Talc and silver nitrate induce systemic inflammatory effects during the acute phase of experimental pleurodesis in rabbits.
OBJECTIVE
s: 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.


METHODS
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.
Marchi
Evaldo
E
Pulmonary Division, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil.
Vargas
Francisco S
FS
Acencio
Milena M P
MM
Antonangelo
Leila
L
Teixeira
Lisete R
LR
Genofre
Eduardo H
EH
Light
Richard W
RW
D000208:Acute Disease; D000818:Animals; D004195:Disease Models, Animal; D007249:Inflammation / Q000503:physiopathology; D018836:Inflammation Mediators / Q000032:analysis*; D015552:Injections, Intralesional; D016209:Interleukin-8 / Q000032:analysis; D007958:Leukocyte Count; D008297:Male; D010996:Pleural Effusion / Q000378:metabolism / Q000628:therapy; D018700:Pleurodesis / Q000379:methods*; D011817:Rabbits; D011897:Random Allocation; D012016:Reference Values; D012680:Sensitivity and Specificity; D012835:Silver Nitrate / Q000009:adverse effects* / Q000494:pharmacology; D013627:Talc / Q000009:adverse effects* / Q000494:pharmacology; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis
D018836:Inflammation Mediators; D016209:Interleukin-8; D042461:Vascular Endothelial Growth Factor A; D013627:Talc; D012835:Silver Nitrate