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Differential roles for sarcKATP and ...
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Kanji, Hussein Diamondali.
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Differential roles for sarcKATP and mitoKATP channels in hypoxia and reoxygenation injury: A study of cell viability and ion channel pharmacology.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Differential roles for sarcKATP and mitoKATP channels in hypoxia and reoxygenation injury: A study of cell viability and ion channel pharmacology./
作者:
Kanji, Hussein Diamondali.
面頁冊數:
104 p.
附註:
Adviser: Robert French.
Contained By:
Masters Abstracts International40-04.
標題:
Health Sciences, Medicine and Surgery. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=MQ64965
ISBN:
0612649652
Differential roles for sarcKATP and mitoKATP channels in hypoxia and reoxygenation injury: A study of cell viability and ion channel pharmacology.
Kanji, Hussein Diamondali.
Differential roles for sarcKATP and mitoKATP channels in hypoxia and reoxygenation injury: A study of cell viability and ion channel pharmacology.
- 104 p.
Adviser: Robert French.
Thesis (M.Sc.)--University of Calgary (Canada), 2001.
Ischemic preconditioning is a novel cardioprotective mechanism in the heart. ATP-sensitive K (K<sub>ATP</sub>) channels have been suggested as key elements of this pathway; however, their mechanisms of activation and involvement remain unclear. To determine the ability of the plasma membrane K<sub>ATP </sub> (sarcK<sub>ATP</sub>) and mitochondrial K<sub>ATP</sub> (mitoK<sub> ATP</sub>) channels to mitigate injury, calcium overload and trypan blue viability assays were conducted. In addition, characterization of a new sarcK<sub>ATP </sub> selective drug, HMR 1098, was performed by patch clamp experiments. Testing of HMR 1098 on a number of different K<super>+</super>-channels showed a selective, dose-dependent block of the cardiac sarcK<sub>ATP</sub> channel. Calcium loading experiments and viability assays demonstrated that both sarcK<sub> ATP</sub> and mitoK<sub>ATP</sub> channels afford some level of protection at different, well-defined stages of the response to metabolic stress. The data also suggest that PKC stimulation as well as adenosine-A<sub> 1</sub> receptor activation can mediate this effect via activation of the sarc and mito K<sub>ATP</sub> channels.
ISBN: 0612649652Subjects--Topical Terms:
1017756
Health Sciences, Medicine and Surgery.
Differential roles for sarcKATP and mitoKATP channels in hypoxia and reoxygenation injury: A study of cell viability and ion channel pharmacology.
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Ischemic preconditioning is a novel cardioprotective mechanism in the heart. ATP-sensitive K (K<sub>ATP</sub>) channels have been suggested as key elements of this pathway; however, their mechanisms of activation and involvement remain unclear. To determine the ability of the plasma membrane K<sub>ATP </sub> (sarcK<sub>ATP</sub>) and mitochondrial K<sub>ATP</sub> (mitoK<sub> ATP</sub>) channels to mitigate injury, calcium overload and trypan blue viability assays were conducted. In addition, characterization of a new sarcK<sub>ATP </sub> selective drug, HMR 1098, was performed by patch clamp experiments. Testing of HMR 1098 on a number of different K<super>+</super>-channels showed a selective, dose-dependent block of the cardiac sarcK<sub>ATP</sub> channel. Calcium loading experiments and viability assays demonstrated that both sarcK<sub> ATP</sub> and mitoK<sub>ATP</sub> channels afford some level of protection at different, well-defined stages of the response to metabolic stress. The data also suggest that PKC stimulation as well as adenosine-A<sub> 1</sub> receptor activation can mediate this effect via activation of the sarc and mito K<sub>ATP</sub> channels.
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