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題 名 | 利用無特定病原豬建立缺血心肌保護機制之研究模式=The Establishment of SPF Pigs Model in Understanding Protective Mechanism of Myocardial Ischemia |
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作 者 | 林志鴻; 王耀宏; 李文權; 李相臺; 林凱元; 陳惠卿; 林寶雪; 黃琇琴; 彭兆昌; 毛仁淡; 楊平政; 朱瑞民; | 書刊名 | 中華民國獸醫學會雜誌 |
卷 期 | 24:4 1998.12[民87.12] |
頁 次 | 頁227-235 |
分類號 | 437.22 |
關鍵詞 | 缺血心肌保護機制; 豬模式; 熱緊迫蛋白; 無特定病原豬; Protective mechanism of myocardial ischemia; Pig model; Heat shock proteins; Specific pathogen free SPF pigs; |
語 文 | 中文(Chinese) |
中文摘要 | 心臟血管疾病在目前世界上人類死亡的原因中佔重要地位。急性心肌梗塞可以造 成心肌缺血以及組織傷害甚或死亡。輕度缺血處理誘導出來的熱緊迫蛋白,已被認為是對抗 再灌流之後維持心肌功能的有利因子之一。最近利用轉殖小鼠表現人類及大鼠熱緊迫蛋白70 可證明熱緊迫蛋白的合成與心肌的保護作用有因果的關係。然而,心肌組織中熱緊迫蛋白表 現之調控機制尚未完全清楚。由於豬的心臟血管系統與人類極為相似,所以在本研究中我們 利用豬來建立缺血心肌保護的研究模式。臺灣養豬科學研究所提供的無特定病原(specific pathogen free, SPF)豬(平均體重29.7±3.8 kg)在麻醉後,施行開胸手術及心肌缺血處理, 過程中監測豬隻之生理狀況包括心跳及血壓。冠狀動脈左前降支分出之後給予輕度缺血處理 (即兩次10分鐘的阻塞及之間30分鐘的灌流過程)。輕度缺血後經過再一次30分鐘之灌流 處理即取出心臟並加以分切。熱緊迫蛋白基因和其蛋白質產物的表現量以反轉錄-多聚合 鏈鎖反應(reverse transcription-polymerase chain reaction, RT-PCR)和蛋白質膠電泳配合西方 免疫吸漬法測定。於手術各步驟進行中,收集豬隻的血液測定血液生化成份。實驗結果顯示, 缺血處理組(n=6)與對照組(n=3)之生理監測值(心跳及血壓)和血液生化成份,無顯 著差異(p>0.05)。相對之下,缺血處理的熱緊迫蛋白70基因之表現,為對照組的2~10倍; 但是蛋白質方面則差異不顯著(p>0.05)。綜合以上結果及前人的研究顯示,我們已成功地 利用SPF豬建立研究心肌缺血之動物模式,此將有利於臨床藥物之評估及熱緊迫蛋白保護 缺血心肌分子機制之深入研究。 |
英文摘要 | Acute myocardial infarction may lead to myocardial ischemia and subsequent myocyte injury or even death. The synthesis of a 70 KDa heat shock protein (HSP70) induced by ischemic pretreatment have been considered to be one of the major causes to protect the ischemic myocardium against severe ischemic episode during the process of reperfusion. Recent evidences from transgenic mouse overexpressing human or rat inducible HSP70 have directly proved the cause-effect relationship between HSP synthesis and myocardial function. However, the regulatory mechanism controlling the expressing of the HSP in the heart has not yet been well-examined. Since the extensive similarity of the cardiovascular system between pig and human, We, Pig Research Institute Taiwan (PRIT) with sophistic technology and dedicated facility, have chosen pig as an animal model to study the molecular mechanism of ischemic preconditioning. Nine specific pathogen free (SPF) pigs weighing about 30 kg were used. After tracheotomy, the left anterior decending coronary artery was gently dissected free of surrounding tissue after second branch and then subjected to a two cycles of 10 minutes occlusion and 30 minutes reperfusion. Three shamed-operated SPF pigs were served as controls. Electrocardiogram and the blood pressure of the pigs were monitored by polygraph showed that were no significant difference between control and experimental animals. (p>0.05) Myocardium samples from infarction and non-infarction regions were collected and protein and mRNA levels for HSP70 were measured. The results from SDS-PAGE followed by immunoblotting showed no apparent difference in HSP70 levels. However, an inducible gene product of HSP70 was found to be increased to 2-10 folds when measured by using RT-PCR. The results indicate that porcine myocardium may augment gene expression of HSP70 in responding the ischemic damage. The successful estalishment of this SPF pigs model will beneficial our understanding to the molecular mechanism of HSP to protect the ischemic myocardium. |
本系統中英文摘要資訊取自各篇刊載內容。