Collan Y, Kivilaakso E, Kalima T V, Lempinen M
Circ Shock. 1977;4(1):13-25.
Ultrastructural changes in the gastric mucosa of 14 piglets subjected to transient hemorrhagic shock (3 hr duration; mean arterial pressure 40 mmHg) are described. After 30 min there was mucosal edema and extravasation of red blood cells. Microthrombi with degranulating thrombocytes and fibrin strands were seen in the capillaries. These changes were also seen in the antral mucosa where no subsequent ulceration usually occurs. At this stage the cells of the neck region of the gastric glands showed mitochondrial dilatation and their apical parts were seen to bulge into the lumen of the gastric glands. Other cell types were affected later and necrosis progressed from the surface into deeper parts of the mucosa. Mast cells and mucosal endocrine cells were relatively resistant, being mostly undamaged at the end of the shock period and later. The findings suggest that, during the shock, local formation of thrombi contributes to mucosal ischemia and ulcer formation, and that the cells at the neck region of the gastric glands form the locus of limited resistance to ulcerogenic effects.
描述了14只经历短暂失血性休克（持续3小时；平均动脉压40mmHg）的仔猪胃黏膜的超微结构变化。30分钟后出现黏膜水肿和红细胞外渗。在毛细血管中可见伴有血小板脱颗粒和纤维蛋白丝的微血栓。在通常不会发生后续溃疡的胃窦黏膜中也观察到了这些变化。在此阶段，胃腺颈部区域的细胞显示线粒体扩张，其顶端部分向胃腺管腔内突出。其他细胞类型稍后受到影响，坏死从表面向黏膜深层发展。肥大细胞和黏膜内分泌细胞相对具有抗性，在休克期结束时及之后大多未受损。这些发现表明，在休克期间，血栓的局部形成导致黏膜缺血和溃疡形成，并且胃腺颈部区域的细胞形成了对致溃疡作用的有限抗性部位。
