Schmidt W, Walther A, Gebhard M M, Martin E, Schmidt H
Department of Anesthesiology, University of Heidelberg, Germany.
Intensive Care Med. 1998 Sep;24(9):967-72. doi: 10.1007/s001340050697.
To determine the influence of N-acetylcysteine (NAC) in a treatment model, its effects on endotoxin-induced leukocyte-endothelial cell adhesion, vascular leakage, and venular microhemodynamics in postcapillary venules of rat mesentery.
Prospective, randomized, controlled, experimental study.
Animal research laboratory.
40 male Wistar rats.
The rats randomly received one of four treatments: infusion of saline (SAL) or Escherichia coli lipopolysaccharides (LPS) followed by treatment with saline (SAL) or NAC (150 mg.kg-1 body weight) 30 min after induction of endotoxemia.
Leukocyte adherence, red blood cell velocity, and vessel diameters in postcapillary venules of rat mesentery were evaluated every 30 min over a period of 120 min using in vivo videomicroscopy. Vascular permeability was determined by measuring the extravasation of fluorescence-labeled albumin. Venular wall shear rate was calculated from red cell velocity, and vessel diameter. NAC in rats without endotoxemia (SAL + NAC group) compared to the control group (SAL + SAL) did not change microcirculatory parameters in postcapillary venules of rat mesentery. In both LPS-treated groups (LPS + SAL and LPS + NAC), leukocyte adherence increased after just 30 min. NAC treatment prevented a further increase in leukocyte adherence and attenuated the extravasation of fluorescence-labeled albumin during endotoxemia. Venular diameters remained unchanged, while erythrocyte velocity decreased in the LPS + SAL group. This led to a lower venular wall shear rate in this group.
Treatment with NAC attenuates endotoxin-induced leukocyte adherence and macromolecular leakage in postcapillary venules of rat mesentery, showing that NAC is also effective after the onset of endotoxemia.
在一个治疗模型中确定N - 乙酰半胱氨酸（NAC）的影响，及其对大鼠肠系膜毛细血管后微静脉中内毒素诱导的白细胞 - 内皮细胞黏附、血管渗漏和微静脉血流动力学的作用。
前瞻性、随机、对照、实验研究。
动物研究实验室。
40只雄性Wistar大鼠。
大鼠随机接受四种治疗之一：输注生理盐水（SAL）或大肠杆菌脂多糖（LPS），然后在内毒素血症诱导30分钟后用生理盐水（SAL）或NAC（150mg·kg-1体重）进行治疗。
使用体内视频显微镜在120分钟内每隔30分钟评估大鼠肠系膜毛细血管后微静脉中的白细胞黏附、红细胞速度和血管直径。通过测量荧光标记白蛋白的外渗来确定血管通透性。根据红细胞速度和血管直径计算微静脉壁剪切率。与对照组（SAL + SAL）相比，无内毒素血症的大鼠（SAL + NAC组）中的NAC并未改变大鼠肠系膜毛细血管后微静脉中的微循环参数。在两个LPS治疗组（LPS + SAL和LPS + NAC）中，仅30分钟后白细胞黏附就增加了。NAC治疗可防止白细胞黏附进一步增加，并在内毒素血症期间减弱荧光标记白蛋白的外渗。微静脉直径保持不变，而LPS + SAL组中的红细胞速度降低。这导致该组微静脉壁剪切率降低。
NAC治疗可减轻大鼠肠系膜毛细血管后微静脉中内毒素诱导的白细胞黏附和大分子渗漏，表明NAC在内毒素血症发作后也有效。
