increase of peak nitrite levels in bacterial peritonitis (n = 13) and a 2.5-fold increase in fungal peritonitis (n = 3) were observed compared to controls. Nitrite gradually declined to control levels (9.3 +/- 7.2 days) after effective antibiotic treatment, but took longer than to normalize leukocyte count in the peritoneal dialysate effluent (3.9 +/- 1.9 days). In four patients with refractory peritonitis (Candida infection in three, Acinetobacter infection in one), the nitrite levels remained elevated 2-fold despite treatment, and the catheters were removed. It is concluded that nitrite levels in peritoneal dialysate effluent may serve as a marker to assess treatment efficacy in CAPD patients with peritonitis.
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PMID:Peritoneal nitric oxide is a marker of peritonitis in patients on continuous ambulatory peritoneal dialysis. 901 24

Nitric oxide (NO) is a regulator of leukocyte adhesion in the microcirculation. This study was designed to examine the effects of a NO synthase inhibitor on neutrophil adhesion in the peritoneum, lung, liver, and kidney in a rat peritonitis model using a fluorescence microscopic method. Sprague-Dawley rats were given normal saline (control) or N omega-nitro-L-arginine methyl ester (L-NAME) at dosages of 10 mg/kg (N10) or 100 mg/kg (N100) (n = 66) intraperitoneally. One hour after pretreatment fluorescein-labeled neutrophils were infused without bacterial challenge (0 hr). Other rats received an injection of 10(7) Escherichia coli into the peritoneal cavity 1 hr after pretreatment. Labeled neutrophils were infused 1 and 5 hr after bacterial challenge. Just 2 min after neutrophil injection, blood samples were obtained and the animals were killed. Five peritoneal samples (omentum, mesentery, parietal peritoneum, colon, and ileum), both lungs, the liver, and the right kidney were harvested for counting of labeled neutrophils under epifluorescent microscopy. Combined plasma nitrite/nitrate levels were determined. In another set of rats (n = 36), an arterial catheter was inserted after L-NAME treatment and bacterial challenge. At 0, 1, 5, and 12 hr after challenge, blood pressure, heart rate, and arterial blood gas data were measured. One hour after E. coli challenge, the number of neutrophils in the peritoneum was significantly lower in both L-NAME-treated groups than in the control group. In contrast, the number of labeled neutrophils in the lungs was significantly higher in the N100 group than in the control group. Neutrophil accumulation in the lungs and peritoneum at 0 and 5 hr and in the liver and kidney at 0, 1, and 5 hr did not differ among groups, nor did combined plasma nitrite/nitrate levels. L-NAME treatment had no influence on either hemodynamic or blood gas data. In conclusion, administration of L-NAME increases neutrophil adhesion in the lung, while decreasing that in the peritoneum. NO plays an important role in neutrophil adhesion at the inflammatory site, as well as in remote organs, during peritonitis. NO inhibition may be detrimental, due to neutrophil sequestration, in this peritonitis model.
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PMID:Nitric oxide inhibition decreases neutrophil adhesion at the inflammatory site, while increasing adhesion in remote organs in peritonitis. 912 99

Nitric oxide (NO) is a short-lived mediator, the synthesis of which is induced by various cytokines during inflammatory processes. Recently, it has been proposed that zymosan, a nonbacterial agent, causes inflammation by inducing the production of various cytokines and proinflammatory mediators. In the present study we investigated the role of NO in a nonseptic shock model induced by zymosan administration in the rat. Administration of zymosan (500 mg/kg, intraperitoneally) in the rat induced acute peritonitis, as assessed by a marked increase in the leukocytes count in the exudate, as well as by an increase in the exudate nitrate/nitrite concentration. Zymosan-treated rats developed a severe hypotension and showed signs of systemic illness, significant loss of body weight, and a high mortality rate (53% of animals died within 72 h). Elevated plasma levels of nitrite and nitrate were also observed in zymosan-treated rats compared with control rats (67 +/- 4 microM and 23 +/- 2 microM, respectively; p < .01). In ex vivo experiments, vascular reactivity was studied in thoracic aorta rings of zymosan-treated rats. The contractile responses to norepinephrine (100 nM) and endothelin-1 (5 nM) were significantly reduced. An impairment of the endothelial-dependent relaxation in response to acetylcholine was also observed. Pretreatment of zymosan-shocked rats with NG-nitro-L-arginine methyl ester (L-NAME) or NG-monomethyl-L-arginine (L-NMA), (10 mg/kg, subcutaneously, 15 min before zymosan) decreased mortality, prevented the development of peritonitis, improved ex vivo vascular reactivity, and significantly reduced hypotension. Our data suggest that overproduction of NO plays a role in the zymosan-induced peritonitis and cardiovascular derangements in the rats.
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PMID:Role of nitric oxide in a nonseptic shock model induced by zymosan in the rat. 916 70

In the present study we tested the hypothesis that nitric oxide may play a role in the pathogenesis of multiple organ failure induced by peritoneal injection of zymosan in the rat. A severe inflammatory response characterized by peritoneal exudation, high plasma and peritoneal levels of nitrate/ nitrite (breakdown products of nitric oxide), prostaglandin E2 and leukocyte infiltration into peritoneal exudate was induced by zymosan administration. This inflammatory process started within 3 h of administration and onset occurred at 18 h, coinciding with damage of lung, small intestine and liver, as assessed by histological examination and by increase of myeloperoxidase activity, indicative of neutrophil infiltration. Furthermore, at 18 h after zymosan-induced peritonitis, expression of inducible nitric oxide synthase enzyme was found mainly in the macrophages of inflamed lungs. Subcutaneously administration of a nonisoform selective nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, reduced formation of peritoneal exudate fluid, blocked plasma and peritoneal nitrate/nitrite accumulation, and attenuated the elevated release of peritoneal prostaglandin E2. In addition, nitric oxide synthase inhibition was effective in preventing the development of organ failure since tissue injury and neutrophil infiltration, by myeloperoxidase evaluation, was reduced in lung, small intestine, and liver. In conclusion, major findings of our study are that nitric oxide exerts a proinflammatory role in the development of multiple organ failure and nitric oxide synthase inhibition is an effective antiinflammatory therapeutic tool, since inhibits not only nitric oxide but also prostaglandin production and cellular infiltration in inflamed organs.
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PMID:Multiple organ failure following zymosan-induced peritonitis is mediated by nitric oxide. 932 28

Overproduction of nitric oxide (NO) upon expression of inducible NO synthase (iNOS) may be responsible for refractory hypotension in septic shock. Whereas high levels of NOS activity have been documented in experimental models of endotoxemia or intravenous challenge with Escherichia coil, much less is known concerning tissue models of Gram-negative infection. We examined NO production (measured as the accumulation of plasma NO3- + NO2-) in a murine model of Gram-negative peritonitis. Plasma NO3- + NO2- increased progressively from 25 microM to peak levels of 50-150 microM 24 h after intraperitoneal challenge with E. coli 0111:B4, similar to values reported for septic shock patients. Treatment of infected mice with NG-monomethyl-L-arginine, an inhibitor of NOS activity, resulted in the efficient inhibition of NO3- + NO2- production. In order to evaluate the roles of interferon-gamma (IFN-gamma) and tumor necrosis factor (TNF-alpha) in the induction of NO synthesis in murine peritonitis, mice deficient in the respective cytokine receptors were studied. In control in vitro experiments, macrophages from IFN-gammaR- or TNFR55-deficient mice, while failing to respond to IFN-gamma or TNF-alpha, respectively, produced high levels of NO under appropriate stimulation. When challenged intraperitoneally with E. coli, IFN-gammaR- or TNFR55-deficient mice exhibited similar levels of bacteremia and NO production as their wild-type controls. These data thus suggest that enhanced NO production during focal Gram-negative infection may occur in the absence of signaling through either IFN-gammaR or TNFR55.
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PMID:Nitric oxide production in experimental gram-negative infection: studies with cytokine receptor-deficient mice. 968 89

In vitro studies have demonstrated that melatonin is a scavenger of oxyradicals and peroxynitrite and an inhibitor of nitric oxide (NO) production. Recently, it has been proposed that zymosan, a non-bacterial agent, causes inflammation by inducing the production of various cytokines and pro-inflammatory mediators. In the present study we evaluated the effect of melatonin treatment in a non-septic shock model induced by zymosan in the rat. Administration of zymosan (500 mg/kg intraperitoneally) in the rat induced acute peritonitis, as assessed by a marked increase in the leukocyte count in the exudate, as well as by an increase in the exudate nitrate/nitrite concentration. This inflammatory process coincided with the damage of lung, small intestine, and liver, as assessed by histological examination and by increase of myeloperoxidase activity, indicative of neutrophil infiltration. Peritoneal administration of zymosan in the rat induced also an significant increase in the plasma levels of nitrite and nitrate, stable metabolites of nitric oxide (NO), and in the levels of peroxynitrite, as measured by the oxidation of the fluorescent dye dihydrorhodamine 123, at 18 hr after zymosan challenge. Immunohistochemical examination demonstrated a marked increase in the immunoreactivity to nitrotyrosine, a specific "footprint" of peroxynitrite, in the lung of zymosan-shocked rats. Pretreatment of zymosan-shocked rats with melatonin (25 and 50 mg/kg, intraperitoneally, 5 min before zymosan) prevented in a dose dependent manner the development of peritonitis and reduced peroxynitrite formation. In addition, melatonin (50 mg/kg, intraperitoneally, 5 min before zymosan) was effective in preventing the development of organ failure since tissue injury and neutrophil infiltration, by myeloperoxidase evaluation, was reduced in lung, small intestine, and liver. Taken together, the present results demonstrate that melatonin exerts potent antiinflammatory effects.
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PMID:Protective effect of melatonin in a non-septic shock model induced by zymosan in the rat. 969 1


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