Protective Effect of FR183998, a Na+/H+ Exchange Inhibitor, Against Postischemic Injury After Normothermic and Prolonged Hypothermic Ischemia in Isolated Perfused Rat Hearts.
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- Ohara Fumihiro
- Department of Cardiovascular Disease, Medicinal Biology Research Laboratories, Fujisawa Pharmaceutical Co., Ltd.
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- Yamamoto Nobuhiro
- Department of Cardiovascular Disease, Medicinal Biology Research Laboratories, Fujisawa Pharmaceutical Co., Ltd.
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- Maeda Kazuhiro
- Research Planning, Fujisawa Pharmaceutical Co., Ltd.
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- Ozaki Toru
- Department of Cardiovascular Disease, Medicinal Biology Research Laboratories, Fujisawa Pharmaceutical Co., Ltd.
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- Seki Jiro
- Department of Cardiovascular Disease, Medicinal Biology Research Laboratories, Fujisawa Pharmaceutical Co., Ltd.
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- Goto Toshio
- Department of Cardiovascular Disease, Medicinal Biology Research Laboratories, Fujisawa Pharmaceutical Co., Ltd.
Bibliographic Information
- Other Title
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- Protective Effect of FR183998, a Na〔+〕/H〔+〕 Exchange Inhibitor, Against Postischemic Injury After Normothermic and Prolonged Hypothermic Ischemia in Isolated Perfused Rat Hearts
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Abstract
Inhibition of Na+/H+ exchanger has been reported to protect hearts from ischemia and reperfusion injury. However, the effect of Na+/H+ exchange inhibition on hypothermic ischemic injury has not been extensively studied and the results are inconsistent. The purpose of this study was to investigate whether inhibition of Na+/H+ exchange with FR183998 (5-(2,5-dichlorothiphen-3-yl)-3-[(2-dimethylaminoethyl)carbamoyl]benzoylguanidine dihydrochloride), a potent Na+/H+ exchange inhibitor, would show protective effects against postischemic cardiac dysfunction after hypothermic as well as normothermic ischemia and furthermore, after hypothermic cardioplegic arrest in isolated rat hearts. FR183998 (3.2 × 10−8 – 3.2 × 10−7 M) improved post-ischemic recovery of left ventricular developed pressure and suppressed the increase of left ventricular end diastolic pressure in a dose-dependent manner, after not only 45 min of normothermic ischemia but also 6 h of hypothermic ischemia. Furthermore, FR183998 (10−7 – 10 −6 M) significantly reduced creatine kinase release during reperfusion after 3 h of hypothermic ischemia with cardioplegia. These results indicate that FR183998 has a potent protective effect on postischemic cardiac dysfunction after normothermic and hypothermic ischemia, and also on reperfusion injury after hypothermic cardioplegic arrest, suggesting that its effect would be additive to cardioplegia.
Journal
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- The Japanese Journal of Pharmacology
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The Japanese Journal of Pharmacology 87 (2), 110-116, 2001
The Japanese Pharmacological Society
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Keywords
Details 詳細情報について
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- CRID
- 1390282679264270464
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- NII Article ID
- 10007368055
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- NII Book ID
- AA00691188
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- COI
- 1:CAS:528:DC%2BD3MXnvF2qurg%3D
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- ISSN
- 13473506
- 00215198
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- NDL BIB ID
- 5950582
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- PubMed
- 11700009
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- Web Site
- http://id.ndl.go.jp/bib/5950582
- https://ndlsearch.ndl.go.jp/books/R000000004-I5950582
- https://api.elsevier.com/content/article/PII:S0021519819302835?httpAccept=text/xml
- https://api.elsevier.com/content/article/PII:S0021519819302835?httpAccept=text/plain
- https://search.jamas.or.jp/link/ui/2002129870
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- Abstract License Flag
- Disallowed