Department of Anesthesiology, University Hospital Duesseldorf, Duesseldorf, Germany.
Shock. 2018 Mar;49(3):326-333. doi: 10.1097/SHK.0000000000000920.
Insufficient microvascular oxygenation (μHBO2) of the intestinal mucosa worsens outcome of septic patients. Hypercapnia ameliorates μHBO2, mediated via endogenous vasopressin release. Under physiological conditions, blockade of the endogenous sympathetic nervous system abolishes this protective effect of hypercapnia. The aim of our study was therefore to evaluate the role of the endogenous sympathetic nervous system during hypercapnia on intestinal μHBO2 under septic conditions.
We randomized 80 male Wistar rats into eight groups. Sepsis was induced via colon ascendens stent peritonitis. The animals were subjected to 120 min of normocapnic (pCO2 35 mm Hg-45 mm Hg) or moderate hypercapnic (pCO2 65 mm Hg-75 mm Hg) ventilation 24 h after surgery. Animals received sympathetic blockade (hexamethonium 15 mg · kg (bolus) followed by 15 mg · kg · h (infusion) intravenously) or the same volume as vehicle (NaCl 0.9%). Microcirculatory oxygenation (μHBO2) and perfusion (μflow) were recorded using tissue reflectance spectrophotometry and laser Doppler.
In septic animals, μHBO2 decreased during normocapnia (-8.9 ± 4%) and increased during hypercapnia (+7.8 ± 7.5%). The additional application of hexamethonium did not influence these effects. μHBO2 declined in normocapnic septic animals treated with hexamethonium similar to normocapnia alone (-6.1 ± 5.4%) and increased in hypercapnic animals treated with hexamethonium similar to hypercapnia alone (+7.9 ± 11.7%). Furthermore, hypercapnic ventilation ameliorated microcirculatory perfusion (μflow) irrespective of whether animals received hexamethonium (from 113 ± 54 [AU] to 206 ± 87 [AU]) or vehicle (from 97 ± 37 [AU]-169 ± 52 [AU]).
The amelioration of the intestinal microcirculation during hypercapnia in sepsis is independent of the endogenous sympathetic nervous system.
肠道黏膜的微血管氧合不足（μHBO2）会使脓毒症患者的预后恶化。高碳酸血症可通过内源性血管加压素的释放来改善 μHBO2。在生理条件下，内源性交感神经系统的阻断会消除高碳酸血症的这种保护作用。因此，我们的研究目的是评估在脓毒症条件下，内源性交感神经系统在高碳酸血症期间对肠道 μHBO2 的作用。
我们将 80 只雄性 Wistar 大鼠随机分为 8 组。通过升结肠支架性腹膜炎诱导脓毒症。手术后 24 小时，动物接受正常碳酸血症（pCO2 35mmHg-45mmHg）或中度高碳酸血症（pCO2 65mmHg-75mmHg）通气。动物接受交感神经阻断（六烃季铵 15mg·kg（推注），然后静脉滴注 15mg·kg·h（输注））或相同体积的载体（NaCl 0.9%）。使用组织反射分光光度法和激光多普勒记录微循环氧合（μHBO2）和灌注（μflow）。
在脓毒症动物中，正常碳酸血症期间 μHBO2 下降（-8.9±4%），高碳酸血症期间 μHBO2 增加（+7.8±7.5%）。额外应用六烃季铵并未影响这些作用。在接受六烃季铵治疗的正常碳酸血症脓毒症动物中，μHBO2 下降类似于单独正常碳酸血症（-6.1±5.4%），在接受高碳酸血症治疗的动物中，μHBO2 增加类似于单独高碳酸血症（+7.9±11.7%）。此外，高碳酸血症通气改善了微循环灌注（μflow），无论动物是否接受六烃季铵（从 113±54[AU]增加到 206±87[AU]）或载体（从 97±37[AU]增加到 169±52[AU]）。
脓毒症时高碳酸血症改善肠道微循环与内源性交感神经系统无关。
