Institute of Neurobiology, Slovak Academy of Sciences, Soltésovej 4, 040 01, Kosice, Slovak Republic.
J Physiol Sci. 2009 Mar;59(2):97-103. doi: 10.1007/s12576-008-0013-7. Epub 2009 Jan 6.
This study was designed in order to consider whether the release of neuronally derived nitric oxide (NO) in the lumbosacral spinal cord during ischemia/reperfusion is region-specific and whether changes in Ca(2+)-dependent NO synthase (cNOS) activity paralell with functional outcome. The cNOS activity was measured in the spinal cord regions after 13-, 15- and 17-min ischemia alone and that followed by 24 h of reperfusion. In addition, the Tarlov's criteria were applied to define the neurological consequences of ischemia/reperfusion in experimental animals. Based on the results, it is evident that only the 17-min ischemia alone was quite sufficient to cause changes in cNOS activity, however, without alterations in functional outcomes. On the other hand, the ischemic episodes followed by reperfusion caused dynamic, region-specific alterations in cNOS activity and consequently led to deterioration of motor function of hindlimbs in affected animals. Our results indicate that the motoneurons in the ventral horns respond more sensitively to ischemia/reperfusion than do neurons localized in the other spinal cord regions and that changes in cNOS activity may also influence the axonal conductance in the white matter and account for the impairment of motoneuronal activity in affected animals.
本研究旨在探讨在缺血/再灌注期间腰骶脊髓中神经元衍生的一氧化氮（NO）释放是否具有区域特异性，以及 Ca(2+)-依赖性一氧化氮合酶（cNOS）活性的变化是否与功能结果平行。在单独缺血 13、15 和 17 分钟以及随后 24 小时再灌注后，测量了脊髓区域中的 cNOS 活性。此外，还应用 Tarlov 标准来定义实验动物缺血/再灌注的神经后果。基于这些结果，显然只有单独的 17 分钟缺血就足以引起 cNOS 活性的变化，但不会改变功能结果。另一方面，缺血后再灌注导致 cNOS 活性的动态、区域特异性改变，从而导致受影响动物后肢运动功能恶化。我们的结果表明，腹角中的运动神经元对缺血/再灌注的反应比定位于脊髓其他区域的神经元更为敏感，并且 cNOS 活性的变化也可能影响白质中的轴突传导，并解释受影响动物中运动神经元活性的损伤。
