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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 蘇銘嘉(Ming-Jai Su) | |
dc.contributor.author | Hsiao-Jung Tseng | en |
dc.contributor.author | 曾筱蓉 | zh_TW |
dc.date.accessioned | 2021-06-08T06:06:49Z | - |
dc.date.copyright | 2007-08-08 | |
dc.date.issued | 2007 | |
dc.date.submitted | 2007-07-20 | |
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/25257 | - |
dc.description.abstract | 在敗血症休克中已知免疫系統會大量活化如巨噬細胞、嗜中性球及內皮細胞,伴隨著過度產生活性氧屬(reactive oxygen species)與活性氮屬(reactive nitrogen species),這些大量的發炎相關物質則是造成多重器官衰竭與低血壓休克導致高死亡率的原因。有許多的研究證實在脂多醣體(lipopolysaccharide, LPS)處理的動物中,在離體血管給予正腎上腺素與活體動物給予血管加壓物質無法使血壓回復是因為過度活化誘導型一氧化氮合成酶(inducible nitric oxide synthase, iNOS )產生一氧化氮(NO | zh_TW |
dc.description.abstract | In endotoxemic shock, the immune system including macrophage, neutrophils and endothelial cells becomes hyperactive to produce powerful inflammatory mediators associated with excessive release of reactive oxygen species and reactive nitrogen species. Production of these excessive mediators may cause multiple organ failure and hypotensive shock with high mortality. Various studies in lipopolysaccharide (LPS)-treated animals have proved that vascular hyporeactivity to norepinephrine in vitro and vasopressor-resistant hypotension in vivo are related to over production of nitric oxide (NO•) by inducible NO synthase (iNOS).
Thaliporphine, a phenolic aporphine alkaloid obtained from Chinese herbs and posessing antioxident and α1 adrenoreceptor antagonistic activity. Our previous study found that thaliporphine attenuated multiple organ failure and improved circulatory failure resulting from LPS-induced endotoxemia and increased the survival rate of endotoxemic rodents. The study aimed to investigate the alternation of cardiac electrophysiological function of rats and guinea pigs suffering from 24 h treatment with LPS (4 mg/kg i.v. in rats and 1 mg/kg i.p. in guinea pigs). The efficacy of thaliporphine treatment (at 30 min before or 2 h after LPS injection) to prevent LPS-induced cardiac dysfunction was examined and compared with the protective efficiency of 3 different agents including selective iNOS inhibitor (1400W), nonselective NOS inhibitor (NG-nitro-L-arginine methyl ester, L-NAME) and anti-inflammatory agent dexamethasone 21 phosphate disodium salt (Dex). The endotoxemic rodents suffering from 24h treatment with LPS showed marked hypotension with reflex tarchycardia, the increase of serum NO× level, leukocytes count and a dramatic decrease of lymphocytes. Pretreated with thaliporphine (1mg/kg, i.v.) or 1400W (3 mg/kg, i.v.), 30 min before LPS injection, significantly attenuated serum NO× level and also improved hypotension in LPS rats. In LPS-induced endotoxemic guinea pigs, pre-and post-treatment with thaliporphine and pretreatment with 1400W all effectively attenuated the lowering of systolic pressure but not the lowering of diastolic pressure. Pretreatment with either L-NAME (2 mg/kg, i.v.) or Dex (1 mg/kg, s.c.)also attenuated hypotension in endotoxemic rats, though L-NAME did not decrease the serum NO• content. Furthermore, thaliporphine (1μM and 10μM)attenuated NO• release from LPS-activated RAW 264.7 macrophage cell. Moreover, the cardioprotective effect of thaliporphine was supported by the decrease of serum CK-MB level in endotoxemic guinea pigs. In cardiac function evaluation, isolated hearts from rats and guinea pigs were mounted on Langendorff apparatus in a mode of the perfusion kept at a constant pressure (80 mmHg in rats and 60 mmHg in guinea pigs). In the initial 10 minutes of perfusion, the level of coronary flow in LPS group was higher than that in sham group, and gradually decreased to a similar level as that in sham group after perfusion for 30 minutes. As in LPS group, thaliporphine-treated groups (either pretreatment or post-LPS-treatment) had higher coronary flow at early phase of perfusion. In electrophysiological study, we found that the ventricular repolarization time (QTc, corrected QT interval)at basal cycle length or at a constant pacing rate was prolonged in LPS-24h-treated rats, and so did the effective refractory period of atria (AERP), ventricle (VERP) and Wenckbach cycle length (WCL). The occurrence of arrhythmia elicited by extra-stimulation protocol on ventricle was also increased in LPS-induced endotoxemic rodents in spite of the prolongation of cardiac effective refractory period. Therefore, the change of intracellular Ca2+ transients in isolated cardiomyocytes loaded with Fluo3-AM was examined to characterize the alteration of intracellular Ca2+ handling and the correlation with the triggered arrhythmia in endotoxemic rats. We found that the rate of Ca2+ releasing from sarcoplasmic reticulum (SR) was unaltered, but the decay rate of the Ca2+ transient was retarded in cells from endotoxemic rats. Besides, the diastole Ca2+ level was markedly elevated when cells were paced at high frequency. The results demonstrated that the pathophysiological characteristic of high occurrence of extrastimulation- induced arrhythmia was due to triggered activity resulted from dysfunction in intracellular Ca2+ handling of endotoxemic rat heart. In thaliporphine-pretreated endotoxemic rats, the occurrence of extrastimulation- induced arrhythmia was significantly decreased in association with the prevention of the cardiac electrical remodeling (CRM) and the recovery of the rate of Ca2+ reuptake. 1400W-pretreatment also preserved cardiac electrophysiological property and abolished the extrastimulation-induced arrhythmia in endotoxemic rats. However, dexamethasone and L-NAME did not affect the CRM but effectively decreased the occurrence of extrastimulation-induced arrhythmia. The NO• content in rat cardiomyocytes was examined by the fluorescence NO• probe, DAF-AM. A higher level of intracellular NO• was detected in cardiomyocytes isolated from endotoxemic rats, and this NO• level was significantly lowered in cardiomyocytes isolated from thaliporphine- or 1400W- pretreated endotoxemic rats. Western blot analysis revealed that the level of nitrotyrosine in total protein was higher in endotoxemic hearts. Thaliporphine-pretreatment could slightly decrease the nitrotyrosine level of endotoxemic hearts. The molecular mechanisms mediating the progress of CRM and the dysfunction of intracellular Ca2+ handling in endotoxemic rat hearts, and the mechanisms for the preservation of cardiac function by thaliporphine remain to be clarified. In conclusion, our results demonstrated the cardiac electrical remodeling including the prolongation of QTc and AERP/VERP in association with a higher incidence of extrastimulation-induced arrhythmia of endotoxemic hearts resulted from the dysfunction of intracellular Ca2+ handling. Thaliporphine slightly inhibited immune cell like macrophage to produce NO•, attenuated the iNOS-dependent excessive NO• synthesis and release in cardiomyocyte, reduced the nitrosylated proteins, and decreased the oxidative stress as well as damage by peroxynitrite in cardiomyocyte. These pharmacological actions may contribute to thaliporphine-mediated preservation of cardiac electrophysiological function and attenuation of the arrhythmogenic activity in endotoxemic rodent models. | en |
dc.description.provenance | Made available in DSpace on 2021-06-08T06:06:49Z (GMT). No. of bitstreams: 1 ntu-96-R94443001-1.pdf: 2374415 bytes, checksum: 473c4ceda2b0bd793eeb69ab1be6ed72 (MD5) Previous issue date: 2007 | en |
dc.description.tableofcontents | 中文摘要 ............................................. i
英文摘要...............................................iv 目錄 ..................................................vii 縮寫.................................................. ix 第一章 緒論...........................................1 第一節 敗血症的定義....................................1 第二節 發炎調節因子在敗血症中所扮演的角色..............2 第三節 發炎物質與敗血症所造成的心臟功能不全........... 3 第四節 一氧化氮(NO•)在敗血症心臟衰竭中所扮演的角色. 5 第五節 敗血症的治療策略............................... 8 第六節 藥物簡介....................................... 9 緒論附圖表............................................ 11 第二章 研究目的與動機................................ 22 第三章 實驗材料與方法................................ 25 第一節 動物活體實驗................................... 25 第二節 離體實驗....................................... 27 第三節 生化檢驗....................................... 29 第四節 LPS誘導巨噬細胞NO•生成實驗.................... 31 第五節 西方點墨法測定蛋白質被Nitrosylation的程度...... 32 第六節 單一心肌細胞實驗.................................................... 34 第七節 組織切片....................................... 35 第八節 試藥及其來源.................................................... 35 第九節 數據分析.................................................... 36 材料與方法附圖表.................................................... 37 第四章 實驗結果.................................................... 40 第一節Thaliporphine與其他藥物在LPS誘導敗血症活體動物實驗 之血液學各項參數的影...................................40 第二節 一氧化氮(nitric oxide,NO•)的測定結果........ 43 第三節Thaliporphine與其他藥物對離體心臟電生理的影響.....................................................44 第四節 Thaliporphine和其他給藥組對離體心臟的冠狀動脈流速與心跳之影響.............................................46 第五節 Thaliporphine和其他給藥組之離體心臟以電刺激驅策誘發心律不整試驗.......................................... 48 第六節 心室肌細胞在電刺激下細胞內Ca2+瞬時釋放之改變... 49 第七節 Thaliporphine可減少分離的心臟細胞內NO•含量,但沒有顯著減少心肌細胞內的蛋白被nitrsosylation的程度.........50 第八節 Thaliporphine可有意義減少LPS誘導RAW 264.7細胞產生的 NO•釋放...............................................50 第九節 組織切片的結果................................. 50 附圖表................................................ 52 第五章 討論.......................................... 72 第六章總結與未來展望.................................. 82 參考文獻...............................................85 | |
dc.language.iso | zh-TW | |
dc.title | Thaliporphine在內毒素血症心臟保護作用之研究 | zh_TW |
dc.title | Studies of Cardiac Protective Effects of Thaliporphine on Endotoxemia | en |
dc.type | Thesis | |
dc.date.schoolyear | 95-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 賴凌平(Ling-pin Lai),林正一(Chia-I Lin),羅時鴻(Shih-Hurng Loh) | |
dc.subject.keyword | 敗血症,沙利醭酚,誘發活性,心律不整,絕對不反應期,細胞內鈣離子, | zh_TW |
dc.subject.keyword | sepsis,thaliporphine,triggered activity,arrhythmia,effective refractory period,intracellular Ca2+, | en |
dc.relation.page | 97 | |
dc.rights.note | 未授權 | |
dc.date.accepted | 2007-07-20 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 藥理學研究所 | zh_TW |
顯示於系所單位: | 藥理學科所 |
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