Adenosine triphosphate-dependent calcium signaling during ventilator-induced lung injury is amplified by hypercapnia.
作者： Arturo Briva , Cristina Santos , Leonel Malacrida , Fabiana Rocchiccioli , Juan Soto
DOI: 10.3109/01902148.2011.598217
关键词: Permissive hypercapnia 、 Tidal volume 、 Fluid transport 、 Hypercapnia 、 Lung injury 、 Internal medicine 、 Anesthesia 、 Reabsorption 、 Lung 、 Endocrinology 、 Calcium in biology 、 Chemistry
摘要: ABSTRACTAdenosine triphosphate (ATP) is released by alveolar epithelial cells during ventilator-induced lung injury (VILI) and regulates fluid transport across epithelia. High CO2 levels are observed in patients with “permissive hypercapnia,” which inhibits reabsorption (AFR) cells. The authors set out to determine whether VILI affects AFR the purinergic pathway modulated exposed hypercapnia. Control group was compared against (tidal volume [Vt] = 35 mL/kg, zero positive end-expiratory pressure [PEEP]) protective ventilation (Vt 6 PEEP 10 cm H2O) groups. Lung mechanics, histology, were evaluated. Alveolar (AECs) loaded Fura 2-AM measure intracellular calcium presence ATP (10 μM) at 5% or 10% as baseline. tidal impairs mechanics AFR. Hypercapnia (HC) increases response stimulation. HC + ATP...
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