Department of Anesthesiology, University Hospital Duesseldorf, Duesseldorf, Germany.
Shock. 2020 Jan;53(1):88-94. doi: 10.1097/SHK.0000000000001323.
In septic patients, adequate microvascular oxygenation (μHBO2) of the intestine is vital for their outcome. Recent studies suggest that statins can ameliorate septic microcirculation in a variety of tissues. However, the effect on intestinal microvascular oxygenation and blood flow is largely unknown. Furthermore, there are indications that statin therapy might not be beneficial in the presence of hypercapnia, as observed in septic acute respiratory distress syndrome (ARDS) patients. Therefore, the present study explores the effect of pravastatin with and without additional moderate acute hypercapnia on intestinal microvascular oxygenation and blood flow in experimental sepsis.
Forty male Wistar rats were randomized into four groups. Half of the animals received 0.2 mg • kg pravastatin s.c., the other half received the same volume as vehicle (NaCl 0.9%). After 18 h, colon ascendens stent peritonitis surgery was conducted in all animals to induce sepsis. Twenty-four hours after surgery, baseline was established and the animals were subjected to either 120 min of normocapnic (pCO2 40 ± 6 mm Hg) or moderate hypercapnic (pCO2 72 ± 10 mm Hg) ventilation. Microcirculatory oxygenation (μHBO2) and perfusion (μflow) of the colon were continuously recorded using tissue reflectance spectrophotometry and laser Doppler, respectively.
In normocapnic septic animals μHBO2 decreased over time (-8.4 ± 8.7%; P < 0.05 vs. baseline), whereas after pravastatin pretreatment μHBO2 remained constant (-1.9 ± 5.7% vs. baseline). However, in hypercapnic septic animals pretreated with pravastatin μHBO2 declined significantly over time (-8.9 ± 11.8%; P < 0.05 vs. baseline) and was significantly lower compared with normocapnic pravastatin-pretreated animals. μflow did not change over time in any group.
Pravastatin pretreatment ameliorates the intestinal microvascular oxygenation in sepsis and thus seems to prevent intestinal hypoxia. Furthermore, we demonstrated that additional hypercapnia abolishes this effect, indicating why septic ARDS patients might not benefit from pravastatin therapy.
在脓毒症患者中,肠道的适当微血管氧合(μHBO2)对其预后至关重要。最近的研究表明,他汀类药物可以改善多种组织中的脓毒症微循环。然而,其对肠道微血管氧合和血流的影响在很大程度上尚不清楚。此外,有迹象表明,他汀类药物治疗在存在高碳酸血症时可能没有益处,正如脓毒症急性呼吸窘迫综合征(ARDS)患者中观察到的那样。因此,本研究探讨了普伐他汀联合和不联合额外中度急性高碳酸血症对实验性脓毒症中肠道微血管氧合和血流的影响。
40 只雄性 Wistar 大鼠随机分为四组。一半的动物接受皮下注射 0.2mg·kg 的普伐他汀,另一半接受相同体积的生理盐水(NaCl 0.9%)。所有动物在 18 小时后接受升结肠支架性腹膜炎手术以诱导脓毒症。手术后 24 小时,建立基线,然后将动物暴露于正常碳酸血症(pCO2 40±6mmHg)或中度高碳酸血症(pCO2 72±10mmHg)通气 120 分钟。使用组织反射光谱光度法和激光多普勒分别连续记录结肠的微血管氧合(μHBO2)和灌注(μflow)。
在正常碳酸血症的脓毒症动物中,μHBO2 随时间推移而降低(-8.4±8.7%;P<0.05 与基线相比),而普伐他汀预处理后μHBO2 保持不变(-1.9±5.7%与基线相比)。然而,在接受普伐他汀预处理的高碳酸血症脓毒症动物中,μHBO2 随时间显著下降(-8.9±11.8%;P<0.05 与基线相比),且显著低于正常碳酸血症普伐他汀预处理动物。在任何一组中,μflow 均未随时间变化。
普伐他汀预处理可改善脓毒症中的肠道微血管氧合,从而预防肠道缺氧。此外,我们还证明,额外的高碳酸血症会消除这种影响,这表明为什么脓毒症 ARDS 患者可能无法从普伐他汀治疗中获益。