The present study was conducted to investigate changes in uncuffed endotracheal tube (ETT) leak during laparoscopic surgery. The study included 31 patients aged between 1 and 6 years scheduled for elective laparoscopic inguinal herniorrhaphy. Inspiratory and expiratory tidal volumes (TVi and TVe) were measured during mechanical ventilation, and ETT leak was calculated using the formula-ETT leak = (TVi - TVe)/TVi × 100 (%), assessed at the following time-points-5 min after the start of mechanical ventilation (T1, baseline), just before the start of surgery (T2), 5 min after the induction of pneumoperitoneum with 15° Trendelenburg tilt (T3), and at the end of surgery (T4).
View Article and Find Full Text PDFOur previous study using apoptosis analysis suggested that Ca(2+) release through inositol 1,4,5-trisphosphate (IP3) receptors and the subsequent Ca(2+) influx through store-operated channels (SOCs) constitute a triggering signal for H2O2-induced β-cell apoptosis. In the present study, we further examined the obligatory role of early Ca(2+) responses in β-cell apoptosis induction. H2O2 induced elevation of the cytosolic Ca(2+) concentration ([Ca(2+)]c) consisting of two phases: an initial transient [Ca(2+)]c elevation within 30 min and a slowly developing one thereafter.
View Article and Find Full Text PDFReactive oxygen species, including hydrogen peroxide (H(2)O(2)), are known to induce β-cell apoptosis. The present study investigated the role of Ca(2+) in H(2)O(2)-induced apoptosis of the β-cell line INS-1. Annexin V assay with flow cytometry and DNA ladder assay demonstrated that treatment of INS-1 cells with 100 µM H(2)O(2) for 18 h significantly increased apoptotic cells.
View Article and Find Full Text PDFAims: Low concentrations of nitric oxide (NO) produced by constitutive NO synthase (cNOS) in pancreatic beta-cells have been suggested to be a physiological regulator of insulin secretion. In contrast, excessive NO produced by inducible NO synthase is known to mediate beta-cell apoptosis. The aim of the present study was to investigate the effect of low concentrations of NO on beta-cell apoptosis.
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