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(Chest. 2004;125:2268-2277.)
© 2004 American College of Chest Physicians

Talc and Silver Nitrate Induce Systemic Inflammatory Effects During the Acute Phase of Experimental Pleurodesis in Rabbits*

Evaldo Marchi, MD, FCCP; Francisco S. Vargas, MD, FCCP; Milena M. P. Acencio, PhD; Leila Antonangelo, MD; Lisete R. Teixeira, MD; Eduardo H. Genofre, MD and Richard W. Light, MD, FCCP

* From the Pulmonary Division (Drs. Marchi, Vargas, Acencio, Antonangelo, Teixeira, and Genofre), Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil; and Saint Thomas Hospital (Dr. Light), Nashville, TN.

Correspondence to: Richard W. Light, MD, FCCP, Director of Pulmonary Disease Program, Saint Thomas Hospital, 4220 Harding Rd, Nashville, TN 37205; e-mail: RLIGHT98{at}yahoo.com


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: To determine whether talc (TL) and silver nitrate (SN), two effective pleurodesis agents, induce a systemic inflammatory response in the acute phase of experimental pleurodesis in rabbits.

Design: Samples of blood and pleural fluid were collected after 6, 24, and 48 h from rabbits injected intrapleurally with 3 mL saline solution, TL (400 mg/kg), or 0.5% SN, and were assayed for WBC count, percentage of neutrophils, and levels of lactate dehydrogenase (LDH), interleukin (IL)-8, and vascular endothelial growth factor (VEGF). The pleural liquid production was compared in the three different groups. A sample of blood collected from animals preinjection was used as the control.

Results: At 6 h after pleural injection, the mean blood WBC count and percentage of neutrophils were significantly elevated in the TL group, whereas the mean LDH and IL-8 levels were significantly increased in the SN group. VEGF was undetectable in the preinjection serum and saline solution-injected animals, but was increased in the serum after the pleural injection of both TL and SN to a comparable degree. SN elicited a more intense acute pleural inflammation reaction than did TL, with higher WBC count and IL-8 levels found in the pleural fluid, mainly within the first 6 h. LDH and VEGF levels, and pleural liquid production were also higher for SN, and they increased with time.

Conclusions: In the acute phase of pleural injection, TL induced a transient increase in blood WBC count and percentage of neutrophils, while SN induced increases in blood LDH and IL-8 levels. Both TL and SN induced significant increases in blood VEGF levels. SN induced an earlier and more intense acute pleural inflammation than TL. Pleural liquid VEGF levels were higher after SN injection and increased, as did pleural liquid production. These findings suggest that the intrapleural injection of TL and SN produce a systemic inflammatory response that may have a role in the pathogenesis of fever and ARDS, which occur with pleurodesis.

Key Words: inflammation • interleukin-8 • pleura • pleurodesis • silver nitrate • talc • vascular endothelial growth factor


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Pleurodesis is routinely used for the treatment of recurrent malignant pleural effusions. Many agents have been used to produce a pleural symphysis, including silver nitrate (SN), quinacrine, tetracycline and its derivatives doxycycline and minocycline, bleomycin, Corynebacterium parvum, and talc (TL), with different degrees of success.1 Therapy with SN, which was one of the first agents used to control recurrent pneumothorax, was abandoned apparently because it caused intense pain.2 The antimalarial agents, particularly quinacrine, are known to induce fever and multiple pleural loculations.34 Tetracycline is no longer commercially available and has been replaced mainly by doxycycline, which also causes intense pain.567891011 Bleomycin, an antineoplastic agent, was once extensively used,1213141516 but it is expensive and did not induce pleurodesis in rabbits.17 C parvum, used mostly in Europe, also was abandoned because its commercial production was stopped.1819 Today, TL is the agent most frequently used for therapy, with a reported success rate of at least 90%. Other advantages of TL include its wide availability, its low cost, and its effectiveness when administered in a minimally invasive procedure (slurry) or by thoracoscopy.20212223 Nonetheless, several cases of ARDS have been reported in association with TL pleurodesis. In one study,24 the insufflation of TL via thoracoscopy in 614 patients with benign and malignant pleural effusions was associated with the development of ARDS in 7 patients (1.2%), which was fatal in 3 patients. Although this is commonly believed to be a rare complication, Rehse and coworkers25 have reported an incidence of 9% in 89 procedures. Experimentally, the presence of TL particles has been demonstrated in multiple organs after its intrapleural injection in normal rats and rabbits.2627 It is not clear whether acute respiratory failure after TL pleurodesis is related to the TL itself. It is thought that TL may induce a systemic inflammatory response due to several factors, including the systemic absorption of TL or its contaminants. These adverse responses to TL have generated interest in alternative agents for pleurodesis.

SN was one of the first agents used for pleurodesis in concentrations varying from 1 to 10% and had a success rate of 75 to 90%.282930 In a rabbit model with normal pleura, the intrapleural injection of 0.5% SN produced a pleurodesis similar to that produced by 35 mg/kg tetracycline31 and was superior to that induced by TL slurry, 400 mg/kg.32 Of concern was the possibility that, due to its intense local caustic effect, SN could produce lung damage. However, in a subsequent 1-year follow-up study, SN induced only minimal microscopic lung damage that decreased after 2 weeks, and was similar to that produced by TL after 21 days.33

In the present study, the effects of the intrapleural injection of TL or SN on WBC count, neutrophil percentage, lactate dehydrogenase (LDH), interleukin (IL)-8, and vascular endothelial growth factor (VEGF) levels in the serum and the pleural fluid 6, 24, and 48 h after injection were studied. IL-8 was chosen because its role in pleural inflammation is well-established, and it is known that inflammatory stimuli, asbestos fibers, and infective agents stimulate significant increases in the production of IL-8 by the mesothelial cells.34 VEGF was chosen because its levels are increased in exudative effusions, and it increases the vascular permeability.34 We hypothesized that the intrapleural injection of TL and SN in doses sufficient to induce pleurodesis would induce an acute systemic inflammatory response.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Pleural Injection
Fifty-four white New Zealand male rabbits (nine groups of 6 rabbits) weighing 2.0 to 2.5 kg were subjected to an intrapleural injection of 3 mL saline solution, TL, 400 mg/kg (USP Pharmacy; Sao Paulo, Brazil), or 0.5% SN (Merck; Darmstadt, Germany). These doses were selected because they have been shown previously313233 to induce pleurodesis in our experimental model in rabbits. Groups of six rabbits receiving each agent were killed after 6, 24, and 48 h. Briefly, the rabbits were anesthetized with ketamine hydrochloride, 35 mg/kg (Cristalia; Sao Paulo, Brazil), plus xylazine hydrochloride, 5 mg/kg (Bayer; Sao Paulo, Brazil), and had their right chests shaved and cleansed with povidone-iodine solution (Rioquimica; Sao Paulo, Brazil). A parasternal 2-cm chest incision was made, and a 21-gauge needle was inserted through the intercostal muscle for the injection of the solution into the pleural space. After the instillation, the muscle and skin were sutured with nylon 5–0. The animals were killed with a lethal injection of pentobarbital (USP Pharmacy). Immediately before the pentobarbital injection, a blood sample from each animal was collected for comparison with normal blood parameters from noninjected rabbits. After death, the animals were exsanguinated by aortic section through a middle abdominal incision, and a 21-gauge needle was inserted through the diaphragm to aspirate the fluid. After the fluid was aspirated, the thoracic cavity was opened and grossly inspected for the presence of TL. Animals injected with saline solution were used as benign noninflammatory controls. Blood samples were collected from a group of six noninjected rabbits as controls on the measurements in the blood of the injected animals. The study was approved by the Ethics Committee of the Heart Institute (InCor), University of Sao Paulo Medical School, which oversees research involving both animals and humans.

Reagents
TL, a magnesium silicate asbestos-free particle with a mean length of 25.4 µm (length range, 6.4 to 50.5 µm), was suspended under sterile conditions in endotoxin-free saline solution to a concentration of 400 mg/kg. SN was suspended in endotoxin-free H2O at a concentration of 0.5% for intrapleural injection.

Cytologic and Biochemical Analysis
Blood and pleural liquid were collected in ethylenediaminetetraacetic acid for cytologic and cytokine analysis, and in dry tubes for LDH evaluation. Samples were placed in a hemocytometer for determination of the total number of leukocytes, and onto slides for Leishman preparation and determination of the percentage of neutrophils. Other samples were centrifuged at 1,000 revolutions per minute for 10 min at 4°C, and the supernatants were withdrawn immediately for LDH analysis and were stored at –80°C for cytokine determination. LDH was measured by a standard biochemical kinetic UV method (range of normal serum values for the method, 120 to 240 IU/L).

Cytokines Analysis
IL-8 (OptEIA, rabbit IL-8 set; Pharmingen; San Diego, CA) and VEGF (R&D Systems; Minneapolis, MN) were measured by enzyme-linked immunosorbent assay according to the manufacturers’ directions. Quantification of IL-8 and VEGF was done by comparison of the optical density in the enzyme-linked immunosorbent assay reader (Power Wave; Bio-Tek; Winooski, VT) using a 450-nm filter with the optical density of controls.

Statistical Analysis
The data are expressed as the mean ± SD. Statistical analyses were performed using statistical computer software (SigmaStat; SPSS; San Rafael, CA). One-way analysis of variance was used to compare the levels among subgroups, and the Tukey test was used to perform multiple comparison procedures. If the log-transformed data did not satisfy the normality and equal variance tests, Kruskal-Wallis one-way analysis of variance on ranks was used to compare the levels among subgroups, and the Dunn method was used to perform multiple comparison procedures. Paired t tests were used to compare the cytokine levels in the blood and pleural fluid. Linear regression was used to analyze the relationship between the serum cytokine (dependent variable) and the pleural fluid cytokine level. A p value of < 0.05 was accepted as being significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Blood
Leukocytes: The intrapleural injection of all three agents led to an increase in the peripheral WBC count, but only the WBC count at 6 h after TL injection (10 ± 3.3 x 103 cells/mm3) was significantly higher than the control value (5.1 ± 1.3 x 103 cells/mm3) [p < 0.05]. The comparison among injected groups at different times showed no significant differences in WBC count (Fig 1 ).



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  		Figure 1.. Blood WBC count in controls, and in rabbits injected with saline solution, TL, and SN. * = p < 0.05 compared with TL-injected rabbits 6 h after injection.

 
Neutrophils: As observed with the blood WBC count, the percentage of blood neutrophils also was increased 6 h after the injection of each of the three agents, but only the TL group (73 ± 11%) differed significantly from the control group (53 ± 7%; p < 0.05). Subsequently, the percentage of neutrophils decreased with time in the TL group, and after 48 h the SN group had a significantly higher mean percentage of neutrophils than did the TL group (55 ± 14% vs 29 ± 9%, respectively). When changes with time in the neutrophil counts in the different groups were analyzed, the neutrophil counts in both the TL and SN groups tended to decrease with time (Fig 2 ).



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  		Figure 2.. Blood neutrophil percentages in controls, and rabbits injected with saline solution, TL, and SN. * = p < 0.05 (TL group at 6 h vs control, saline solution at 6 h, and the TL group at 24 and 48 h); # = p < 0.05 (TL group at 24 h vs TL group at 48 h and the SN group at 24 h); x = p < 0.05 (SN group at 6 h vs SN group at 24 h); + = p < 0.05 (SN group at 48 h vs TL group at 48 h).

 
LDH: The intrapleural injection of SN, but not TL or saline solution, led to a short-term increase in serum LDH levels. The mean serum LDH level was significantly higher 6 h after the injection of SN (540 ± 215 IU/L) than after the injection of TL (300 ± 91 IU/L) or saline solution (238 ± 150 IU/L), or compared to the levels in the controls (217 ± 84 IU/L). The increase in the serum LDH level following SN injection had disappeared by 24 and 48 h (Fig 3 ).



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  		Figure 3.. Serum LDH levels in controls, and in rabbits injected with saline solution, TL, and SN. * = p < 0.05 (SN group at 6 h vs controls, and animals injected with saline solution and TL at 6 h, and those injected with SN at 24 and 48 h).

 
IL-8: The intrapleural injection of all three agents led to an increase in serum IL-8 levels. The serum IL-8 levels tended to increase with time in all groups. The serum levels of IL-8 after the intrapleural injection of SN were significantly higher than those after the intrapleural injection of saline solution at all three time periods, and those after the intrapleural injection of TL at 6 and 24 h (Fig 4 ).



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  		Figure 4.. Serum IL-8 levels in controls, and in rabbits injected with saline solution, TL, and SN. * = p < 0.05 (controls vs all other measurements); # = p < 0.05 (rabbits injected with saline solution at 24 and 48 h vs those injected at 6 h); x = p < 0.05 (TL group at 48 h vs TL group at 6 and 24 h); + = p < 0.05 (SN group at 6 h vs TL group 6 h).

 
VEGF: The intrapleural injection of both TL and SN led to significant increases in the serum levels of VEGF. Serum VEGF was undetectable (< 15 pg/mL) in the serum samples of controls and of animals injected with saline solution. The mean serum levels of VEGF in the TL and SN groups were significantly greater than those in the control group or those in the animals injected with saline solution. There was no statistical difference between the mean levels of VEGF in the TL and SN groups (Fig 5 ).



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  		Figure 5.. Serum VEGF levels in controls, and in rabbits injected with saline solution, TL, and SN. * = p < 0.05 (all TL group and all SN group vs controls and all saline solution group; there was no difference between the TL and SN groups).

 
Pleural Fluid
Leukocytes: The pleural fluid WBC count was higher in the SN group than in the TL group, and the difference was statistically significant at 48 h (Table 1 ).


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  		Table 1.. Pleural Fluid WBC Counts, Neutrophil Percentages, LDH Levels, and Pleural Fluid Volume in Rabbits Injected With TL and SN*

 
Neutrophils: The predominant pleural fluid cells at all time points in both the TL and SN groups were neutrophils. The percentage of neutrophils decreased significantly with time in only the TL group (Table 1).

LDH: After the intrapleural injection of TL, the highest pleural fluid LDH level was at 6 h, and there was a significant decrease by 48 h. In contrast, after the intrapleural injection of SN, the highest pleural fluid LDH level was at 48 h, and, indeed, the pleural fluid LDH level at that time point was significantly higher than that at 6 or 24 h in the SN group, or at any time point in the TL group (Table 1).

Pleural Fluid Volume: The pleural fluid volume was significantly greater after the intrapleural injection of SN than it was after the intrapleural injection of TL at each time point (Table 1). The amount of pleural fluid tended to increase with time in both groups.

IL-8: There were detectable levels of IL-8 in the pleural fluid after the intrapleural injection of both TL and SN. The highest level of pleural fluid IL-8 occurred in the SN group 6 h after injection, and this level was significantly higher than the levels occurring at 24 or 48 h after SN injection or at any time after the injection of TL (Table 2 ). The pleural fluid levels of IL-8 were comparable to those in serum, except for the level 6 h after SN injection, which was significantly higher than the serum level (Table 2).


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  		Table 2.. Comparison Between Serum and Pleural Fluid Levels of IL-8 and VEGF in TL and SN-Injected Rabbits*

 
VEGF: The pleural fluid VEGF levels tended to increase after the injection of both agents. The pleural fluid VEGF levels were significantly higher in the SN groups at 6 and 24 h.

Comparison Between Serum and Pleural Fluid IL-8 and VEGF Levels
IL-8 levels were significantly higher in the pleural fluid than in the serum at 6 h in the SN group. In contrast, IL-8 levels were significantly higher in the serum than in the pleural fluid at 48 h in both groups (Table 2). VEGF levels were significantly higher in the pleural fluid than in the serum at all time points for both agents (Table 2). The serum levels of VEGF were significantly correlated with the pleural fluid levels of VEGF in both groups (TL group: r = 0.74; p < 0.001; SN group: r = 0.72; p < 0.001) [Fig 6 , 7 ]. In contrast, the serum levels of IL-8 did not correlate as well with the pleural fluid levels (TL group: r = 0.45; p = 0.04; SN group: r = 0.50; p = 0.03).



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  		Figure 6.. Comparison of VEGF levels (pg/mL) in the serum and pleural fluid of TL-injected rabbits.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The present study demonstrates that both TL and SN, when injected intrapleurally, induce an acute systemic inflammatory response. After 6 h, TL induced a predominant cellular response, with an increased blood WBC count and neutrophil percentage that decreased with time, equaling those of the control group after 48 h. The serum levels of VEGF also increased in the short term in animals injected with TL and remained elevated at 48 h after pleural injection.

SN also induced a systemic response, with increases in serum LDH, IL-8, and VEGF levels. The serum LDH level increased 6 h after injection, and decreased after 24 and 48 h. The serum levels of IL-8 were higher than those of animals injected with saline solution at all three time periods, and were higher than those of animals injected with TL at 6 and 24 h. The serum VEGF levels in the SN group were significantly greater than those in the control group or in animals injected with saline solution.

There have been only a limited number of previous studies that examined changes in the blood or serum after the intrapleural injection of sclerosing agents. In one study in rabbits,35 the intrapleural injection of TL led to a significant increase in the angiotensin-converting enzyme activity in serum, whereas the intrapleural injection of doxycycline led to increases in liver function enzymes and produced lung toxicity for 30 days. In a clinical study,36 the intrapleural injection of both TL and tetracycline induced significant increases in serum C-reactive protein levels 48 h after the injection, but the increases after TL injection were significantly greater than the increases after tetracycline injection. In the same study, the intrapleural injection of TL, but not of tetracycline, led to decreased levels of oxygen saturation and to decreases in lung clearance, as measured by a 99mTc-diethylenetriaminepentaacetate scan 48 h after the injection.

The mechanisms by which TL induces a systemic inflammatory response remain unknown. One possible mechanism is the migration of TL particles to other organs such as the lung, spleen, liver, and kidneys, where its presence could elicit an inflammatory response. Indeed, after the intrapleural administration of TL in rats26 and rabbits,27 TL particles have been found in various organs. Moreover, TL particles were found disseminated throughout the body in one patient who died of ARDS following TL administration.37 It has been hypothesized that this systemic dissemination of TL is more likely if TL with a smaller mean particle size is used.27383940 TL particles have been shown to vary markedly in median particle size.2739 It is hypothesized that small TL particles can enter the lymphatic system in the parietal pleura and subsequently can gain access to the systemic circulation. It should be noted that in the present study, TL with a relatively high mean particle size was used. It would be interesting to compare the systemic responses to animals that receive relatively large and relatively small TL particles. A second possible mechanism for the systemic inflammatory response induced by the administration of TL intrapleurally is the transpleural transfer of TL, which then could induce inflammation in the lung.27 A third possible mechanism is the systemic absorption of TL contaminants such as endotoxin.38 A fourth possible mechanism is the intrapleural generation of large amounts of cytokines that could be absorbed systemically to induce a systemic inflammatory response. Indeed, the observation in the present study that the pleural fluid levels of VEGF were significantly higher than the serum levels, and that there was a significant correlation between the serum and pleural fluid levels of VEGF supports this hypothesis.

One possible explanation for the delayed maximal responses after the intrapleural injection of TL could be its persistence in the pleural space. In fact, in this study TL was visible intrapleurally at autopsy as a patchy aggregation in all rabbits that had received it.

The present study also demonstrates that the intrapleural administration of SN induced systemic effects. Although the increases in serum VEGF levels were comparable after the intrapleural injection of both agents, the intrapleural injection of TL elicited a greater increase in LDH and IL-8, and a smaller increase in the blood WBC count and percentage of neutrophils.

Although there have been reports of adverse systemic effects in humans when TL has been administered intrapleurally, there have been limited reports on the systemic effects after the intrapleural administration of this low dose of SN. One study (an abstract)41 injected the same concentration of SN in an attempt to induce pleurodesis in patients with malignant pleural effusions. In that clinical study, 47 patients were randomized to receive 5 g TL slurry or 20 mL 0.5% SN. In that study, TL was effective in 21 of 24 patients (87.5%), and SN was effective in 22 of 23 patients (95.6%). The only significant side effect was pain requiring therapy with analgesics. No patient receiving either drug developed ARDS.41

We also observed that both agents produced an acute and intense pleural inflammation, which was more pronounced with SN. For the TL group, pleural fluid WBC count, neutrophil percentage, and LDH level increased in the first 6 h and tended to decrease with time, which is similar to what was observed in the blood. For the SN group, the cellular influx to the pleural cavity was acute and was sustained with a progressive increase in LDH level.

As observed in serum, the IL-8 level in pleural fluid increased within the first 6 h after injection only in the SN group, and the VEGF level increased with time after injection with both agents, following the pattern of pleural fluid production. These findings suggest that SN tends to produce an intense compartmentalized inflammatory response that is characterized predominantly by biochemical and cytokine local production, and that IL-8 plays an important role in the recruitment of inflammatory cells to the pleural cavity in the acute phase of pleurodesis with SN. The decreased level of IL-8 in pleural fluid with time may be due to intense proteolysis, the presence of an unknown antagonist, or the action of another predominant inflammatory mediator in the pleural cavity. Pleural VEGF levels in serum increased by twofold to 12-fold for TL, and by 10-fold to 20-fold for SN, in comparison with serum levels in the control group and in animals injected with saline solution. We speculate that VEGF may be one of mediators involved in the maintenance of the inflammatory process when the levels of pleural fluid IL-8 decrease and may influence the pleural fluid production.

In conclusion, both TL and SN injected intrapleurally induced an acute systemic inflammatory response of variable degree. TL induced a predominantly cellular inflammatory response in the first 6 h. SN also produced a systemic response, with predominant increases in LDH, IL-8, and VEGF production. We think that further studies are needed in experimental animals and in patients receiving these agents for pleurodesis to determine the significance of these acute systemic inflammatory effects.



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  		Figure 7.. Comparison of VEGF levels (pg/mL) in the serum and pleural fluid of SN-injected rabbits.

 

   Footnotes
 
Abbreviations: IL = interleukin; LDH = lactate dehydrogenase; SN = silver nitrate; TL = talc; VEGF = vascular endothelial growth factor

This research was supported by the Foundation to Support Research from the State of Sao Paulo (FAPESP) and by the National Board of Scientific and Technologic Development (CNPq) of Brazil.

Received for publication April 7, 2003. Accepted for publication December 10, 2003.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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