Higgins Brendan D, Costello Joseph, Contreras Maya, Hassett Patrick, O' Toole Daniel, Laffey John G
Department of Anaesthesia, Clinical Science Institute, and Lung Biology Group, National Centre for Biomedical Engineering Science, National University of Ireland, Galway, Ireland.
Anesthesiology. 2009 Dec;111(6):1317-26. doi: 10.1097/ALN.0b013e3181ba3c11.
Acute hypercapnic acidosis protects against lung injury caused by nonseptic insults and after both pulmonary and systemic sepsis. The authors wished to dissect the contribution of the acidosis versus hypercapnia per se to the effects of hypercapnic acidosis on the hemodynamic profile and severity of lung injury induced by systemic sepsis.
In the hypercapnic acidosis series, adult male Sprague-Dawley rats were randomized to normocapnia or hypercapnic acidosis-produced by adding 5% carbon dioxide to the inspired gas-and cecal ligation and puncture performed. In the buffered hypercapnia series, animals were first randomized to housing under conditions of environmental normocapnia or hypercapnia-produced by exposure to 8% carbon dioxide-to allow renal buffering. After 96 h, cecal ligation and puncture was performed. In both series, the animals were ventilated for 6 h, and the severity of the lung injury and hemodynamic deterioration were assessed.
Both hypercapnic acidosis and buffered hypercapnia attenuated the development and severity of hypotension and reduced lactate accumulation compared to normocapnia. Hypercapnic acidosis reduced lung injury and inflammation, decreased mean (+ or - SD) bronchoalveolar lavage protein concentration (232 + or - 50 versus 279 + or - 27 microg x ml(-1)) and median neutrophil counts (3,370 versus 9,120 cells x ml(-1)), and reduced histologic lung injury. In contrast, buffered hypercapnia did not reduce the severity of systemic sepsis induced lung injury.
Both hypercapnic acidosis and buffered hypercapnia attenuate the hemodynamic consequences of systemic sepsis. In contrast, hypercapnic acidosis, but not buffered hypercapnia, reduced the severity of sepsis-induced lung injury.
急性高碳酸性酸中毒可预防由非感染性损伤以及肺部和全身性脓毒症引起的肺损伤。作者希望剖析酸中毒与高碳酸血症本身对高碳酸性酸中毒对全身脓毒症所致血流动力学特征和肺损伤严重程度的影响。
在高碳酸性酸中毒组中，成年雄性Sprague-Dawley大鼠被随机分为常碳酸血症组或通过向吸入气体中添加5%二氧化碳产生的高碳酸性酸中毒组，并进行盲肠结扎和穿刺。在缓冲高碳酸血症组中，动物首先被随机分为环境常碳酸血症或通过暴露于8%二氧化碳产生的高碳酸血症环境中饲养，以进行肾脏缓冲。96小时后，进行盲肠结扎和穿刺。在两个组中，动物均通气6小时，并评估肺损伤的严重程度和血流动力学恶化情况。
与常碳酸血症相比，高碳酸性酸中毒和缓冲高碳酸血症均减轻了低血压的发展和严重程度，并减少了乳酸积累。高碳酸性酸中毒减轻了肺损伤和炎症，降低了支气管肺泡灌洗蛋白平均浓度（标准差）（232±50对279±27μg·ml⁻¹）和中性粒细胞计数中位数（3370对9120个细胞·ml⁻¹），并减轻了组织学肺损伤。相比之下，缓冲高碳酸血症并未减轻全身脓毒症诱导的肺损伤严重程度。
高碳酸性酸中毒和缓冲高碳酸血症均减轻了全身脓毒症的血流动力学后果。相比之下，高碳酸性酸中毒而非缓冲高碳酸血症降低了脓毒症诱导的肺损伤严重程度。
