| Nisoldipine selectively induces coronary vasodilation and improves mild myocardial ischemia in dogs: a potential role of cellular acidosis. | |
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MedLine Citation:
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PMID: 10410823 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We examined whether nisoldipine, a calcium (Ca) channel blocker, increases coronary blood flow (CBF) without decreasing aortic blood pressure (AoP) with ischemic and nonischemic hearts, and whether the presence of cellular acidosis in ischemic myocardium contributes to the augmentation of coronary vasodilation due to nisoldipine. In 42 dogs, coronary perfusion pressure (CPP) was reduced so that CBF decreased to 60% of the baseline, and CPP was maintained constant thereafter. First, we administered nisoldipine into a systemic vein in the ischemic and nonischemic hearts. Second, nisoldipine was administered into the canine coronary artery of the ischemic myocardium, with and without administration of either sodium bicarbonate (NaHCO3), sodium hydroxide (NaOH), or amiloride. Nisoldipine (0.25-4.0 mg/kg, i.v.) increased CBF by 59% in the ischemic myocardium more than the nonischemic myocardium (by 34%) without reducing AoP. The infusion of nisoldipine (40 ng/kg/min, IC) increased CBF markedly by about 55% in the ischemic myocardium with increases in fractional shortening (FS; 11 +/- 2% to 21 +/- 2%) and lactate extraction ratio (LER; -19 +/- 4% to 15 +/- 2%). Increases in CBF, FS, and LER were markedly attenuated during administration of nisoldipine with concomitant administration of either NaHCO3 or NaOH. Furthermore, the extent of increases in CBF (54 +/- 2 mL/100 g/min), FS (13 +/- 2%), and LER (-17 +/- 4%) were also markedly attenuated due to the concomitant treatment with amiloride. We conclude that myocardial cellular acidosis plays an important role in mediating coronary vasodilation affected by nisoldipine in the ischemic myocardium. H+ may modulate the property of voltage-dependent Ca channels via Na(+)-H+ exchange. |
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Authors:
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M Kitakaze; H Funaya; K Komamura; K Node; T Minamino; H Mori; H Takeda; T Kuzuya; M Hori |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy Volume: 12 ISSN: 0920-3206 ISO Abbreviation: Cardiovasc Drugs Ther Publication Date: 1998 Dec |
Date Detail:
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Created Date: 1999-09-14 Completed Date: 1999-09-14 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8712220 Medline TA: Cardiovasc Drugs Ther Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 533-41 Citation Subset: IM |
Affiliation:
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First Department of Medicine, Osaka University School of Medicine, Suita, Japan. Kitakaze@medone.med.osaka-u.ac.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acidosis
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physiopathology* Amiloride / pharmacology Animals Bicarbonates / pharmacology Blood Pressure / drug effects Buffers Coronary Circulation / drug effects* Diuretics / pharmacology Dogs Injections, Intravenous Myocardial Ischemia / drug therapy*, physiopathology Nisoldipine / therapeutic use* Oxygen / blood Vasodilator Agents / therapeutic use* |
| Chemical | |
Reg. No./Substance:
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0/Bicarbonates; 0/Buffers; 0/Diuretics; 0/Vasodilator Agents; 2609-46-3/Amiloride; 63675-72-9/Nisoldipine; 7782-44-7/Oxygen |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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