Sharma H S, Westman J, Nyberg F, Cervos-Navarro J, Dey P K
Institute of Neuropathology, Free University, Berlin, Federal Republic of Germany.
Acta Neurochir Suppl (Wien). 1994;60:65-70. doi: 10.1007/978-3-7091-9334-1_17.
The possibility that serotonin and prostaglandins participate in edema formation following heat stress (HS) was examined in young rats. Exposure of conscious young animals (8-9 weeks old) to heat at 38 degrees C in a biological oxygen demand (BOD) incubator (relative humidity 50-55%; wind velocity 20-25 cm/s) for 4 h resulted in marked increase in the whole brain water content (about 3%) as compared to animals kept at room temperature (21 degrees C). A marked extravasation of Evans blue and 131I-sodium occurred in the brain of heat exposed animals as compared to normal animals. Morphological examination using electron microscopy of selected brain regions of heat stressed animals showed profound cell changes. Thus perivascular edema, swollen neuronal and glial cells, membrane damage, vesiculation of myelin, axonal swelling and synaptic damage was frequent in this group of untreated animals. Pretreatment with ketanserin (a selective serotonin2 receptor antagonist) or indomethacin (an inhibitor of prostaglandin synthesis) markedly reduced edema formation after 4 h HS in young animals. These heat stressed animals had considerably less extravasation of protein tracers as compared to the untreated group. Cell changes and edema at the ultrastructural level were mainly absent. Our results suggest that serotonin and prostaglandins are involved in heat stress induced breakdown of the BBB permeability, edema formation, and cell damage.
在幼鼠中研究了血清素和前列腺素参与热应激(HS)后水肿形成的可能性。将清醒的幼龄动物(8 - 9周龄)置于生物需氧量(BOD)培养箱中,在38℃下受热(相对湿度50 - 55%;风速20 - 25厘米/秒)4小时,与置于室温(21℃)的动物相比,全脑含水量显著增加(约3%)。与正常动物相比,受热动物脑内伊文思蓝和131I - 钠明显外渗。对受热应激动物选定脑区进行电子显微镜形态学检查显示细胞有深刻变化。因此,在这组未经处理的动物中,血管周围水肿、神经元和神经胶质细胞肿胀、膜损伤、髓鞘空泡化、轴突肿胀和突触损伤很常见。用酮色林(一种选择性血清素2受体拮抗剂)或吲哚美辛(一种前列腺素合成抑制剂)预处理可显著减少幼龄动物热应激4小时后的水肿形成。与未处理组相比,这些受热应激动物的蛋白质示踪剂外渗明显减少。超微结构水平的细胞变化和水肿基本不存在。我们的结果表明,血清素和前列腺素参与了热应激诱导的血脑屏障通透性破坏、水肿形成和细胞损伤。