Pluta R, Salińska E, Lazarewicz J W
Department of Neuropathology, Polish Academy of Sciences, Warsaw.
Acta Neurobiol Exp (Wars). 1990;50(4-5):295-302.
The authors made a study of the effect of prostacyclin (PGI2) on ischemic morphological changes in the brain, extracellular calcium concentration (Ca2+e) and the blood-brain barrier (BBB) permeability. This was combined with physiological and neurophysiological measurements. Complete cerebral ischemia (CCI) lasting 15 or 20 min was produced by the ligation of the brachiocephalic trunk, the left subclavian and both internal thoracic arteries. The experiments with PGI2 were carried out in two groups. In group I, the rabbits received PGI2 3 min before CCI, during it and for 15 min after it. In group II PGI2 was infused in the last 3 min of CCI and for 40 min after it. Control animals with CCI of the same duration were not given PGI2 medication. The rabbits treated with PGI2 were found to have recovery of the bioelectric activity of the brain in half the time that its return took in the untreated cases. PGI2 was noted to have a positive effect on some parameters of the peripheral blood system after CCI. Application of PGI2 reduced the depth of ischemia-evoked drop of Ca2+e by 50% without accelerating recovery during recirculation; the post-ischemic increase of BBB permeability to fluorescein was also diminished. PGI2 reduced edema and the spectrum of neuronal changes and decreased the number of pathologically changed neurons in the brain. In the group that received PGI2 ischemic ultrastructural changes in the cytoplasm of neurons were abolished, but PGI2 did not prevent pathological changes in the neuronal nuclei after CCI. Those changes were manifested in numerous vesicular structures and nuclear inclusions.(ABSTRACT TRUNCATED AT 250 WORDS)
作者研究了前列环素(PGI2)对脑缺血形态学变化、细胞外钙浓度(Ca2+e)和血脑屏障(BBB)通透性的影响。这与生理和神经生理测量相结合。通过结扎头臂干、左锁骨下动脉和双侧胸廓内动脉产生持续15或20分钟的完全性脑缺血(CCI)。PGI2实验分两组进行。在第一组中,兔子在CCI前3分钟、期间及之后15分钟接受PGI2。在第二组中,PGI2在CCI的最后3分钟及之后40分钟输注。相同持续时间的CCI对照动物未给予PGI2药物治疗。发现用PGI2治疗的兔子脑生物电活动恢复的时间是未治疗病例的一半。PGI2被认为对CCI后外周血液系统的一些参数有积极作用。应用PGI2可使缺血引起的Ca2+e下降深度降低50%,但在再灌注期间不加速恢复;缺血后BBB对荧光素通透性的增加也减少。PGI2减轻了水肿和神经元变化的范围,并减少了脑中病理改变神经元的数量。在接受PGI2的组中,神经元细胞质中的缺血超微结构变化被消除,但PGI2并未预防CCI后神经元细胞核的病理变化。这些变化表现为大量囊泡结构和核内包涵体。(摘要截短于250字)