| Cardioprotective effects of amlodipine in the ischemic-reperfused heart. | |
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MedLine Citation:
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PMID: 2530882 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Amlodipine is a dihydropyridine derivative belonging to the group of pharmacologic calcium entry blocking agents and is characterized as having a slow onset and relatively long duration of action with minimal effects on cardiac electrophysiology and myocardial contractility. The protective effect of amlodipine was studied in isolated blood-perfused feline hearts made globally ischemic for 60 minutes followed by reperfusion for 60 minutes. Ischemic-induced alterations of left ventricular developed pressure and complicance were monitored. In 11 control and 7 drug-treated hearts, amlodipine produced significant decreases in myocardial oxygen consumption (6.2 +/- 0.4 to 4.4 +/- 0.4 ml oxygen/min/100 g) and coronary vascular resistance, as assessed by changes in perfusion pressure (120 +/- 1 to 100 +/- 4 mm Hg). Amlodipine administered before the onset of global ischemia decreased the development of ischemic contracture as reflected by a progressive increase in resting left ventricular diastolic pressure. The return of contractile function, 60 minutes afer reperfusion, improved significantly in the amlodipine-treated group compared with controls, and there was better maintenance of the tissue concentration of Na+, Ca2+ and K+. A canine model of regional myocardial ischemia (90 minutes) followed by 6 hours of reperfusion was used to assess the cardioprotective effects of amlodipine, 150 micrograms/kg, administered 15 minutes before reperfusion. Infarct size, expressed as a percentage of the area at risk, was smaller in the amlodipine-treated group (n = 10) than in the control group (n = 10) (34.5 +/- 3.8% vs 45.9 +/- 2.8%, p = 0.027). Risk region size did not differ between groups and both groups were comparable with respect to the hemodynamic parameters of heart rate, blood pressure and rate-pressure product. Amlodipine prevented the gradual reduction in coronary blood flow observed in the control group. It is concluded that amlodipine reduces myocardial ischemic injury by mechanism(s) that may involve a reduction in myocardial oxygen demand as well as by positively influencing transmembrane Ca2+ fluxes during ischemia and reperfusion. |
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Authors:
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P T Hoff; Y Tamura; B R Lucchesi |
Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The American journal of cardiology Volume: 64 ISSN: 0002-9149 ISO Abbreviation: Am. J. Cardiol. Publication Date: 1989 Nov |
Date Detail:
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Created Date: 1989-12-12 Completed Date: 1989-12-12 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0207277 Medline TA: Am J Cardiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 101I-115I discussion 115I-116I Citation Subset: AIM; IM |
Affiliation:
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Department of Pharmacology, University of Michigan Medical School, Ann Arbor 48109-0626. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amlodipine Animals Blood Pressure / drug effects Calcium / metabolism Calcium Channel Blockers Cats Compliance / drug effects Coronary Circulation / drug effects Electrophysiology Female Heart / drug effects*, physiopathology Heart Ventricles Male Myocardial Contraction / drug effects Myocardial Infarction / pathology Myocardial Reperfusion Injury / prevention & control* Myocardium / metabolism Nifedipine / pharmacology Rest |
| Grant Support | |
ID/Acronym/Agency:
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HL-19782-10/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Calcium Channel Blockers; 21829-25-4/Nifedipine; 7440-70-2/Calcium; 88150-42-9/Amlodipine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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