Department of Anesthesiology, University Hospital Duesseldorf, Germany.
Microvasc Res. 2013 Nov;90:180-6. doi: 10.1016/j.mvr.2013.07.008. Epub 2013 Jul 31.
The deterioration of microcirculatory oxygenation of the gut plays a vital role in the development of sepsis. Acute hypercapnia enhances the microcirculatory oxygenation of the splanchnic region under physiological conditions, while the effect of hypercapnia under sepsis is unknown. The aim of this study was to investigate the effects of acute hypercapnia and hypercapnic acidosis on the colonic microcirculation and early cytokine response in polymicrobial sepsis.
Experiments were performed on 103 male Wistar rats. Colon ascendens stent peritonitis (CASP) surgery with varying stent diameters was conducted to establish a moderate polymicrobial sepsis model. In a second series, 24h of sepsis development induced by CASP surgery was followed by 120min of volume-controlled and pressure-limited ventilation with either normocapnic (pCO2 45±5mmHg) or moderate hypercapnic ventilation targets (pCO2 75±5mmHg) via exogenous carbon dioxide application. The effect of acidosis was investigated by metabolically buffering the hypercapnic acidosis with tromethamine. Microcirculatory oxygenation of the colon wall (tissue reflectance spectrophotometry) and hemodynamic variables were recorded continuously and arterial blood gas and cytokine (TNF-α, IL-6, IL-10) levels were analyzed intermittently.
In septic animals the microcirculatory oxygenation of the colon deteriorated under normocapnia (-7.0±7.6% at 90min) but was maintained under hypercapnic acidosis (+3.6±7.6%) and buffered hypercapnia (+1.5±4.4%). Cytokine levels were significantly higher in septic animals as opposed to sham animals but did not differ between normocapnic and hypercapnic groups.
Acute hypercapnic acidosis and buffered hypercapnia both improve splanchnic microcirculatory oxygenation in a septic animal model, thereby counteracting the adverse effect induced by sepsis. The circulating pro- and anti-inflammatory cytokine levels are not modulated after 120min of hypercapnia.
肠道微循环氧合的恶化在脓毒症的发展中起着至关重要的作用。在生理条件下，急性高碳酸血症增强内脏区域的微循环氧合，而脓毒症下高碳酸血症的影响尚不清楚。本研究旨在探讨急性高碳酸血症和高碳酸酸中毒对多微生物脓毒症结肠微循环和早期细胞因子反应的影响。
对 103 只雄性 Wistar 大鼠进行了实验。采用升结肠支架腹膜炎（CASP）手术，通过改变支架直径来建立中度多微生物脓毒症模型。在第二个系列中，通过外源性二氧化碳应用，对 CASP 手术后 24 小时的脓毒症发展进行 120 分钟的容量控制和压力限制通气，分别采用正常碳酸血症（pCO2 45±5mmHg）或中度高碳酸血症通气目标（pCO2 75±5mmHg）。通过三羟甲基氨基甲烷代谢缓冲高碳酸酸中毒来研究酸中毒的影响。连续记录结肠壁微循环氧合（组织反射分光光度法）和血流动力学变量，并间歇性分析动脉血气和细胞因子（TNF-α、IL-6、IL-10）水平。
在脓毒症动物中，正常碳酸血症下结肠微循环氧合恶化（90 分钟时为-7.0±7.6%），但高碳酸血症酸中毒下和缓冲高碳酸血症下得到维持（分别为+3.6±7.6%和+1.5±4.4%）。与假手术动物相比，脓毒症动物的细胞因子水平显著升高，但正常碳酸血症组和高碳酸血症组之间没有差异。
急性高碳酸酸中毒和缓冲高碳酸血症均可改善脓毒症动物模型内脏微循环氧合，从而抵消脓毒症引起的不利影响。120 分钟高碳酸血症后，循环促炎和抗炎细胞因子水平没有调节。
