The magnitude of pleural fibrosis was not affected by the pH of the sclerosing solution. Although previous investigators showed that hydrochloric acid does not induce pleural fibrosis, this is the first study (to our knowledge) to show that DOXY pleurodesis is effective at a neutral pH. It is possible that the initial injection of neutralized solution is less painful, although this information cannot be extracted from this study in anesthetized animals.
The combination of adhesions, pleural thickening, and fluid accumulation severely compressed the underlying lung. This compression is not ordinarily seen in clinical pleurodesis, presumably because the pleural space is usually drained after DOXY instillation. Although the widespread fibrosis that we observed indicates that successful pleurodesis does not require posttreatment drainage of the pleural space, failure to do so does risk atelectasis and impaired gas exchange canadian neighbor pharmacy.
The histologic changes that we observed are similar to those previously reported in rabbits treated with TCN or minocycline. The earliest changes include damage to the surface mesothelium and the deposition of fibrin within both the pleural space and the submesothelial connective tissue. As with other forms of serosal injury, the fibrin is believed to result from increased vascular permeability to plasma coagulation factors, including fibrinogen.
Progression of this process to collagen deposition correlates with the infiltration of fibroblasts but may also depend on the presence or absence of fibrinolytic mechanisms in the pleural space. Pleural fluids from patients with exudates have depressed fibrinolytic activity as compared with transudates. Idell et al showed that this depression of fibrinolysis was due both to an inhibition of plasminogen activation (by plasminogen activator inhibitors) and of plasmin (by a2-antiplasmin).