ABSTRACT
BACKGROUND: Insulin directly changes the sheep pleural electrophysiology. The aim of this study was to investigate whether insulin induces similar effects in human pleura, to clarify insulin receptor's involvement, and to demonstrate if glibenclamide (hypoglycemic agent) reverses this effect. METHODS: Human parietal pleural specimens were mounted in Ussing chambers. Solutions containing insulin or glibenclamide and insulin with anti-insulin antibody, anti-insulin receptor antibody, and glibenclamide were used. The transmesothelial resistance (R(TM)) was determined. Immunohistochemistry for the presence of Insulin Receptors (IRa, IRb) was also performed. RESULTS: Insulin increased R(TM) within 1st min (P = .016), when added mesothelially which was inhibited by the anti-insulin and anti-insulin receptor antibodies. Glibenclamide also eliminated the insulin-induced changes. Immunohistochemistry verified the presence of IRa and IRb. CONCLUSION: Insulin induces electrochemical changes in humans as in sheep via interaction with its receptor. This effect is abolished by glibenclamide.
Subject(s)
Insulin/pharmacology , Pleura/drug effects , Receptor, Insulin/physiology , Glyburide/pharmacology , Humans , Pleura/physiology , Receptor, IGF Type 1/physiology , Receptor, Insulin/analysisABSTRACT
We present a case of human pulmonary dirofilariasis, diagnosed in a 55-year-old heavy smoker (male) by wedge resection of the pulmonary lesion and histologic examination. The dirofilaria lesion had the clinical and radiographic appearance of a peripheral pulmonary lesion invading the anterior chest wall and mediastinum. The reported radiographic image of the disease is different from the usually described picture of a pulmonary coin lesion.
