Acute alcohol intoxication potentiates neutrophil-mediated intestinal tissue damage after burn injury
Acute alcohol intoxication potentiates neutrophil-mediated intestinal tissue damage after burn injury
复制标题
DOI：
10.1097/shk.0b013e31815abe80
复制
发表时间：
2008-03-01
期刊：
影响因子：
3.1
通讯作者：
Choudhry, Mashkoor A.
中科院分区：
文献类型：
--
作者：
Li, Xiaoling;Schwacha, Martin G.;Choudhry, Mashkoor A.
本研究旨在探讨烧伤前急性酒精（EtOH）中毒是否会加重烧伤后肠组织的损伤，以及中性粒细胞在这些条件下是否在损伤中起任何作用。雄性大鼠（类似于250 g）用EtOH灌胃以达到约100 mg/dL的血液EtOH水平，或用盐水灌胃，并接受约12.5%或约25%的总体表面积（TBSA）烧伤或假损伤。分别于伤后4 h和24 h处死大鼠，测定各项指标。与假手术动物相比，单独烧伤（无论大小）导致肠组织髓过氧化物酶（MPO;中性粒细胞浸润指数）活性和IL-18水平损伤后4小时显着增加。此外，大鼠接受25%TBSA，而不是12.5%，烧伤表现出肠水肿。12.5%TBSA烧伤大鼠伤后24 h IL-18和MPO活性恢复正常，而25%烧伤大鼠伤后24 h IL-18和MPO活性仍明显升高。在烧伤时大鼠体内乙醇的存在加剧了烧伤后4和24 h的IL-18、MPO活性和水肿水平。用抗IL-18抗体或抗中性粒细胞抗血清治疗大鼠可防止EtOH和烧伤后上述参数的增加，但中性粒细胞的耗竭不能防止IL-18的增加。总之，这些研究结果表明，急性乙醇中毒加重烧伤后肠组织损伤后，它是，在一定程度上，中性粒细胞介导的。
This study examined whether acute alcohol (EtOH) intoxication before burn injury potentiates postburn intestinal tissue damage and whether neutrophils have any role in the damage under those conditions. Male rats (similar to 250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dL or with saline and received either approximately 12.5% or approximately 25% total body surface area (TBSA) burn or sham injury. Rats were killed at 4 or 24 h after injury, and various parameters were measured. As compared with sham animals, burn injury alone (regardless of size) resulted in a significant increase in intestinal tissue myeloperoxidase (MPO; an index of neutrophil infiltration) activity and IL-18 levels 4 h after injury. Furthermore, rats receiving 25% TBSA, but not 12.5%, burn exhibited intestine edema. The IL-18 and MPO activity were normalized at 24 h after injury in rats receiving 12.5% TBSA burn, whereas these parameters remained elevated at 24 h in rats with 25% burn. The presence of EtOH in rats at the time of burn injury exacerbated the levels of IL-18, MPO activity, and edema at 4 and 24 h after burn injury. Treatment of rats with anti-IL-18 antibodies or with anti-neutrophil antiserum prevented the increase in the above parameters after EtOH and burn injury, except that the depletion of neutrophils did not prevent the IL-18 increase. In summary, these findings suggest that acute EtOH intoxication exacerbates postburn intestinal tissue damage after burn injury, and that it is, in part, neutrophil mediated.