Frontczak-Baniewicz M
Laboratory of the Cell Ultrastructure, Medical Research Centre Polish Academy of Sciences, Pawiñskiego St. 5, 02-106 Warsaw, Poland.
Neuro Endocrinol Lett. 2001 Apr;22(2):81-6.
In our investigations we have reported that photochemical reaction leading to brain ischemia can also be precipitated with visible light from a non-coherent light source. It was revealed that focal cerebral ischemia after photochemical reaction cause the alterations in the capillaries ultrastructure and perivascular spaces of the barrier-competent regions of the brain. The purpose of this study is to first characterize the ultrastructural morphological consequences of photochemically induced ischemia in the cerebral cortex on the capillaries of neurohypophysis as the barrier-free region of the brain.
We used a model of ischemic brain damage due to obliteration of microvessels following the photochemical reaction. Rats were treated with an intravenous injection of rose bengal and irradiated from a halogen lamp source through an intact cranium to precipitate microvascular damage. Material for electron microscopic studies were sampled from the neurohypophysis 1 and 4 days after irradiation (4 animals in each group) in experimental group and 1 and 4 days after a rose bengal injection in control group.
Investigations in transmission electron microscopy revealed platelet aggregation on the endothelium preceded by its early ultrastructural damage. In the capillaries of the neurohypophysis, one and four days after irradiation, numerous microthrombi adhering to the damaged endothelium were present. The capillary vessels contained a continuous, rather than a fenestrated endothelium. The basement membrane was thickened, blurred and locally multiplicated.
Our results show that experimentally-induced thrombosis of cortical microvessels leads to alterations in the capillaries of neurohypophysis.
在我们的研究中,我们报告了导致脑缺血的光化学反应也可由非相干光源发出的可见光引发。结果显示,光化学反应后的局灶性脑缺血会导致脑屏障功能区毛细血管超微结构和血管周围间隙的改变。本研究的目的是首先描述作为脑无屏障区域的神经垂体毛细血管在大脑皮层光化学诱导缺血后的超微结构形态学后果。
我们使用了光化学反应后微血管闭塞导致的缺血性脑损伤模型。给大鼠静脉注射孟加拉玫瑰红,然后通过完整的颅骨用卤素灯源照射,以引发微血管损伤。实验组在照射后1天和4天(每组4只动物)从神经垂体采集用于电子显微镜研究的材料,对照组在注射孟加拉玫瑰红后1天和4天采集。
透射电子显微镜研究显示,内皮细胞早期超微结构损伤之前有血小板聚集。在照射后1天和4天的神经垂体毛细血管中,存在大量附着在受损内皮细胞上的微血栓。毛细血管的内皮是连续的,而非有窗孔的。基底膜增厚、模糊且局部增生。
我们的结果表明,实验诱导的皮质微血管血栓形成会导致神经垂体毛细血管发生改变。