THE ANALYSES OF LIPID MEDIATORS RELATED TO MULTIPLE ORGAN FAILURE AND MECHANISMS THAT PROVOKE BRAIN DAMAGE

我们按照原来的技术进行了动物实验。脑组织提取物用于核磁共振（NMR）代谢组学研究。使用“Alice2 for metabolome^<TM>”和“Adome Works/Modelbuilder （Fujitsu Co.）”进行数据分析。从肠缺血再灌注（I/R）后的大鼠脑中提取水溶性提取物，用于1H-NMR研究。(1)主成分分析允许在第1、3、5和7天比较I/R组或sham组的数据时区分不同的区域。SIMCA方法也能区分各组。(2)主成分分析显示，在I/R组和假手术组中，每天的数据。1与第3、5、7天的分布区域不同，说明这些代谢方面与第1天不同。ATP、磷酸肌酐和无机磷酸盐等物质对能量代谢很重要。31P-MRS对于测量这些物质至关重要，这一想法促使我们为31P-MRS测量制作了一种新颖的表面线圈。这个线圈将使我们能够评估磷脂的前体和降解的最终产物，磷脂是细胞膜的主要成分，并估计脑组织的代谢变化。我们还分析了失血性休克前后啮齿动物肠道和肺部的代谢变化。在肠道中，复苏后120分钟的代谢状态倾向于恢复到休克前的状态。另一方面，在肺部，复苏后120分钟的代谢状态与休克前不同。利用从血浆和淋巴中获得的核磁共振数据，我们还对失血性休克模型进行了代谢组学分析。在休克前和复苏后比较低分子化合物和脂类物质时，结构元素的变化清晰可见。

We underwent animal experiments following our original technique. Brain tissue extracts were provided for the study of Nuclear Magnetic Resonance (NMR) metabolomics. Data analyses were performed using "Alice2 for metabolome^<TM>" and "Adome Works/Modelbuilder (Fujitsu Co.)". The water-soluble extract was collected from rat brain after intestinal ischemia-reperfusion (I/R) and used for the 1H-NMR study. (1) The principal component analysis allowed discrimination of different regions, when data from I/R or sham groups were compared on days 1, 3, 5, and 7. The SIMCA method was also able to discriminate each group. (2) The principal component analysis revealed that, in both I/R and sham groups, the data on day.1 distributed in a different region from those on days 3, 5, and 7, suggesting that these metabolic aspects are different from that on day 1. Substances such as ATP, creatinine phosphate, and inorganic phosphate are important for energy metabolism. The idea that 31P-MRS is essential for measuring these substances led us to make an original new surface-coil for 31P-MRS measurements. This coil will allow us to evaluate precursors and degradated endproducts of phospholipids which are main components of cell membranes, and to estimate metabolic changes in the brain tissue. We also analyzed metabolic changes in the rodent intestine and lung before and after hemorrhagic shock. In the intestine, the metabolic state at 120 minutes after resuscitation tended to return to that demonstrated prior to shock. On the other hand, in the lung, the metabolic state at 120 minutes after resuscitation was different from that shown before shock. Using NMR data obtained from the plasma and lymph, we also performed metabolomics analyses in the hemorrhagic shock model. The change in structural elements were clearly shown, when low molecular compounds and lipid-type substances were compared before shock and after resuscitation.