Kremer Thomas, Harenberg Patrick, Hernekamp Frederick, Riedel Katrin, Gebhardt Martha M, Germann Guenter, Heitmann Christoph, Walther Andreas
Department of Hand, Plastic and Reconstructive Surgery, Burn Center-BG Trauma Center Ludwigshafen, Plastic- and Hand Surgery, University of Heidelberg, Ludwigshafen, Germany.
J Burn Care Res. 2010 May-Jun;31(3):470-9. doi: 10.1097/BCR.0b013e3181db5199.
Oxidative stress after burn injuries leads to systemic capillary leakage and leukocyte activation. This study evaluates whether antioxidative treatment with high-dose vitamin C leads to burn edema reduction and prevention of leukocyte activation after burn plasma transfer. Donor rats underwent a burn (n = 7; 100 degrees C water, 12 seconds, 30% body surface area) or sham burn (37 degrees C water; n = 2) procedure and were killed after 4 hours for plasma harvest. This plasma was administered to study rats (continuous infusion). Rats were randomized to four groups (n = 8 each; burn plasma alone [BP]; burn plasma/vitamin C-bolus 66 mg/kg and maintenance dose 33 mg/kg/hr [VC66]; burn plasma/vitamin C-bolus 33 mg/kg and maintenance dose 17.5 mg/kg/hr [VC33]; and sham burn plasma [SB]). Intravital fluorescence microscopy in the mesentery was performed at 0, 60, and 120 minutes for microhemodynamic parameters, leukocyte adherence, and fluorescein isothiocyanate-albumin extravasation. No differences were observed in microhemodynamics at any time. Burn plasma induced capillary leakage, which was significantly higher compared with sham burn controls (P < .001). VC66 treatment reduced microvascular barrier dysfunction to sham burn levels, whereas VC33 had no significant effect. Leukocyte sticking increased after burn plasma infusion, which was not found for sham burn. Vitamin C treatment did not influence leukocyte activation (P > .05). Burn plasma transfer leads to systemic capillary leakage. High-dose vitamin C treatment (bolus 66 mg/kg and maintenance dose 33 mg/kg/hr) reduces endothelial damage to sham burn levels, whereas half the dose is inefficient. Leukocyte activation is not influenced by antioxidative treatment. Therefore, capillary leakage seems to be independent from leukocyte-endothelial interactions after burn plasma transfer. High-dose vitamin C should be considered for parenteral treatment in every burn patient.
烧伤后的氧化应激会导致全身毛细血管渗漏和白细胞活化。本研究评估大剂量维生素C抗氧化治疗是否能减轻烧伤水肿,并预防烧伤血浆输注后白细胞的活化。供体大鼠接受烧伤(n = 7;100摄氏度水,12秒,30%体表面积)或假烧伤(37摄氏度水;n = 2)处理,4小时后处死以采集血浆。将该血浆给予研究大鼠(持续输注)。大鼠被随机分为四组(每组n = 8;单纯烧伤血浆[BP];烧伤血浆/维生素C - 推注剂量66 mg/kg,维持剂量33 mg/kg/小时[VC66];烧伤血浆/维生素C - 推注剂量33 mg/kg,维持剂量17.5 mg/kg/小时[VC33];以及假烧伤血浆[SB])。在0、60和120分钟时,通过活体荧光显微镜观察肠系膜的微循环动力学参数、白细胞黏附以及异硫氰酸荧光素 - 白蛋白外渗情况。在任何时间点,微循环动力学均未观察到差异。烧伤血浆诱导了毛细血管渗漏,与假烧伤对照组相比显著更高(P < .001)。VC66治疗将微血管屏障功能障碍降低至假烧伤水平,而VC33没有显著效果。烧伤血浆输注后白细胞黏附增加,假烧伤未出现这种情况。维生素C治疗未影响白细胞活化(P > .05)。烧伤血浆输注导致全身毛细血管渗漏。大剂量维生素C治疗(推注剂量66 mg/kg,维持剂量33 mg/kg/小时)将内皮损伤降低至假烧伤水平,而剂量减半则无效。抗氧化治疗不影响白细胞活化。因此,烧伤血浆输注后毛细血管渗漏似乎独立于白细胞 - 内皮细胞相互作用。对于每位烧伤患者的肠外治疗,应考虑使用大剂量维生素C。