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At least 19 recordsLinked to original sources
PubMed1987

Differential effects of anti-inflammatory drugs on fluid accumulation and cellular infiltration in reverse passive arthus pleurisy and carrageenan pleurisy in rats.

At 4 h following induction of pleural inflammation in rats using either an immune stimulus (reverse passive Arthus reaction, RPAR) or a chemical stimulus (carrageenan), the cellular infiltration and fluid accumulation responses were quantitated. The bell-shaped antigen (BSA) dose-response curve describing the fluid response was increased upward as the anti-BSA dose was increased from 0.25 to 1 mg, whereas the dose-response curve for cellular infiltration was both shifted upward and to the right. Both nonsteroidal anti-inflammatory drugs and a mixed lipoxygenase-cyclooxygenase inhibitor (BW 755C) preferentially inhibited fluid accumulation in RPAR pleurisy elicited with 5 mg BSA and 1 mg anti-BSA and in carrageenan pleurisy. In contrast, these drugs inhibited cellular infiltration preferentially in RPAR pleurisy elicited with 1 mg BSA and 1 mg anti-BSA. These results demonstrate that the fluid and cellular responses in rat pleural inflammation can be differentially regulated by anti-inflammatory drugs depending upon the doses of antigen and antibody employed in RPAR pleurisy and the identity of the inflammatory stimulus.

Animals↗
PubMed1989

[T-lymphocyte subsets in peripheral blood and pleural effusion in tuberculous pleurisy and carcinomatous pleurisy: analysis by monoclonal antibodies].

By using monoclonal antibodies, OKT8(pant), OKT4(inducer/helper),OKT8(suppressor/cytotoxic) T-lymphocyte subsets were examined in 25 patients with tuberculous pleurisy and 15 patients with carcinomatous pleurisy. The results showed that percent and absolute counts of OKT8,OKT4,OKT8 in tuberculous pleural effusion were significantly higher than those in carcinomatous pleural effusion. Percent and absolute counts of OKT8, OKT4, in tuberculous pleural effusion were significantly higher than those in peripheral blood. OKT8% in peripheral blood of carcinomatous pleural effusion was significantly lower than that in peripheral blood of control group. When OKT8% greater than 65, OKT4% greater than 45, OKT8 number/mm8 greater than 1,000, OKT4 number/mm8 greater than 800, OKT8 number/mm8 greater than 500 in pleural effusion, it suggests pleural effusion is tuberculous. when OKT8% less than 55, OKT4% less than 45, OKT5 number/mm8 less than 500, OKT4 number/mm8 less than 300, OKT8 number/mm8 less than 200, it suggests pleural effusion is carcinomatous pleural effusion.

Adenocarcinoma↗
PubMed1982

Effects of anti-inflammatory drugs on triple vaccine-induced pleurisy in rats.

Effects of various anti-inflammatory drugs on triple vaccine-induced pleurisy, a model of delayed hypersensitivity, were examined and compared with those on carrageenin-induced pleurisy in rats. Steroidal drugs depressed markedly the volume of exudate and the number of leucocytes in both types of pleurisy. Gold compounds also depressed both types of pleurisy. Non-steroidal anti-inflammatory drugs were apt to show depressive effects on carrageenin-induced pleurisy, especially on increased exudate volume. BW755C produced a depressive effect on carrageenin-induced pleurisy, but on triple vaccine-induced pleurisy, BW755C produced only a slight depressive effect. Cyproheptadine produced a slight depressive effect on carrageenin-induced pleurisy, but not on triple vaccine-induced pleurisy. Promethazine had a slight depressive effect on both types of pleurisy. D-penicillamine and levamisole did not show any depressive effects on triple vaccine-induced pleurisy. The results show that reported mediators in carrageenin-induced pleurisy (prostaglandin, serotonin, leukotriene B, etc.) are not relevant to triple vaccine-induced pleurisy. Specific lymphokines and/or degradated products of complement may participate in the latter. This triple vaccine-induced pleurisy seems to be a good model for screening non-steroidal anti-inflammatory drugs which have steroidal-like activity.

Animals↗
PubMed1997

Differential diagnosis of tuberculous pleurisy by measurement of cytokine concentrations in pleural effusion.

STUDY OBJECTIVE: Measurement of cytokine concentration in serum and pleural effusion may be useful in the differential diagnosis of tuberculous pleurisy. PATIENTS AND METHODS: We compared the biochemical properties and concentrations of cytokines in serum and pleural effusion samples of 18 patients with tuberculous pleurisy, 7 patients with parapneumonic pleurisy, and 25 patients with malignant pleurisy. RESULTS: A high value of adenosine deaminase (ADA) was observed in pleural effusion of patients with tuberculosis. The serum concentrations of interleukin (IL)-1-beta, IL-2, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha were similar among the three groups. However, the concentration of IFN-gamma in pleural effusion was high in tuberculous patients, and that of TNF-alpha was high in tuberculous and parapneumonic pleural fluid, but both cytokines were low in malignant pleural fluid. The sensitivity, specificity and accuracy of IFN-gamma in the diagnosis of tuberculous pleurisy were 94%, 100% and 98%, respectively. Similarly, those of TNF-alpha for the diagnosis of infectious pleurisy including tuberculous and parapneumonic pleurisy were 88%, 80% and 84%, respectively. CONCLUSIONS: Our results indicate that simultaneous measurement of IFN-gamma and TNF-alpha in pleural effusion is a useful diagnostic tool for differentiating tuberculous pleurisy from parapneumonic and malignant pleurisy.

Adult↗
PubMed2002

[Surgical policy in tuberculous pleurisy].

Two hundred and eighty seven cases of tuberculous pleurisy are analyzed. According to the pleural contents, four phases of development of this disease are identified. These include: 1) free pleurisy; 2) partially encysted pleurisy; 3) encysted pleurisy, and 4) adhesive pleurisy. An algorithm of use of draining procedures and surgical interventions depending on the phase of pleurisy is proposed. Among other things, indications for thoracoscopy that was performed in 66 patients with tuberculous pleurisy for its therapy were stated. Thoracoscopy is ineffective in adhesive pleurisy, in the presence of a rigid residual cavity in particular, and thus preference should be given to thoracotomy with pleurectomy and decortication of the lung. This operation was made in 39 cases. Timely use of draining procedures and surgical interventions make it possible to achieve recovery from tuberculous pleurisy over shorter periods of time and with minimal residual changes.

Adolescent↗
PubMed1986

Roles of leukotrienes in two rat allergic inflammatory models; IgE-mediated and IgG-antigen complex-induced pleurisies.

Rat IgE pleurisy was induced by the injection of di-nitrophenol-conjugated bovine serum albumin (DNP-BSA) 48 hours after the intrapleural injection of rat anti-DNP-IgE serum. IgG-BSA complex pleurisy was also induced by the intrapleural injection of IgG-BSA complexes produced at the optimum ratio in vitro. Plasma exudation was markedly increased in the first 20 minutes, but not observed thereafter, in IgE pleurisy, whereas marked plasma exudation in the first 20 minutes was followed by weak exudation at three and five hours in IgG-BSA complex pleurisy. Leukotrienes (LTs) E4 (100 ng/rat), D4 (32) and B4 (16) were detected on HPLC in the pleural exudate in the first 20 minutes of IgG-BSA complex pleurisy, but less (9 ng/rat) LTE4 alone was detected in the five-hour exudate. The first 20-minute pleural exudate contained 13 ng/rat of LTE4 in IgE pleurisy. The plasma was completely inhibited by simultaneous treatment of rats with pyrilamine (2.5 mg/kg, i.p.) and methysergide (3 mg/kg, i.p.), as it was in compound 48/80-induced pleurisy. In IgG-BSA complex pleurisy, 90% of the pleural exudate for the first 20 minutes was inhibited by the same treatment, and the rest was completely suppressed by simultaneous treatment with an intrapleural injection of AA-1777, a selective 5-lipoxygenase inhibitor. AA-1777 alone did not reduce the plasma exudation significantly. The 5-lipoxygenase inhibitor was also very effective in reducing the migrating numbers of polymorphonuclear and mononuclear leukocytes to half, without affecting the eosinophils of mast cells.

Animals↗
PubMed1998

Characterization of the receptor and the mechanisms underlying the inflammatory response induced by des-Arg9-BK in mouse pleurisy.

1 The characterization of the B1 kinin receptor, and some mediators involved in the inflammatory response elicited by intrathoracic (i.t.) administration of des-Arg9-bradykinin (BK) in the mouse model of pleurisy, was investigated. 2 An i.t. injection of des-Arg9-BK (10-100 nmol per site), a selective B1 agonist, caused a significant and dose-related increase in the vascular permeability observed after 5 min, which peaked at 1 h, associated with an increase in cell influx, mainly neutrophils, and, to a lesser extent, mononuclear cell influx, peaking at 4 h and lasting for up to 48 h. The increase in fluid leakage caused by des-Arg9-BK was completely resolved 4 h after peptide injection. I.t. injection of Lys-des-Arg9-BK (30 nmol per site) caused a similar inflammatory response. 3 Both the exudation and the neutrophil influx elicited by i.t. injection of des-Arg9-BK were significantly antagonized (P<0.01) by an i.t. injection of the selective B1 antagonists des-Arg9-[Leu8]-BK (60 and 100 nmol per site) or des-Arg9-NPC 17731 (5 nmol per site), administered in association with des-Arg9-BK (P<0.01), or 30 and 60 min before the cellular peak, respectively. In contrast, an i.t. injection of the B2 bradykinin selective receptor antagonist Hoe 140 (30 nmol per site), at a dose which consistently antagonized bradykinin (10 nmol per site)-induced pleurisy, had no significant effect on des-Arg9-BK-induced pleurisy. 4 An i.t. injection of the selective tachykinin receptor antagonists (NK1) FK 888 (1 nmol per site), (NK2) SR 48968 (20 nmol per site) or (NK3) SR 142801 (10 nmol per site), administered 5 min before pleurisy induction, significantly antagonized neutrophil migration caused by i.t. injection of des-Arg9-BK. In addition, FK 888 and SR 142801, but not SR 48968, also prevented the influx of mononuclear cells in response to i.t. injection of des-Arg9-BK (P<0.01). However, the NK3 receptor antagonist SR 142801 (10 nmol per site) also significantly inhibited des-Arg9-BK-induced plasma extravasation. An i.t. injection of the calcitonin gene-related peptide (CGRP) receptor antagonist CGRP8-37 (1 nmol per site), administered 5 min before pleurisy induction, inhibited des-Arg9-BK-induced plasma extravasation (P<0.01), without significantly affecting the total and differential cell migration. 5 The nitric oxide synthase inhibitors L-NOARG and L-NAME (1 pmol per site), administered 30 min beforehand, almost completely prevented des-Arg9-BK (i.t.)-induced neutrophil cell migration (P<0.01), and, to a lesser extent, mononuclear cell migration (P<0.01). The D-enantiomer D-NAME had no effect on des-Arg9-BK-induced pleurisy. At the same dose range, L-NOARG and L-NAME inhibited the total cell migration (P<0.01). L-NAME, but not L-NOARG caused significant inhibition of des-Arg9-BK-induced fluid leakage. Indomethacin (1 mg kg(-1), i.p.), administered 1 h before des-Arg9-BK (30 nmol per site), inhibited the mononuclear cell migration (P<0.05), but, surprisingly, increased the neutrophil migration at 4 h without interfering with plasma extravasation. The administration of terfenadine (50 mg kg(-1), i.p.), 30 min before des-Arg9-BK (30 nmol per site), did not interfere significantly with the total cell migration or with the plasma extravasation in the mouse pleurisy caused by i.t. injection of des-Arg9-BK. 6 Pretreatment of animals with the lipopolysaccharide of E. coli (LPS; 10 microg per animal, i.v.) for 24 h did not result in any significant change of the inflammatory response induced by i.t. injection of des-Arg9-BK compared with the saline treated group. However, the identical treatment of mice with LPS resulted in a marked enhancement of des-Arg9-BK induced paw oedema (P<0.01). 7 In conclusion, we have demonstrated that the inflammatory response induced by i.t. injection of desArg9-BK, in a murine model of pleurisy, is mediated by stimulation of constitutive B1 receptors. (These responses are largely mediated by release of neuropeptides such as substanceP or CGRP and also by NO, but products derived from cyclo-oxygenase pathway and histamine seem not to be involved. Therefore, these results further support the notion that the B1 kinin receptor has an important role in modulating inflammatory responses, and it is suggested that selective B1 antagonists may provide therapeutic benefit in the treatment of inflammatory and allergic conditions.

Animals↗