Mechanical ventilation during experimental sepsis increases deposition of advanced glycation end products and myocardial inflammation.
Mechanical ventilation during experimental sepsis increases deposition of advanced glycation end products and myocardial inflammation.
复制标题
DOI：
10.1186/cc7911
复制
发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Plötz FB
中科院分区：
文献类型：
--
作者：
Kneyber MC;Gazendam RP;Niessen HW;Kuiper JW;Dos Santos CC;Slutsky AS;Plötz FB
越来越多的证据表明，包括N-ε-(羧甲基)赖氨酸在内的晚期糖基化终末产物(AGE)与心力衰竭的发生有关。AGE的积聚导致心肌炎症，这被认为是脓毒症引起心功能障碍的可能机制之一。我们假设机械通气(MV)增加了脓毒症引起的心肌CML沉积和炎症。采用改良盲肠结扎穿孔(CLP)技术建立36只成年雄性SD大鼠脓毒症模型。脓毒症诱导后24小时，随机分为低潮气量(LTV：6ml/kg，PEEP 5cmH2O，n=10)和高潮气量(HTV：15ml/kg，PEEP 3cmH2O，n=10)两组。8只大鼠作为败血症、非通风对照组，8只作为非败血症、非通风对照组。28小时后处死所有大鼠。血管外中性粒细胞(PMN)、巨噬细胞和淋巴细胞的数量以阳性细胞数/mm2表示。根据强度评分对CML阳性内皮细胞的数量进行半定量。CML强度评分与炎症细胞数相关，以研究CML沉积与炎症之间的关系。通气组之间的气体交换是相似的。脓毒症引起的慢性粒细胞白血病沉积显著增加，与非机械通气的脓毒症对照组相比，MV显著增加(左心室1.1±1.0vs0.7±0.1，P=0.030；右心室2.5±0.5vs0.6±0.1，P=0.037)。在右室，HTV组与脓毒症、非呼吸机对照组相比，CML沉积无明显增加趋势(1.0±0.1vs0.7±0.09，P=0.07)。与未经机械通气的脓毒症对照相比，脓毒症诱导的巨噬细胞和中性粒细胞数量显著增加，而机械通气增加了巨噬细胞和中性粒细胞的数量，而与机械通气策略无关。CML沉积与心脏巨噬细胞和中性粒细胞数量显著相关。脓毒症导致慢性粒细胞白血病在心脏沉积，右室炎症占主导地位，无论采用何种机械通气策略，右室炎症均显著加重。
Increasing evidence links advanced glycation end products (AGE) including Nε-(carboxymethyl)lysine (CML) to the development of heart failure. Accumulation of AGE leads to myocardial inflammation, which is considered as one of the possible mechanisms underlying sepsis-induced cardiac dysfunction. We hypothesized that mechanical ventilation (MV) augmented sepsis-induced myocardial CML deposition and inflammation. Sepsis was induced using a modified cecal ligation and perforation (CLP) technique in 36 male adult Sprague Dawley rats. Rats were randomized to four hours of MV with low tidal volume (LTV: 6 ml/kg, PEEP 5 cmH2O, n = 10) or high tidal volume (HTV: 15 ml/kg, PEEP 3 cmH2O, n = 10) 24 hours after the induction of sepsis. Eight rats served as septic, non-ventilated controls and eight as non-septic, non-ventilated controls. After 28 hours all rats were killed. The number of extravascular polymorphonuclear (PMN) leucocytes, macrophages, and lymphocytes was measured as the number of positive cells/mm2. The number of CML positive endothelial cells were semi-quantified based upon an intensity score. The CML intensity score was correlated with the number of inflammatory cells to study the association between CML depositions and inflammation. Gas exchange was comparable between the ventilated groups. Sepsis induced a significant increase in CML deposition in both ventricles that was significantly augmented by MV compared with non-ventilated septic controls (left ventricle 1.1 ± 1.0 vs 0.7 ± 0.1, P = 0.030; right ventricle 2.5 ± 0.5 vs 0.6 ± 0.1, P = 0.037), irrespective of ventilatory strategy. In the right ventricle there was a non-significant tendency towards increased CML deposition in the HTV group compared with septic, non-ventilated controls (1.0 ± 0.1 vs 0.7 ± 0.09, P = 0.07). Sepsis induced a significant increase in the number of macrophages and PMNs compared with non-ventilated septic controls that was augmented by MV, irrespective of ventilatory strategy. CML deposition was significantly correlated with the number of macrophages and PMNs in the heart. Sepsis induces CML deposition in the heart with a predominant right ventricular inflammation that is significantly augmented by MV, irrespective of the ventilatory strategy.
登录
查看更多内容
影响因子：
5.7
作者：
Begieneman, M. P. V.;de Goot, F. R. W. van;Niessen, H. W. M.
通讯作者：
Niessen, H. W. M.
DOI：
10.1016/j.echo.2006.06.011
发表时间：
2006-12-01
影响因子：
6.5
作者：
Plante, Eric;Lachance, Dominic;Couet, Jacques
通讯作者：
Couet, Jacques
影响因子：
15.9
作者：
Anderson, MM;Requena, JR;Heinecke, JW
通讯作者：
Heinecke, JW
影响因子：
2.2
作者：
Bopp, Christian;Hofer, Stefan;Weigand, Markus A.
通讯作者：
Weigand, Markus A.
DOI：
10.1186/cc6164
发表时间：
2008
期刊：
Critical care (London, England)
影响因子：
--
作者：
Bopp C;Bierhaus A;Hofer S;Bouchon A;Nawroth PP;Martin E;Weigand MA
通讯作者：
Weigand MA