作者: Christopher Beck , Franziska Barthel , Anna-Maria Hahn , Christian Vollmer , Anna Herminghaus
DOI: 10.1016/J.MVR.2015.02.009
关键词: Hypercapnia 、 Glibenclamide 、 Oxygenation 、 Normocapnia 、 Splanchnic 、 Sepsis 、 Hemodynamics 、 Medicine 、 Anesthesia 、 Breathing
摘要: Abstract Background Acute hypercapnia maintains the microcirculatory oxygenation of splanchnic region during sepsis. The first aim this study was to characterize role K + ATP channels on flow and acute moderate hypercapnia. second investigate whether a short period induces detrimental effects in an otherwise undamaged rodent lung. Methods Experiments were performed 60 male Wistar rats. A polymicrobial sepsis induced by colon ascendens stent peritonitis (CASP) surgery. 24 h after induction volume-controlled pressure-limited ventilation established for 120 min, with either normocapnic (pCO 2 35–45 mm Hg) or hypercapnic targets 65–75 mm Hg) without non-selective channel blockade glibenclamide. Microcirculatory blood colonic wall as well oxygen delivery consumption assessed tissue laser Doppler reflectance spectrophotometry. Hemodynamic variables recorded plasma cytokine levels myeloperoxidase lungs analyzed. Results In septic animals deteriorated progressively normocapnia (− 11.7 ± 11.8%) but maintained (− 2.9 ± 5.6%) This effect associated increased (+ 25.7 ± 37.1%) that decreased groups (− 7.2 ± 28.1%). not altered additional (− 5.7 ± 32.7%). Hypercapnia neither inflammatory response nor systemic response. Conclusions observed beneficial microvascular does seem be mediated via channels.