Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The alterations in peritoneal permeability characteristics during peritonitis can only partly be explained by the increased concentrations of prostaglandins and cytokines in the dialysate. Fifteen patients undergoing continuous ambulatory peritoneal dialysis (CAPD) with 16 peritonitis episodes were examined in the acute phase of the infection by using standard peritoneal permeability analyses (SPAs). In 9 of these patients, a control SPA could be performed. The contribution of nitric oxide (NO), prostaglandins, and the acute phase reactants C-reactive protein (CRP) and secretory phospholipase A2 (sPLA2) were analyzed. The mass transfer area coefficients (MTACs) of low-molecular-weight solutes increased during peritonitis: urea 26%, creatinine 45%, and urate 45%. The MTAC of CO2, calculated to estimate peritoneal blood flow, was 71 mL/min (34 to 254 mL/min) during peritonitis and 55 mL/min (42 to 63 mL/min) after recovery, P < or = .05. The peritoneal protein clearances were also greater during peritonitis, but this increase was not related to the molecular weight of the protein. Therefore the restriction coefficients to macromolecules were not different. The net ultrafiltration in all peritonitis episodes was lower as compared with the control dwells: -97 mL (-196 to 19 mL) versus 25 mL (-132 to 216 mL), P = .03. The prostaglandin concentrations in dialysate were greater during peritonitis than after recovery. The median increase was 199% for prostaglandin E2 (PGE2), 68% for 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha), and 44% for thromboxane B2 (TxB2). Plasma sPLA2 values were 22.7 microg/L (7.3 to 407.6) during peritonitis and 8.9 microg/L (5.5 to 11.5) after recovery, P < .01. The increased plasma sPLA2 during peritonitis correlated with plasma CRP (r = .6; P = .02). The peritoneal clearances of sPLA2 were greater during peritonitis, but this could be attributed completely to the increased peritoneal transport. Both during peritonitis and after recovery, the sPLA2 clearances did not exceed the predicted values based on transport from the circulation to the dialysate. No evidence was found for local production of nitrite or nitrate. However, the MTAC of cyclic guanosine monophosphate (cGMP) was greater during the experiments performed 48 to 72 hours after the onset of peritonitis, which suggests the synthesis of NO. It can be concluded that peritonitis does not induce detectable local release of sPLA2 and that the inflammation-induced increase in the vascular surface area could not be attributed to NO in the acute phase. The activation of inducible NO synthase may occur after 48 hours.
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PMID:Are phospholipase A2 and nitric oxide involved in the alterations in peritoneal transport during CAPD peritonitis? 979 5

Levels of procalcitonin (ProCT) have been found to be elevated in individuals with severe bacterial infections such as sepsis and peritonitis, and this correlates well with the severity of the disease. Recently, increased levels have been described in melioidosis and Plasmodium falciparum malaria. In this study ProCT levels were measured in 27 Thai patients with complicated malaria before and during/after treatment with artesunate and mefloquine. Initial parasite counts averaged 290,680/microl (range = 533-1,147,040). On admission, ProCT levels were elevated in all but one patient (median = 40 ng/ml, range = 0.04-662, normal values < 0.5 ng/ml). With treatment, levels decreased to 1.3 ng/ml (range = 0.01-6.5). Nitrite/nitrate levels in patients were higher than in controls throughout the study. The ProCT levels correlated with initial parasite density (P < 0.05), which is a marker of disease severity, and with nitrite/nitrate levels (P < 0.05). Based on the changes of ProCT levels over the course of the disease a possible role in the acute-phase reaction seems likely.
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PMID:Serum procalcitonin levels in severe Plasmodium falciparum malaria. 988 89

Several recent studies have suggested that nitric oxide (NO) derived from the inducible isoform of NO synthase (NOS) may act as an endogenous modulator of the inflammatory response by inhibiting adhesion of leukocytes to endothelial cells in vitro. Few studies have addressed specifically the role of iNOS in regulating leukocyte recruitment in vivo in a model of acute inflammation. Thus, the objective of this study was to assess the role of iNOS in modulating neutrophil (PMN) extravasation in an oyster glycogen-induced model of acute peritonitis in rats. Data obtained in the present study demonstrates that injection (IP) of oyster glycogen induces massive and selective PMN recruitment into the peritoneal cavity of rats at 6 hrs following OG administration. These extravasated cells were found to contain significant amounts of iNOS protein as assessed by Western blot analysis. Treatment of rats with the selective iNOS inhibitor L-iminoethyl-lysine (L-NIL) dramatically reduced NO levels in lavage fluid as measured by decreases in nitrate and nitrite concentrations without significantly affecting iNOS protein levels. Although L-NIL inhibited NO production by >70%, it did not alter oyster glycogen-induced PMN recruitment when compared to vehicle-treated rats. We conclude that PMN-associated, iNOS-derived NO does not play an important role in modulating extravasation of these leukocytes in this model of acute inflammation.
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PMID:Role of inducible nitric oxide synthase in leukocyte extravasation in vivo. 1020 44

In the present study, we used IL-6 knock-out mice (IL-6KO) to evaluate a possible role of IL-6 in the pathogenesis of non-septic shock induced by peritoneal injection of zymosan. A severe inflammatory response characterized by peritoneal exudation, high peritoneal levels of nitrate/nitrite, and leukocyte infiltration into peritoneal exudate was induced by zymosan administration in wild-type control (WT) mice. This inflammatory process coincided with the damage to the lung and small intestine, as assessed by histological examination. Lung, small intestine and liver myeloperoxidase (MPO) activity, indicative of neutrophil infiltration and lipid peroxidation, were significantly increased in zymosan-treated WT mice. Peritoneal administration of zymosan in the WT mice also induced a significant increase in the plasma levels of nitrite/nitrate and in the levels of peroxynitrite, 18 hours after zymosan challenge. Immunohistochemical examination demonstrated a marked increase in the immunoreactivity to nitrotyrosine in the lung of zymosan-treated WT mice. Zymosan-treated IL-6KO showed significantly decreased mortality and inhibition of the development of peritonitis. In addition, IL-6KO mice showed significant protection from the development of organ failure, since tissue injury and MPO was reduced in the lung, small intestine and liver. Furthermore, a significant reduction of suppression of mitochondrial respiration, DNA strand breakage and reduction of cellular levels of NAD+ was observed in ex vivo macrophages harvested from the peritoneal cavity of IL-6KO mice subjected to zymosan-induced non-septic shock. In vivo treatment with anti-IL-6 (5,000 ng/day per mouse, 24 and 1 hour before zymosan administration) significantly reduced the inflammatory process. Taken together, the present study clearly demonstrates that IL-6 exerts a role in zymosan-induced non-septic shock.
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PMID:Role of interleukin-6 in a non-septic shock model induced by zymosan. 1040 Aug 25

1 The therapeutic efficacy of Mn(III)tetrakis (4-benzoic acid) porphyrin (MnTBAP), a novel superoxide dismutase mimetic which scavenges peroxynitrite, was investigated in rats subjected to shock induced by peritoneal injection of zymosan. 2 Our data show that MnTBAP (given at 1, 3 and 10 mg kg-1 intraperitoneally, 1 and 6 h after zymosan injection) significantly reduce in dose dependent manner the development of peritonitis (peritoneal exudation, high nitrate/nitrite and peroxynitrite plasma levels, leukocyte infiltration and histological examination). 3 Furthermore, our data suggest that there is a reduction in the lung, small intestine and liver myeloperoxidase (MPO) activity and lipid peroxidation activity from MnTBAP-treated rats. 4 MnTBAP also reduced the appearance of nitrotyrosine immunoreactivity in the inflamed tissues. 5 Furthermore, a significant reduction of suppression of mitochondrial respiration, DNA strand breakage and reduction of cellular levels of NAD+ was observed in ex vivo macrophages harvested from the peritoneal cavity of zymosan-treated rat. 6 In vivo treatment with MnTBAP significantly reduced in a dose-dependent manner peroxynitrite formation and prevented the appearance of DNA damage, the decrease in mitochondrial respiration and the loss of cellular levels of NAD+. 7 In conclusion our results showed that MnTBAP was effective in preventing the development of zymosan-induced shock.
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PMID:Beneficial effects of Mn(III)tetrakis (4-benzoic acid) porphyrin (MnTBAP), a superoxide dismutase mimetic, in zymosan-induced shock. 1057 38

The aim of this study was to determine whether nitric oxide (NO) production is altered during peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD), and if so, whether there is an association between this alteration and the severity and prognosis of CAPD-induced peritonitis. The study population comprised 30 patients with 30 episodes of peritonitis. Thirteen patients without peritonitis were used as CAPD-control, and eighteen patients with normal renal function were used as normal-control. Total NO metabolites (NOx; nitrite + nitrate) were measured by the Griess method to reflect nitric oxide production. Peritoneal dialysate effluent and plasma were collected from 30 patients during episodes of peritonitis every day for the first 3 days, and then every 3 days for 2 weeks or until the patients were discharged. Plasma NOx levels in the control, CAPD-control, and CAPD-peritonitis groups were 87.0 +/- 11.5, 163.0 +/- 30.7 and 146.3 +/- 18.1 microM, respectively. Dialysate NOx levels in the CAPD-control and CAPD-peritonitis groups were 91.8 +/- 13.1 and 103.8 +/- 14.1 microM, respectively, and dialysate NOx levels did not differ between the two groups. The peak dialysate/plasma (D/P) ratios during the acute phase exceeded 1.0 in 46.7% of the patients of the CAPD-peritonitis group. The D/P ratios of NOx levels before and after treatment were 1.03 +/- 0.07 and 0.56 +/- 0.05, respectively. On the contrary, NOx levels in dialysate after treatment were not decreased, but those in plasma were increased after effective treatment. The peak D/P ratio increased 2.1-fold in the bacterial peritonitis group and 2.3-fold in the fungal peritonitis group, compared with the CAPD-control group. The lowest D/P ratios after treatment were similar to those in the CAPD-control group in patients with effective treatment, but remained 1.5-fold higher in patients for whom treatment was ineffective. In the evolutional study, the D/P ratios of NOx levels gradually declined to CAPD-control group levels (6.6 +/- 2.5 days) after effective antibiotic treatment, but it took longer for leukocyte counts in the peritoneal dialysate effluents (3.8 +/- 1.2 days) to normalize. In 5 patients with refractory peritonitis (Candida infection in three, Staphylococcus aureus infection in two), the D/P ratios of NOx levels remained elevated by 1.5-fold despite treatment, and the catheters were removed. These results suggest that dialysate NOx may be influenced not only by local NO production, but also by plasma NO or NOx diffusion. Therefore, we can suppose that the D/P ratio of NOx levels provides more clinical significance than dialysate NOx levels only. In conclusion, the D/P ratios of NOx levels may serve as a marker to assess the severity of peritoneal inflammation, treatment efficacy, and progression of refractory peritonitis in CAPD patients with peritonitis.
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PMID:Nitric oxide is a marker of peritonitis in patients on continuous ambulatory peritoneal dialysis. 1064 19

In order to elucidate the contribution of hereditary factor (dose of ribosome genes) to the realization of organ dysfunction syndromes in children with surgical infection, the total size of silver nitrate-stained nucleoli-forming regions (Ag-NFR) of acrocentric chromosomes in karyotypes was assessed in 22 patients aged from 14 months to 12 years, 17 of these with appendicular peritonitis, 4 with destructive pneumonia, and 1 with acute hematogenic osteomyelitis. Pyoseptic diseases involved no organ dysfunction in 10 patients, and in 12, multiple organ dysfunction was diagnosed. Our findings indicate that the carriers of low-copy variants of ribosome genes are characterized by hereditary predisposition to lowered individual resistance of the organism. Therefore, children with surgical infection with a decreased size of Ag-NFR (low dose of ribosome genes) in the karyotype potentially represent a group at risk of multiple organ dysfunction realization.
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PMID:[Significance of hereditary factors in multiple organ dysfunction syndrome in children with infections]. 1076 61

Intra-abdominal infection is one of the major causes of septic shock and multiple organ failure. To date, what causes the disease's progression remains unclear and therefore the relevance of immune modulating therapies remains speculative. The primary outcome measure of this study was to investigate immune modulating mediators at the onset of peritonitis before the development of subsequent septic shock. The secondary outcome measure was to investigate the usefulness of these immune parameters in predicting progression from peritonitis to septic shock. Fifty-eight peritonitis patients were included in this study: 14 patients subsequently developed septic shock. All patients were examined on "diagnosis of peritonitis" (<4 h within establishment of diagnosis), during "early septic shock" (<12 h following the onset of septic shock), and once again during "late septic shock" (within 72-98 h following the onset of septic shock). The immune modulating parameters tumor necrosis factor-alpha (TNF-alpha), the soluble TNF-alpha receptors I and II (sTNF-alpha RI and sTNF-alpha RII), interleukines (IL) -1beta, -6, -8, and -10, and the adhesions molecules endothelial-leukocyte-adhesion-molecule (E-Selectin), intercellular-adhesion-molecule-1 (ICAM-1), and vascular-adhesion-molecule-1 (VCAM-1), in addition to nitrate and nitrite, were determined. In the peritonitis group with subsequent septic shock, TNF-alpha, sTNF-alpha RI + RII IL-1beta, IL-8, IL-10, and nitrate were significantly increased before the onset of septic shock. TNF-alpha had an area under the receiver operating characteristics curve (AUC) of 0.84 and was reliable in predicting the progression from peritonitis to septic shock. The AUC of the other immune modulating parameters, despite being significantly elevated, ranged from 0.71 to 0.76. The AUC of the conventional laboratory markers such as leukocytes and C-reactive protein ranged from 0.64 to 0.68. In peritonitis that progressed to septic shock, an early immune response had already occurred before the onset of septic shock. The progression was best predicted by TNF-alpha. Therefore, mediator therapy might be considered in high-risk peritonitis patients who show an exaggerated immune response before the progression to septic shock.
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PMID:The value of immune modulating parameters in predicting the progression from peritonitis to septic shock. 1122 Jun 48

Erythrocyte deformability has been recognized as a determinant of microvascular perfusion. Because nitric oxide (NO) is implicated in the modulation of red blood cell (RBC) deformability and NO levels increase during sepsis, we tested the hypothesis that a NO-mediated decrease in RBC deformability contributes to decreased functional capillary density (CD) in remote organs. With the use of a peritonitis model of sepsis in the rat [cecal ligation and perforation (CLP)] and aminoguanidine (AG) to prevent increases in NO, we measured CD in skeletal muscle (intravital microscopy), mean erythrocyte membrane deformability (; micropipette aspiration), systemic NO production [plasma nitrite/nitrate (NO(x)) chemiluminescence], and NO accumulation in RBC [NO bound to hemoglobin (HbNO) detected by electron paramagnetic resonance spectroscopy]. In untreated CLP animals relative to sham, NO(x) increased 254% (P < 0.05), stopped flow capillaries increased 149% (P < 0.05), and decreased 12.7% (P < 0.05), with a subpopulation (5%) of RBC with deformabilities below the normal range. AG prevented increases in NO(x), accumulation of HbNO, and decreases in both and functional CD. We found no evidence of leukocyte plugging postcapillary venules. Our findings suggest that decreased functional CD during sepsis resulted from a NO-mediated decrease in erythrocyte deformability.
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PMID:Erythrocyte deformability is a nitric oxide-mediated factor in decreased capillary density during sepsis. 1135 44

In the present study, by comparing the responses in wild-type mice (+/+) and mice lacking (-/-) the inducible (or type 2) nitric oxide synthase (iNOS), we investigated the role played by iNOS in the development of non-septic shock. A severe inflammatory response characterized by peritoneal exudation, high peritoneal levels of nitrate/nitrite, and leukocyte infiltration into peritoneal exudate was induced by zymosan administration in iNOS +/+ mice. This inflammatory process coincided with the damage of lung, liver, and small intestine, as assessed by histological examination. Lung, small intestine, and liver myeloperoxidase (MPO) activity, indicative of neutrophil infiltration and lipid peroxidation, were significantly increased in zymosan-treated iNOS +/+ mice. Peritoneal administration of zymosan in the iNOS +/+ mice induced also a significant increase in the plasma levels of nitrite/nitrate and in the levels of peroxynitrite at 18 h after zymosan challenge. Immunohistochemical examination demonstrated a marked increase in the immunoreactivity to nitrotyrosine and to poly ADP-ribose synthetase (PARS) in the lung, liver, and intestine of zymosan-treated iNOS +/+ mice. The intensity and degree of nitrotyrosine and PARS were markedly reduced in tissue section from zymosan-iNOS -/- mice. Zymosan-treated iNOS -/- mice showed a significantly decreased mortality and inhibition of the development of peritonitis. In addition, iNOS -/- mice showed a significant protection on the development of organ failure since tissue injury and MPO were reduced in lung, small intestine, and liver. Furthermore, a significant reduction of suppression of mitochondrial respiration, DNA strand breakage, and reduction of cellular levels of NAD+ was observed in ex vivo macrophages harvested from the peritoneal cavity of iNOS -/- mice subjected to zymosan-induced non-septic shock. In vivo treatment with aminoguanidine (300 mg/kg 1 and 6 h after zymosan administration) significantly prevents the inflammatory process. Taken together, our results clearly demonstrate that iNOS plays an important role in zymosan-induced non-septic shock.
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PMID:Inducible nitric oxide synthase knockout mice exhibit resistance to the multiple organ failure induced by zymosan. 1144 16


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