Cardioprotective effects of KRN2391 and nicorandil on ischemic dysfunction in perfused rat heart
Autor: | Ohta Hideo, Fukushima Hideaki, Ogawa Nobuyuki, Nishikori Koji, Jinno Yasuhiro, Harada Katsuhiko |
---|---|
Rok vydání: | 1991 |
Předmět: |
Male
Niacinamide Agonist Pyridines medicine.drug_class Vasodilator Agents Potassium Ischemia chemistry.chemical_element Coronary Disease Vasodilation In Vitro Techniques Pharmacology Glibenclamide Cytosol Heart Rate Glyburide medicine Animals Nicorandil business.industry Myocardium Rats Inbred Strains medicine.disease Potassium channel Rats Perfusion chemistry Anesthesia cardiovascular system business medicine.drug |
Zdroj: | European Journal of Pharmacology. 204:171-177 |
ISSN: | 0014-2999 |
DOI: | 10.1016/0014-2999(91)90702-r |
Popis: | The cardioprotective effect of KRN2391 (N-cyano-N-(2-nitroxymethyl)-3- pyridinecarboximidamide methanesulfonate), a novel vasodilator, was studied in the isolated perfused rat heart and compared with that of nicorandil. The isolated buffer-perfused rat heart was subjected to 25 min ischemia followed by 30 min reperfusion. The heart was pretreated with 0.1-10 microM KRN2391, 10-1000 microM nicorandil or vehicle. Before ischemia, KRN2391 (1-10 microM) and nicorandil (10-1000 microM) increased coronary flow, but did not modify the cardiac mechanical function. KRN2391 (1-10 microM) and nicorandil at high doses (300-1000 microM) resulted in significant improvements of cardiac functions and coronary flow during reperfusion and significantly reduced the release of cytosolic enzymes. The protective effects of 3 microM KRN2391 and 300 microM nicorandil were completely reversed by 3 microM glibenclamide, a blocker of ATP-sensitive potassium channels. Thus, KRN2391 and nicorandil at high doses have a direct cardioprotective effect, which may be related to activation of ATP-sensitive potassium channels. |
Databáze: | OpenAIRE |
Externí odkaz: |