Balentine J D, Greene W B
Acta Neuropathol. 1987;73(3):233-9. doi: 10.1007/BF00686616.
This study defines the conditions required to provoke myelopathic changes by dripping lactic acid onto the surgically exposed spinal cord of adult male rats. A severe necrotizing myelopathy was observed after 24 h, principally in the posterior half of the cord at the level of lactic acid (pH 1.8) application. A profound early effect on small blood vessel walls, appearing necrotic after 30 min to 2 h, was identified. Nerve fiber alterations (axonal stasis, granular axoplasm, axonal calcification, and vesicular myelin), identical to those appearing early in the myelopathies of trauma and calcium toxicity, were apparent. However, the pathogenesis of these alterations in this model remains unclear, because of the vascular events and the presumed alterations of calcium metabolism by the acid. Further studies are required to elucidate the precise mechanisms of these important reactions of myelinated axons to the injuries provoked by acid, calcium, and trauma.
本研究确定了通过将乳酸滴加到成年雄性大鼠手术暴露的脊髓上引发脊髓病性改变所需的条件。24小时后观察到严重的坏死性脊髓病，主要发生在应用乳酸（pH 1.8）水平的脊髓后半部。发现对小血管壁有深远的早期影响，在30分钟至2小时后出现坏死。观察到与创伤和钙毒性脊髓病早期出现的神经纤维改变（轴突停滞、颗粒状轴浆、轴突钙化和泡状髓鞘）相同。然而，由于血管事件以及酸对钙代谢的假定改变，该模型中这些改变的发病机制仍不清楚。需要进一步研究以阐明有髓轴突对酸、钙和创伤引发的损伤的这些重要反应的确切机制。
