Seemayer T A, Osborne C, de Chadarévian J P
Hum Pathol. 1985 Dec;16(12):1231-4. doi: 10.1016/s0046-8177(85)80035-6.
Variable degrees of injury of the pancreatic islets of Langerhans, with sparing of the acinar pancreas, were observed in three infants (age range, 1 day to 3 months) who died of profound shock. The duration of shock varied from 19 to 48 hours. In two of the infants, the shock stemmed from hypovolemia; in the remaining infant, the shock followed blood loss, sepsis, and heart failure. The islet lesions were devoid of cellular infiltrates, hemorrhage, and fibrin thrombi. Tissue manifestations of shock included acute renal tubular necrosis, massive hepatic centrilobular necrosis, ischemic enteropathy, and "shock" lung. Study of pancreatic sections from 30 children (age range, 13 hours to 15 years) with clinical and/or morphologic evidence of shock showed no additional instances of islet injury. These findings suggest that pancreatic islets in the young may be vulnerable to shock-induced ischemia. Studies are in progress in an animal model to test this hypothesis.
在三名死于深度休克的婴儿（年龄范围为1天至3个月）中，观察到胰岛有不同程度的损伤，而胰腺腺泡未受影响。休克持续时间为19至48小时。其中两名婴儿的休克源于低血容量；另一名婴儿的休克是在失血、败血症和心力衰竭之后发生的。胰岛病变没有细胞浸润、出血和纤维蛋白血栓。休克的组织表现包括急性肾小管坏死、大量肝小叶中心坏死、缺血性肠病和“休克”肺。对30名有临床和/或形态学休克证据的儿童（年龄范围为13小时至15岁）的胰腺切片研究显示，没有发现其他胰岛损伤的病例。这些发现表明，幼儿的胰岛可能易受休克诱导的缺血影响。正在用动物模型进行研究以验证这一假设。
