Kajihara H, Hirata S, Miyoshi N
Virchows Arch B Cell Pathol. 1977 Jan 20;23(1):1-16. doi: 10.1007/BF02889115.
Blood catcholamine levels and ultrastructural changes in adrenal medullary cells were followed during the course of oligemic and normovolemic shock in dogs. Blood adrenaline concentration rose promptly after hemorrhage, reaching a maximum that was 10-fold greater than normal during the early period of hemorrhagic hypotension. Thereafter, adrenaline levels gradually declined until the end of the critical stage of hemorrhagic shock when the blood concentration rose to a level 8-fold that of normal. Following the critical stage, and throughout the irreversible stages of shock, adrenaline levels remained near normal. Noradrenaline, which was initially undetectable, first appeared in the impending stage of hemorrhagic hypotension and showed little change during the course of severe hemorrhagic hypotension. Ultrastructural studies demonstrated A-cell degranulation as early as 5 min after initiation of hemorrhage. Degranulation continued throughout the impending stage of hemorrhagic hypotension and was associated with an increasing number of autophagic vacuoles containing empty vesicles. At the end of the critical stage, all A cells showed complete degranulation and degenerative hydropic change. Progression to necrosis rather than arrest or reversal of hydropic change was observed after reinfusion of blood. In contrast to the marked alterations in A cells, most N cells were morphologically unchanged.
在犬的低血容量性休克和正常血容量性休克过程中，对血中儿茶酚胺水平及肾上腺髓质细胞的超微结构变化进行了跟踪观察。出血后血中肾上腺素浓度迅速升高，在出血性低血压早期达到比正常水平高10倍的最大值。此后，肾上腺素水平逐渐下降，直至出血性休克关键期结束时血浓度升至正常水平的8倍。在关键期之后以及整个休克不可逆阶段，肾上腺素水平维持在接近正常的水平。去甲肾上腺素最初检测不到，最早在出血性低血压即将发生阶段出现，在严重出血性低血压过程中变化不大。超微结构研究表明，出血开始后5分钟，A细胞就出现脱颗粒现象。脱颗粒现象在出血性低血压即将发生阶段持续存在，并伴有越来越多含有空泡的自噬泡。在关键期结束时，所有A细胞均表现为完全脱颗粒和退行性水肿改变。输血后观察到细胞向坏死发展，而不是水肿改变停止或逆转。与A细胞的显著变化形成对比的是，大多数N细胞在形态上没有改变。
