Jonas J, Heimann A, Alebrahim-Dehkordy A, Kempski O
Klinik für Allgemein- und Abdominalchirurgie, Johannes-Gutenberg-Universität, Mainz.
Langenbecks Arch Chir. 1996;381(2):95-101. doi: 10.1007/BF00183939.
The epithelial damage and the accumulation of the leucocytes within intestinal wall layers after ischemia and reperfusion was investigated in a pig model. Superior mesenteric artery (SMA) was occluded for 1 h (group 2, n = 9), 2 h (group 3, n = 6) and 3 h (group 4, n = 7) with a consecutive 2 h reperfusion period. The histological evaluation was performed on hematoxylin-eosine and Naphtol AS-D chloracetate stained preparations. The intensity of reperfusion shock depended on the duration of the intestinal ischemia. After 1 h SMA occlusion systolic blood pressure stabilized at a lower level with a normalization of the serum lactate level and the intestinal intramural pHi within the reperfusion period. After 2 h SMA occlusion the decrease of the systolic blood pressure was intensified (54-69 mm Hg) with a persistent elevated serum lactate concentration and a delayed increase of the ischemic pHi values. Reperfusion after 3 h SMA occlusion caused an irreversible shock. The epithelial damage also depended on the duration of the SMA occlusion. There were no significant changes of the leucocytic accumulation within the submucosa. But a significant increase of the number of the leucocytes was seen within the inner and the outer layer of the muscularis after 1 h SMA occlusion (106+/-5/mm2 resp. 280/mm2; p<0.05). This increase was less pronounced after 2 h (92+/-5/mm2*resp. 189+/-4/mm2; *p<0.05) and 3 h of SMA occlusion (84+/-5/mm2 resp. 185+/-23/mm2). Intestinal ischemia and reperfusion caused no changes of the leucocytic accumulation within the submucosa but a significantly increased accumulation within the muscularis after 1 h SMA occlusion, which was not seen after a more elongated occlusion period. A reperfusion shock without normalization of the serum lactate level and the intramural pHi suggesting intestinal perfusion disturbances may also lead to a depression of the leucocytic accumulation within the muscularis.
在猪模型中研究了缺血再灌注后肠壁层内的上皮损伤和白细胞积聚情况。肠系膜上动脉（SMA）闭塞1小时（第2组，n = 9）、2小时（第3组，n = 6）和3小时（第4组，n = 7），随后进行连续2小时的再灌注。对苏木精-伊红和萘酚AS-D氯乙酸酯染色的制剂进行组织学评估。再灌注休克的强度取决于肠缺血的持续时间。SMA闭塞1小时后，收缩压在较低水平稳定，再灌注期血清乳酸水平和肠壁内pH值恢复正常。SMA闭塞2小时后，收缩压下降加剧（54 - 69 mmHg），血清乳酸浓度持续升高，缺血pH值延迟升高。SMA闭塞3小时后再灌注导致不可逆休克。上皮损伤也取决于SMA闭塞的持续时间。黏膜下层白细胞积聚无明显变化。但SMA闭塞1小时后，肌层内层和外层白细胞数量显著增加（分别为106±5/mm²和280/mm²；p<0.05）。2小时（分别为92±5/mm²和189±4/mm²；*p<0.05）和3小时SMA闭塞后这种增加不太明显（分别为84±5/mm²和185±23/mm²）。肠缺血再灌注未引起黏膜下层白细胞积聚变化，但SMA闭塞1小时后肌层内积聚显著增加，较长闭塞期后未见此现象。血清乳酸水平和壁内pH值未恢复正常提示肠灌注紊乱的再灌注休克也可能导致肌层内白细胞积聚减少。
