Dietrich W D, Watson B D, Busto R, Ginsberg M D, Bethea J R
Acta Neuropathol. 1987;72(4):315-25. doi: 10.1007/BF00687262.
Cerebral ischemia leading to infarction was produced in rats by intravascular thrombosis induced by a photochemical reaction between systemically injected rose bengal and green light (560 nm) transmitted through the intact skull for a 2-min period. At 2 or 15 min following photochemical sensitization, animals were perfusion-fixed for scanning (SEM) and transmission (TEM) electron microscopic analyses of the cerebral vasculature. At 2 minutes, ultrastructural examination of cortical regions destined to undergo infarction revealed numerous platelet aggregates within both pial and intraparenchymal vessels. Platelets close to the endothelial walls were routinely degranulated with pseudopodia. Endothelial cells were frequently swollen and contained dilated mitochondria and granular endoplasmic reticulum. The endothelial luminal membrane structure was shown by high-power TEM to be focally damaged. If brain temperature was reduced by 4 degrees C during the photochemical sensitization period, the platelet response was inhibited without interfering with other ultrastructural changes. These results are consistent with the hypothesis that photochemically induced endothelial alterations stimulate platelet activation and implicate abnormal endothelial function as a primary event in the pathogenesis of photochemically induced cerebral infarction.
通过将全身注射的孟加拉玫瑰红与透过完整颅骨传输的绿光（560纳米）进行光化学反应诱导血管内血栓形成，从而在大鼠中产生导致梗死的脑缺血。在光化学致敏后2分钟或15分钟，对动物进行灌注固定，以对脑血管进行扫描（SEM）和透射（TEM）电子显微镜分析。在2分钟时，对注定要发生梗死的皮质区域进行超微结构检查，发现软脑膜和实质内血管内有大量血小板聚集。靠近内皮壁的血小板通常会脱颗粒并形成伪足。内皮细胞经常肿胀，含有扩张的线粒体和粗面内质网。高倍透射电镜显示内皮腔膜结构有局灶性损伤。如果在光化学致敏期间将脑温降低4摄氏度，血小板反应会受到抑制，而不会干扰其他超微结构变化。这些结果与以下假设一致，即光化学诱导的内皮改变刺激血小板活化，并表明异常的内皮功能是光化学诱导的脑梗死发病机制中的主要事件。
