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題 名 | The Interference of Uptake of Thallium-201 in Cultured Rat Myocardial Cells with Existence of Potassium Related Pharmaceuticals--A Preliminary Report=鉀相關藥物對鉈201進入幼鼠心肌培養細胞的影響--初步報告 |
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作 者 | 陳毓雯; 葉竹來; 黃允志; 陳英俊; 黃英峰; 劉金昌; | 書刊名 | The Kaohsiung Journal of Medical Sciences |
卷 期 | 16:3 2000.03[民89.03] |
頁 次 | 頁134-140 |
分類號 | 418.346 |
關鍵詞 | 鉀離子相關藥物; 鉈201; 幼鼠; 心肌培養細胞; Thallium-201; Potassium channel openers and blockers; Sodium-potassium ATPase pump; |
語 文 | 英文(English) |
中文摘要 | 鉈201心肌灌注掃描造影,臨床上廣泛地運用於偵測心肌缺血,以輔助 診斷冠心症,及評估心肌梗塞後,心肌存活狀態,和可能存在其他心肌缺血區。 近年來大量鉀離子通道阻斷及促進劑研發,本研究目的在於了解這些鉀離子相關 藥物存在,對鉈201離子在心肌細胞的攝取是否有所影響。首先分別將各種不同 的鉀離子相關藥物,例如:氯化鉀,鈉-鉀幫浦抑制劑(ouabain),鍶化合物,各種 鉀離子通道阻斷及促進劑等,與幼鼠心肌培養細胞反應,加入鉈201六十分鐘 後,以伽瑪計測器記錄進入心肌細胞內鉈201的放射量。實驗發現鉈與鉀離子在 幼鼠心肌培養細胞中,表現相似生物性,兩種細胞外不同濃度鉀離子(2.5mM, 5mM) 皆明顯減少鉈201離子進入幼鼠心肌細胞,0.5mM ouabain,一種鈉-鉀幫浦抑制 劑可阻斷40%的鉈201離子進入幼鼠心肌培養細胞內,另一鉀離子拮抗劑-鍶離 子同樣造成減少鉈201進入心肌細胞,此次結果中,我們發現鉀離子通道阻斷 劑,尤其是glibenclamide及TEA可阻斷部分鉈201離子為心肌培養細胞所攝取, 而鉀離子通道促進劑則對鉈201進入心肌培養細胞無明顯影響,由實驗結果,我 們有以下結論:鈉-鉀幫浦抑制劑(ouabain)可減少40%的鉈201離子為幼鼠心肌培 養細胞所攝取,間接證明部份鉈201離子進入心肌細胞經由鈉-鉀幫浦主動運輸, 鉀離子、鍶離子及鉀離子通道阻斷劑,如glibenclamide及TEA,抑制不同比例量 的鉈201離子進入幼鼠心肌培養細胞。 |
英文摘要 | Thallium-201 myocardial perfusion imaging is wildly used to detect and assess the extent of jeopardized myocardial ischemia in the coronary artery disease and the viability of myocardium post infarction. In recent years, there has been a great deal of pharmacological development of blockers and openers of potassium channel. In this study, we will discuss the interference of uptake of thallium-201 ion in cultured neonatal rat myocytes with existence of a variety of pharmacological agents. The cultures of neonatal rat myocardial cells were incubated with different agents such as potassium chloride, sodium-potassium ATPase pump inhibitor (ouabain), cesium compound, variable potassium channel blockers ( 4 AP, TEA and glibenclamide) and their openers (minoxidil, and cromakalim). The radioactivity of intracellular thallium-201 that could enter rat myocardial cells was detected by gamma counter sixty minutes after thallium-201 was added. In this study we found that thallium and potassium ions behave in an analogous manner in cultured rat myocardial cells. Both 2.5 mM and 5 mM concentration of extracellular potassium ion significantly result in reduction of thallium-201 ion influx in rat myocardial cells. 0.5 mM ouabain, an inhibitor of sodium-potassium ATPase pump, reduced about 40% of influx of thallium-201 ion in cultured rat myocardial cells via active transport. Combination of both potassium ion and ouabain inhibit most of thallium-201 ions influx in myocardial cells, but it is not completely inhibited. Cesium, a potassium antagonist, also interferes with the uptake of thallium-201 in cultured rat myocytes in our study. The most interesting finding in our investigation is that potassium channel blockers such as TEA and glibenclamide, inhibit the influx of thallium-201 in myocytes. However, potassium channel openers have no overt effect on influx of thallium-201 in cultured rat myocytes. We indirectly observe about 60% of influx of thallium-201 ion into cultured rat myocardial cells via active sodium-potassium ATPase pump. Potassium, cesium and potassium channel blockers, such as TEA and glibenclamide, inhibited the different percentage of influx of thallium-201 in cultured rat myocardial cells in this study. |
本系統中英文摘要資訊取自各篇刊載內容。