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At least 19 recordsLinked to original sources
PubMed1987

Antitumor activity of pleural cavity macrophages and its regulation by pleural cavity lymphocytes in patients with lung cancer.

Antitumor activities of pleural cavity macrophages (PCM) and pleural cavity lymphocytes (PCL) in lung cancer patients were examined. The effect of coculture supernatants of PCL and autologous tumor cells on the cytostatic activity of macrophages was also examined. Cytostatic activity of PCM was not affected by an advance of metastasis to regional lymph nodes or increase of tumor size and difference of histological type. However, the cytostatic activity of PCM was markedly augmented when pleural invasion was limited to within the visceral pleura although it was low when pleural invasion was absent or extended beyond the visceral pleura. On the other hand, PCL did not exert any cytolytic activity against various tumor target cells. However, coculture supernatants of PCL and autologous tumor cells exhibited the activity of macrophage-activating factor against guinea pig peritoneal macrophages. Furthermore, the higher the cytostatic activity of PCM, the higher the macrophage-activating factor activity of the coculture supernatant of PCL and autologous tumor cells was. These results suggested that antitumor activity of PCM was controlled by specifically sensitized PCL through lymphokines.

Animals↗
PubMed1998

A case of ruptured descending thoracic aortic aneurysm into the right pleural cavity: importance of preoperative drainage of the right pleural cavity.

We present an unusual case of a ruptured descending thoracic aortic aneurysm into the right pleural cavity of a patient with pectus carinatum. The presence of pectus carinatum played an important role in the development of the aneurysm at the atypical site and the rupture into the right pleural cavity. A small amount of right pleural bleeding on admission can increase and develop to massive hemothorax until emergency operation. Massive bleeding in the right pleural cavity where the dependent lung is located causes atelectasis and increased shunt fraction under one lung ventilation. Therefore, continuous drainage of the right pleural cavity is essential to prevent serious hypoxia during graft replacement in a case of ruptured descending thoracic aneurysm into the right hemithorax.

Aged↗
PubMed1989

Breakage and detachment of an Abrams needle in the pleural cavity during performance of a pleural biopsy.

This is the report of a case of breakage and detachment in the pleural cavity of the tip of a nearly new Abrams needle during performance of a pleural biopsy. We have not found any reference in the literature to similar accidents and do not know what later complications may be produced by the metal body in the pleural cavity. In this case, there have been no complications 12 months after the incident.

Aged↗
PubMed1984

The value of pleural fluid carcinoembryonic antigen estimation in the diagnosis of malignant tumours of the pleural cavity.

Measurement of pleural fluid and blood carcinoembryonic antigen (CEA) concentrations as well as estimations of pleural fluid protein, lactic acid dehydrogenase and sugar levels were carried out in 45 patients with pleural effusions in order to determine the value of these biochemical parameters in the diagnosis of malignant tumours involving the pleural space. The study population included individuals with epithelial and non-epithelial malignant tumours involving the pleural cavity as well as patients with inflammatory effusions and patients with transudates due to cardiac, renal or hepatic disease. Pleural fluid CEA content was the single most useful measurement in distinguishing epithelial malignant tumours from other causes of pleural effusion. In addition, the pleural fluid CEA/blood CEA ratio was greater than 1 in most patients with epithelial cancer of the pleural space, suggesting that local production of CEA is responsible for elevated values in the pleural fluid.

Carcinoembryonic Antigen↗
PubMed1993

Phenotypes and lymphokine-activated killer activity of pleural cavity lymphocytes of lung cancer patients without malignant effusion.

We examined the phenotypes of lymphocytes in the pleural cavity of 23 lung cancer patients without malignant effusion. The ability of those lymphocytes to develop lymphokine-activated killer (LAK) activity and the regulation of LAK by pleural cavity macrophages were also compared with their counterparts in the peripheral blood. Mononuclear cells (MNC) were obtained simultaneously from the blood and by lavage of the pleural cavity of patients with lung cancer. The proportion of the T-cell subset of HLA-DR+ cells was significantly higher in the pleural cavity than in the peripheral blood, but the proportions of CD3+ and CD8+ cells in the pleural cavity were similar to the corresponding proportions in the blood. The proportions of CD4+ and CD16+ cells were lower in the pleural cavity than in the blood. The LAK activity could be developed by MNC from the pleural cavity following incubation with interleukin 2 (IL-2), but the LAK activity of pleural cavity MNC was significantly less than that of peripheral MNC. Pleural cavity lymphocytes alone also developed LAK activity following incubation with IL-2. Pleural macrophages from the patients were regulated to augment in vitro induction of LAK activity by IL-2 from autologous blood lymphocytes and pleural cavity lymphocytes. Lymphocytes in the pleural cavity without malignant pleural effusion could be developed by LAK activity and this activity was augmented by pleural cavity macrophages. The LAK activity developed by pleural cavity lymphocytes was significantly lower than that developed by peripheral blood lymphocytes. However, they can change their population to include cells with higher activities on exposure to IL-2 against the invasion of lung cancer cells into the pleural cavity. Thus, the population of lymphocytes in the pleural cavity of patients with lung cancer without malignant pleural effusion was different from that in malignant pleural effusion.

Aged↗
PubMed1997

The role of gammadelta T lymphocytes in lipopolysaccharide-induced eosinophil accumulation into the mouse pleural cavity.

LPS induces an accumulation of eosinophils in the pleural cavity that requires resident macrophages and lymphocytes, but is independent of IL-5 production. In the present study we investigated the involvement of different T lymphocyte subsets on the modulation of LPS-induced eosinophil accumulation into the pleural cavity of mice. Within 4 h after LPS injection the number of neutrophils in the pleural cavity increased significantly. Mononuclear cell counts increased after 12 h, while a significant rise on eosinophil counts was observed only after 24 h. T lymphocytes counts were increased in the pleural cavity 24 and 48 h after LPS administration. This T lymphocyte accumulation was accounted for by an influx of the gammadelta+ subset, while CD4+ and CD8+ subsets did not accumulate in the pleural cavity after LPS stimulation. All those changes had resolved 96 h after LPS injection. Depletion of T lymphocytes by treatment with mAb anti-Thy 1.0 inhibited the eosinophil accumulation triggered by LPS. Aiming to clarify which T lymphocyte subset would be involved in the LPS-induced eosinophil accumulation, we depleted mice of various T lymphocyte subpopulations using specific Abs. Depletion of either CD4+ or CD8+ subsets failed to inhibit LPS-induced eosinophil migration. In contrast, when mice were treated with anti-gammadelta+ T lymphocyte mAb, a significant reduction of LPS-induced eosinophil accumulation was observed. Similarly, the administration of LPS in BALB/c-nu/nu mice induced the expected significant influx of eosinophils into the pleural cavity. Our results indicate that the gammadelta+ T lymphocytes are centrally involved in LPS-induced eosinophil accumulation in mice.

Animals↗
PubMed2001

Diffusion of nitrous oxide into the pleural cavity.

We postulated that nitrous oxide transfer into the pleural cavity can occur by diffusion from the alveoli, independent of vascular transport. Under general anaesthesia, six sheep were studied in two phases, a control and an experimental phase. The sheep were anaesthetized, intubated, and received positive pressure mechanical ventilation. A catheter was placed in the right pleural cavity and 150 ml air injected. The animals were ventilated with 100% oxygen. The inspired gas was changed to a mixture of 50% nitrous oxide and 50% oxygen, and the rate of increase of nitrous oxide concentration in the pleural space was measured. The animals were then ventilated with 100% oxygen and then killed by exsanguination while ventilation was continued. The inspired mixture was changed to 50% nitrous oxide and 50% oxygen and the rate of increase in nitrous oxide concentration was measured in the pleural space again. During venitilation with nitrous oxide in the living animals, the concentration of nitrous oxide in the pleural cavity increased rapidly and decreased to zero during ventilation with 100% oxygen. During ventilation without circulation, the rate of increase in the concentration of nitrous oxide in the pleural cavity was the same as in the control phase. This suggests that nitrous oxide enters the pleural space by diffusion, rather than by vascular delivery. This mechanism may explain the rapid increase in the volume of pneumothorax if nitrous oxide is given in the inspired gas.

Anesthetics, Inhalation↗
PubMed1994

Epstein-Barr virus-associated primary malignant lymphomas of the pleural cavity occurring in longstanding pleural chronic inflammation.

Primary pleural non-Hodgkin's lymphomas (NHLs) have been described mostly in Japan and occasionally in western countries. We report three cases occurring in nonimmunocompromised patients demonstrating close similarities to the Japanese cases. These lymphomas occurred more than 20 years after thoracoplasty for the treatment of pleural or pulmonary tuberculosis. They were all high grade lymphomas of B phenotype (two immunoblastic with plasmocytoid differentiation and one immunoblastic with anaplastic large cells). In situ hybridization (ISH) detected small nuclear RNAs encoded by Epstein-Barr virus (EBERs) in most lymphomatous cells in all cases. This suggests a link between primary pleural lymphoma and the longstanding chronic inflammation, which could favor a clonal evolution of Epstein-Barr virus (EBV)-infected B cells through the production of growth factors or immunosuppressive cytokines produced by inflammatory cells.

Aged↗
PubMed2003

Morphological analysis of leucocyte transmigration in the pleural cavity.

The role that pleural mesothelial cells play in leucocyte transmigration into the pleural cavity was investigated in lipopolysaccharide-stimulated mice. Changes in mesothelial cell morphology and changes in expression of adhesion molecules on mesothelial cells and leucocytes were analysed by light microscopy, immunohistochemistry, transmission electron microscopy (TEM) and immuno-scanning electron microscopy (immuno-SEM). After stimulation, the mesothelial cells separated completely from one another before leucocyte penetration across the mesothelial layer occurred. These changes occurred primarily in the immediate vicinity of ribs, where a large number of leucocytes accumulated. Immuno-SEM showed that the expression of intercellular adhesion molecule-1 (ICAM-1) on the parietal pleural mesothelial cells was significantly up-regulated by lipopolysaccharide stimulation, and that of vascular cell adhesion molecule-1 (VCAM-1) was induced. Both were restricted to the microvilli of the mesothelial cells. By contrast, expression of intercellular adhesion molecule-2 (ICAM-2), platelet/endothelial cell adhesion molecule-1 (PECAM-1), mucosal addressin cell adhesion molecule-1 (MAdCAM-1), endothelial leucocyte adhesion molecule-1 (ELAM-1), peripheral node addressin (PNAd) and fibronectin were not detected. Lymphocyte function associated antigen-1 (LFA-1), macrophage-1 molecule (Mac-1) and very late appearing antigen-4 (VLA-4), all ligands of ICAM-1 and VCAM-1, were present on the transmigrated neutrophils and macrophages. These findings demonstrate that the immediate vicinity of ribs is a source of leucocyte migration into the pleural space.

Animals↗
PubMed1985

[Response and pharmacokinetics of cisplatin instilled into the pleural cavity].

The response and pharmacokinetics of cisplatin instilled into the pleural cavity were studied in 11 patients with malignant pleural effusion; 10 patients had primary lung cancer and one had breast cancer. All of them were adenocarcinoma histologically. In five of the 11 patients effusion disappeared and its cytology became negative for malignancy after four weeks. In the other six patients effusion was reduced and its cytology became negative for malignancy after four weeks. Toxicity was almost similar to that in systemic administration of cisplatin but a few patients had chest pain and fever possibly due to local irritation. The pharmacokinetics showed that a high concentration of cisplatin (free-form, 48.9 micrograms/ml) was maintained over a long period (free from (t 1/2) beta = 33.6 hours) in the pleural cavity. This was regarded as the reason for the high response to this therapy. The intrapleural instillation of cisplatin into the pleural cavity therefore seems to be an effective modality for malignant pleural effusion.

Aged↗
PubMedDate not supplied

Pharmacokinetics of hypotonic cisplatin chemotherapy administered into the peritoneal and the pleural cavities in experimental model.

The pharmacokinetics of intraperitoneal (i.p.) and intrapleural (i.pl.) hypotonic cisplatin (CDDP) were compared under the same experimental conditions. The same dose of CDDP was administered in hypotonic (62 mOsm/L) and isotonic (308 mOsm/L) solutions to the peritoneal and pleural cavities of Ehrlich carcinoma cell bearing mice. The intracellular amount of platinum increased for more than 60 minutes after an i.pl. injection of the hypotonic solution of CDDP, whereas it increased for up to 30 minutes after an i.p. injection. Although hypotonic conditions augmented the amount of platinum taken-up by Ehrlich cells, the amount was significantly greater in the pleural cavity than in the peritoneal cavity. In Donryu rats, the levels of platinum in the i.p. and i.pl. fluids decreased rapidly after injection of hypotonic solution as compared with isotonic solution. The extent of this decrease was greater in the peritoneal cavity than in the pleural cavity. In the hypotonic condition, the area under the curve of concentration versus time (AUC) for platinum of i.pl. fluid was greater than that of i.p. fluid. When i.p. and i.pl. hypotonic CDDP were administered, the osmolarity of the fluid returned rapidly to the isotonic level, with equilibration in 30 or 180 minutes respectively. The lower osmolarity continued for a longer duration in the pleural cavity than in the peritoneal cavity. These results indicate that the pleural cavity may require a smaller amount of CDDP to achieve the same effect on intracellular uptake of platinum than the peritoneal cavity.

Animals↗
PubMed1998

Talc-induced inflammation in the pleural cavity.

Talc administration into the pleural cavity induces pleurodesis. To obtain further insight into the inflammatory process that causes pleurodesis, the cellular kinetics in the pleural space after the administration of talc was studied, along with its relation to chemokine concentrations in the pleural fluid. Thirteen consecutive patients with idiopathic spontaneous pneumothorax and eight patients with malignant pleural effusions received talc pleurodesis. The first group was treated with talc poudrage, whereas the second group was treated with talc slurry. Pleural fluids were isolated before talc administration as well as 3, 6, 24, 48 and 72 h afterwards. The talc induced a rapid polymorphonuclear neutrophil (PMN) influx followed by an accumulation of macrophages. In addition, increased production of interleukin (IL)-8 and monocyte chemotactic protein (MCP)-1 was observed. The talc-induced PMN influx reached its maximum after 3-24 h, and was related to the IL-8 concentration. In contrast, the MCP-1 was not related to the macrophage accumulation. Talc-induced inflammation in patients with idiopathic spontaneous pneumothorax and malignant pleural effusion is characterized by an influx of polymorphonuclear neutrophils related to interleukin-8, followed by an accumulation of monocytes.

Adult↗