Ischemic tolerance phenomenon from an approach of energy metabolism

从能量代谢途径观察缺血耐受现象

• 批准号: 06454281
• 负责人: KATAYAMA Yasuo
• 金额: $ 0.32万
• 依托单位: Nippon Medical School
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (B)
• 财政年份: 1994
• 资助国家: 日本
• 起止时间: 1994 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06454281/
• 关键词: ischemic tolerance; energy matabolism; pyruvate dehydrogenase (PDH); protein synthesis

The effect of 5 min lethal ischemia on cerebral metabolism and a mitochondrial enzyme, pyruvate dehydrogenase (PDH) activity in the animals treated with or without 2 min sublethal ischemia was studied using mongolian gerbils. Protein synthesis was also studied.The animals with or without pretreatment were induced 5 min lethal ischemia and allowed reperfusion for designated periods. The pretreated animals were given 2 min ischemia 24 hr prior to 5 min ischemic insult.Brain metabolites of ATP,PCr and lactate and PDH activity were determined in the cortex and hippocampus mainly including CA_1 region. Protein synthesis was determined by autoradiography method ; after injecting [^<14>C]-leucine the uptake was measured in CA_1, CA_3', dentate and cortex in the both groups.In 10 min reperfusion lactate levels in the non-pretreated group were lower than those of the pretreated group in cortex, otherwise, there was no difference in metabolism between the pretreated and the non-pretread animals … More in the both areas by reperfusion 3 days. However, the elevation of PDH activity in the hippocampus in the pretreated animals was suppressed in 5 min ischemia. In reperfusion 7 days, marked decrease of ATP and PCr concentrations in hippocampus in the non-pretreated animals, which reflects delayd neuronal death, was noticed, while that in cortex was not noticed.Protein synthesis in the all areas measured markedly decreased compared to each sham controls 1 hr after ischemia. After 1 day, in CA_1 region, protein synthesis in the pretreated animals recovered to 50% of the control, while that in the non-pretreated was about 20% of the control. In other areas protein synthesis quickly recovered to more than 60% of the control in the both groups.In conclusion, the pretreatment of sublethal ischmia prior to lethal ischemia does not influence the degree of the secondary ischemic insult. However it may have some effect on cellar organ molecular activity like a mitochondrial enzyme PDH,and influences protein synthesis in CA_1 region, which may be essentials to induce ischemic tolerance. Less

本实验观察了5 min致死性缺血对沙土鼠脑代谢及线粒体丙酮酸脱氢酶（PDH）活性的影响。采用5 min致死性缺血再灌注模型，观察缺血前和缺血后不同时间的蛋白质合成情况。缺血2 min后再行5 min缺血24 h，测定脑内ATP、PCr、乳酸代谢产物及海马（主要包括CA_1区）PDH活性。用放射自显影法测定蛋白质合成，注射[^<14>C]-亮氨酸后测定两组大鼠海马CA_1、CA_3 ′、齿状回和皮质的摄取，再灌注10 min时，未预处理组皮质乳酸含量低于预处理组，而代谢无差异 ...更多信息 再灌注3天后，两个区域均恢复正常。然而，在预处理的动物海马中的PDH活性的升高在5分钟缺血中被抑制。再灌注7天，未预处理组海马ATP和PCr含量明显降低，反映了神经元的延迟性死亡，而皮层则无明显变化，缺血后1小时各区域蛋白质合成均明显低于假手术对照组。1d后，预处理组CA_1区蛋白质合成恢复到对照组的50%，而未预处理组仅为对照组的20%左右。在其他领域的蛋白质合成迅速恢复到60%以上的控制在两个groups.In结论，预处理的亚致死性缺血前致死性缺血不影响继发性缺血损伤的程度。但它可能与线粒体酶PDH一样，对细胞器官分子活性有一定影响，并影响CA_1区蛋白质合成，这可能是诱导缺血耐受的必要条件。少

项目成果

Katayama Y et al.: "Studies of ischemic tolerence -An approach from erergy metabolism and protein synthesis-." Jpn J Stroke. 17 (in press). (1996)

Katayama Y 等人：“缺血耐受性的研究 - 来自能量代谢和蛋白质合成的方法 -”。

yasuo KATAYAMA: "Ischemic tolerance phenomenon from an approach of energy metabolism and the mitochondrial enzyme activity of pyruvate dehydrosenase in gerbils" J CBF and Metabol.Vol.15,suppl.1. S197 (1995)

yasuo KATAYAMA：“沙鼠能量代谢方法和丙酮酸脱氢酶线粒体酶活性的缺血耐受现象”J CBF 和 Metabol.Vol.15，suppl.1。

Katayama Y: "Ischemic tolerance phenomenon from an approach of energy metabolism." J.Nippon Med.Sch.61. 134-140 (1994)

Katayama Y：“来自能量代谢途径的缺血耐受现象。”

yasuo KATAYAMA: "lschemic tolerance phenomenon from an approach of energy metabolism and the mitochondrial enzyme activity of pyruvate dehydrogenase in gerbils" J CBF and Metabol.Vol.15,suppl.1.S197 (1995)

yasuo KATAYAMA：“来自能量代谢方法和沙鼠丙酮酸脱氢酶线粒体酶活性的缺血耐受现象”J CBF and Metabol.Vol.15,suppl.1.S197 (1995)

片山 泰朗: "脳代謝よりみた虚血耐性現象" 日医大誌. 61. 134-140 (1994)

Yasuo Katayama：“从脑代谢的角度观察缺血耐受现象”日医大学学报61. 134-140（1994）。