| Effect of prostaglandin I2 analogues on left ventricular diastolic function in vivo. | |
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MedLine Citation:
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PMID: 15993879 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The prostaglandin I2 analogues epoprostenol and iloprost increase left ventricular contractility. Therefore, we hypothesize that the prostaglandin I2 analogues epoprostenol and iloprost improve also left ventricular diastolic function. To test this hypothesis, the effects of epoprostenol and iloprost on left ventricular diastolic function were assessed in vivo and compared to two vasodilators sodium nitroprusside and adenosine, not formerly associated with changes of left ventricular contractility. Eleven pigs (25.9+/-2.8 kg, balanced anaesthesia) were exposed to the short-acting intravenous vasodilators sodium nitroprusside, adenosine and epoprostenol in a randomized cross over design. The long-acting iloprost was administered at the end of the protocol. The drugs are titrated to achieve a 25% reduction of diastolic aortic pressure. Active isovolumic relaxation properties of the left ventricle were assessed by the maximum velocity of left ventricular pressure drop. Passive phase of relaxation and filling was assessed by the determination of end diastolic compliance during a preload reduction manoeuvre. The maximum velocity of left ventricular pressure drop worsened during the infusion of sodium nitroprusside (baseline: -1950; sodium nitroprusside: -1293 mm Hg/s, p<0.05, Wilcoxon signed rank test versus vs. baseline) and adenosine (baseline: -2015; adenosine: -1345 mm Hg/s, p<0.05), but remained stable during the infusion of the prostaglandins (baseline: -1943; epoprostenol: -1785 mm Hg/s; baseline: -2042; iloprost: -1923 mm Hg/s). End diastolic compliance was not altered significantly by any vasodilator. Interstitial myocardial cAMP increased during the infusion of epoprostenol (7.60 to 13.87 fmol/ml, p<0.05) and tended to increase during the infusion of iloprost (7.56 to 11.66 fmol/ml, p=0.21). The prostaglandin I(2) analogues epoprostenol and iloprost preserved the early phase of active isovolumic relaxation, presumably mediated by myocardial cAMP, whereas sodium nitroprusside and adenosine impaired early active isovolumic relaxation. Passive relaxation and filling properties remained stable during the infusion of each applied vasodilator in the intact left ventricle in vivo. |
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Authors:
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Hille Kisch-Wedel; Gregor Kemming; Franz Meisner; Michael Flondor; Sebastian Bruhn; Carolina Koehler; Konrad Messmer; Bernhard Zwissler |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: European journal of pharmacology Volume: 517 ISSN: 0014-2999 ISO Abbreviation: Eur. J. Pharmacol. Publication Date: 2005 Jul |
Date Detail:
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Created Date: 2005-07-12 Completed Date: 2005-09-12 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 1254354 Medline TA: Eur J Pharmacol Country: Netherlands |
Other Details:
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Languages: eng Pagination: 208-16 Citation Subset: IM |
Affiliation:
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Clinic of Anesthesiology, Ludwig Maximilian University, Marchioninistr. 15, D-81377 Munich, Germany. Hille.Kisch-Wedel@med.uni-muenchen.de |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine
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administration & dosage,
pharmacology Animals Antihypertensive Agents / administration & dosage, pharmacology Blood Pressure / drug effects Cyclic AMP / metabolism Diastole Epoprostenol / administration & dosage, pharmacology* Heart Rate / drug effects Heart Ventricles / drug effects, metabolism Iloprost / administration & dosage, pharmacology* Infusions, Intravenous Nitroprusside / administration & dosage, pharmacology Random Allocation Swine Systole Time Factors Vasodilator Agents / administration & dosage, pharmacology Ventricular Function Ventricular Function, Left / drug effects*, physiology |
| Chemical | |
Reg. No./Substance:
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0/Antihypertensive Agents; 0/Vasodilator Agents; 15078-28-1/Nitroprusside; 35121-78-9/Epoprostenol; 58-61-7/Adenosine; 60-92-4/Cyclic AMP; 78919-13-8/Iloprost |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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