Lukácová N, Jalc P, Marsala J
Neurobiologický ústav Slovenskej akadémie vied v Kosiciach.
Bratisl Lek Listy. 1998 Jul;99(7):359-63.
Degradation of membrane bound phospholipids in CNS during ischaemia begins with extreme rapidity. Sublethal ischaemia influences ischaemic tolerance in the affected neurons and is stressful enough to induce neuronal changes such as postischaemic hypoperfusion, transient suppression of protein synthesis and induction of stress (HSP) proteins. It seems, that the nature of factors responsible for ischaemic tolerance may involve the activation of multiple different systems.
The aim of this study was to investigate the changes of phospholipids in gray matter regions of spinal cord following sublethal ischaemia repeated in long intervals of reperfusion.
Male rabbits, weight range 2.5-3.5 kg were used in the experiment. They were divided in following groups : 1. control animals; 2. animals subjected to 25 min ischaemia; 3. animals subjected to 25 min ischaemia and 3 h of reperfusion; 4. animals subjected to sublethal (8-8-9 min) ischaemia repeated in long-lasting (8-8-24 h) intervals of reperfusion. Phospholipids were separated by thin layer chromatography, lipidic phosphorus was assessed spectrophotometrically.
Sublethal ischaemia repeated in long-lasting intervals of reperfusion increased the concentration of phospholipids to control levels in all gray matter regions. The resynthesis in the dorsal horns, of PC and PE in the ventral horns and of PC in the intermediate zone.
An excessive renewal of phospholipids after sublethal ischaemia repeated in longer intervals of reperfusion was most pronounced in the eh dorsal horns of the spinal cord and can be the result of many defensive cellular mechanisms.
中枢神经系统(CNS)在缺血期间,膜结合磷脂的降解极其迅速地开始。亚致死性缺血会影响受影响神经元的缺血耐受性,其压力足以诱导神经元发生变化,如缺血后灌注不足、蛋白质合成的短暂抑制以及应激(热休克蛋白,HSP)蛋白的诱导。似乎,负责缺血耐受性的因素的性质可能涉及多个不同系统的激活。
本研究的目的是调查在长时间再灌注间隔下重复亚致死性缺血后脊髓灰质区域磷脂的变化。
实验使用体重范围为2.5 - 3.5千克的雄性兔子。它们被分为以下几组:1. 对照动物;2. 经历25分钟缺血的动物;3. 经历25分钟缺血和3小时再灌注的动物;4. 在长时间(8 - 8 - 24小时)再灌注间隔下重复亚致死性(8 - 8 - 9分钟)缺血的动物。通过薄层色谱法分离磷脂,用分光光度法评估脂质磷。
在长时间再灌注间隔下重复亚致死性缺血使所有灰质区域的磷脂浓度增加至对照水平。在背角中磷脂的重新合成,腹角中磷脂酰胆碱(PC)和磷脂酰乙醇胺(PE)的重新合成,以及中间带中PC的重新合成。
在较长再灌注间隔下重复亚致死性缺血后磷脂的过度更新在脊髓背角最为明显,这可能是多种细胞防御机制的结果。