Hotz H G, Schmidt J, Ryschich E W, Foitzik T, Buhr H J, Warshaw A L, Herfarth C, Klar E
Department of Surgery, University of Heidelberg, Germany.
Am J Surg. 1995 Jan;169(1):161-6. doi: 10.1016/s0002-9610(99)80126-3.
Previous studies demonstrated that intravenous contrast medium (CM), as used in contrast enhanced computed tomography, aggravates the impairment of pancreatic microcirculation (PM) characteristic of severe pancreatitis and increases necrosis and mortality in necrotizing pancreatitis (NP) in rats. This study evaluates the use of isovolemic hemodilution, which can enhance the microcirculation in severe pancreatitis, for preventing CM-induced injury.
NP was induced in 30 dextran-tolerant Wistar rats by intraductal glycodeoxycholic acid and intravenous cerulein for 6 hours. PM was quantified by intravital microscopy using fluorescein isothiocyanate labeled erythrocytes. Based on previous results, areas with low blood flow (< 1.6 nL/min/cap) were identified and baseline recordings of capillary blood flow taken. A reduction of hematocrit to 75% of baseline was achieved by replacement of 5 mL/kg of blood with 25 mL/kg Ringer's lactate (RL) or by exchange of 8 mL/kg of blood for the same amount of dextran 70.6%. Thereafter, the nonionic CM iopamidol (Solutrast, Byk Gulden, Konstanz, Germany) was injected during 1 minute and PM measurements repeated after 30 and 60 minutes.
Despite hemodilution with RL, pancreatic capillary perfusion was significantly decreased to 87% of baseline (0.83 +/- 0.04 mL/min/cap; n = 216) 60 minutes after CM infusion (P < 0.05). In contrast, capillary blood flow was significantly increased to 161% (1.56 +/- 0.05 nL/min/cap; n = 278) in the group treated with dextran. Moreover, the percentage of capillaries developing complete stasis was significantly lower in the dextran group (2.3 +/- 1.2%) compared to animals diluted with RL (22.3 +/- 4.8%) (P < 0.002).
Isovolemic hemodilution with dextran prevents the additional impairment of pancreatic microcirculation induced by CM in NP.
先前的研究表明，在增强CT中使用的静脉造影剂（CM）会加重重症胰腺炎所特有的胰腺微循环（PM）损伤，并增加大鼠坏死性胰腺炎（NP）的坏死率和死亡率。本研究评估采用等容血液稀释（可增强重症胰腺炎时的微循环）预防CM诱导损伤的效果。
通过导管内注入甘氨脱氧胆酸和静脉注射雨蛙肽6小时，在30只右旋糖酐耐受的Wistar大鼠中诱导产生NP。使用异硫氰酸荧光素标记的红细胞，通过活体显微镜对PM进行定量。根据先前的结果，识别出血流较低（<1.6 nL/分钟/毛细血管）的区域，并记录毛细血管血流的基线值。通过用25 mL/kg乳酸林格液（RL）替代5 mL/kg血液，或将8 mL/kg血液换成等量的6%右旋糖酐70，使血细胞比容降至基线的75%。此后，在1分钟内注射非离子型CM碘帕醇（Solutrast，拜耳先灵医药公司，康斯坦茨，德国），并在30分钟和60分钟后重复测量PM。
尽管用RL进行血液稀释，但在注入CM后60分钟，胰腺毛细血管灌注显著降至基线的87%（0.83±0.04 mL/分钟/毛细血管；n = 216）（P < 0.05）。相比之下，在接受右旋糖酐治疗的组中，毛细血管血流显著增加至161%（1.56±0.05 nL/分钟/毛细血管；n = 278）。此外，与用RL稀释的动物相比，右旋糖酐组中出现完全停滞的毛细血管百分比显著更低（2.3±1.2%）（22.3±4.8%）（P < 0.002）。
用右旋糖酐进行等容血液稀释可预防CM在NP中诱导的胰腺微循环的额外损伤。
