The aim of the study was to investigate if human pleura from different anatomical locations presents electrophysiology differences. Specimens were stripped over the 2nd-5th rib (cranial), 8th-10th rib (caudal), and mediastinum during open surgery and were mounted between Ussing chambers. Amiloride and ouabain were added towards mesothelial surface and trans-mesothelial potential difference (PD) was measured after 1, 5, 10 and 20 min. Trans-membrane resistance (R) was calculated from Ohm's law. R increased after amiloride addition, for cranial (net increase of 0.40 Omega x cm(2)) and caudal (1.16 Omega x cm(2)) pleural pieces. Mediastinal pleura R remained unchanged (0.09 Omega x cm(2)). R increase was higher for caudal than cranial (P=0.029) or mediastinal tissues (P=0.002). R increased after ouabain addition for caudal (1.35 Omega x cm(2)) and cranial (0.56 Omega x cm(2)) pleural pieces. Mediastinal pleural tissue did not respond (0.20 Omega x cm(2)). Caudally located pleura responded greater than cranial (P=0.043) or mediastinal (P=0.003) pleural tissues. Human pleura shows electrophysiology differences according to the location within the pleural cavity. Surgeons may waste mediastinal pleura when needed but should leave intact caudal parietal pleura, which seems to be electrophysiologically the most important part of the pleural cavity.
The postoperative length of hospital stay did not differ significantly between OA and LA for men. Laparoscopic appendectomy required more time and did not offer any advantages compared with OA.
We report the case of a 56-y-old male admitted with a left-sided post-pneumonic empyema. Clostridium sordellii DNA was directly detected in its pleural fluid by a broad-range 16S rRNA PCR, after 24 h of specimen collection. This is the third case of pleural infection caused by C. sordellii in the literature.
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.
Insulin induces electrochemical alterations that vary depending on the location of specimens within the pleural cavity which possibly is not correlated with insulin receptors variations.
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