| Perfusion of ischemic myocardium during anesthesia with sevoflurane. | |
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MedLine Citation:
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PMID: 7943851 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Sevoflurane produces direct vasodilation of coronary arteries in vitro and decreases coronary vascular resistance in vivo, pharmacologic properties that may contribute to the development of "coronary steal." This investigation examined the effects of sevoflurane on the distribution of regional myocardial perfusion in chronically instrumented dogs with steal-prone coronary artery anatomy. METHODS: Dogs were chronically instrumented for measurement of aortic and left ventricular pressure, diastolic coronary blood flow velocity and subendocardial segment length. After recovery from surgery, dogs underwent repetitive, brief, left anterior descending coronary artery (LAD) occlusions via an implanted hydraulic vascular occluder to enhance collateral development. A progressive left circumflex coronary artery (LCCA) stenosis was also obtained using an ameroid constrictor. After development of LCCA stenosis, the LAD was totally occluded to produce a model of multivessel coronary artery disease. Systemic hemodynamics, regional contractile function and myocardial perfusion measured with radioactive microspheres were assessed in the conscious state and during sevoflurane anesthesia at 1.0 and 1.5 MAC with and without restoration of arterial blood pressure and heart rate to conscious levels. RESULTS: Total LAD occlusion with simultaneous LCCA stenosis increased heart rate, mean arterial pressure, left ventricular systolic and end-diastolic pressures, end-diastolic segment length, and rate-pressure product in conscious dogs. Subsequent administration of sevoflurane caused dose-related decreases in arterial pressure, left ventricular systolic pressure, double product, and peak rate of increase of left ventricular pressure at 50 mmHg. Perfusion of normal myocardium was unchanged during sevoflurane anesthesia. In contrast, sevoflurane caused dose-dependent decreases in blood flow to myocardium supplied by the stenotic LCCA, which returned to control levels after restoration of heart rate and arterial pressure. No reduction in collaterally derived blood flow to the occluded region was produced by 1.0 or 1.5 MAC sevoflurane. No redistribution of blood flow away from the occluded LAD region to normal or stenotic myocardium occurred during sevoflurane anesthesia. In fact, increases in the ratio of blood flow between occluded and normal zones or occluded and stenotic zones were observed in the subepicardium during 1.5 MAC sevoflurane with maintenance of the heart rate and arterial pressure at conscious levels. CONCLUSIONS: The results demonstrate that sevoflurane does not reduce or abnormally redistribute myocardial blood flow derived from coronary collateral vessels in a chronically instrumented canine model of multivessel coronary artery obstruction. |
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Authors:
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J R Kersten; A P Brayer; P S Pagel; J P Tessmer; D C Warltier |
Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Anesthesiology Volume: 81 ISSN: 0003-3022 ISO Abbreviation: Anesthesiology Publication Date: 1994 Oct |
Date Detail:
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Created Date: 1994-11-08 Completed Date: 1994-11-08 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 1300217 Medline TA: Anesthesiology Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 995-1004 Citation Subset: AIM; IM |
Affiliation:
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Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Anesthesia, Intratracheal Anesthetics* / pharmacology* Animals Blood Pressure / drug effects, physiology Coronary Disease / physiopathology Dogs Dose-Response Relationship, Drug Ethers / pharmacology* Female Heart Rate / drug effects, physiology Hemodynamics / drug effects, physiology Male Methyl Ethers* Myocardial Ischemia / physiopathology* Vascular Resistance / drug effects, physiology Vasodilation / drug effects, physiology |
| Grant Support | |
ID/Acronym/Agency:
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GM 08377/GM/NIGMS NIH HHS; HL 36144/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Anesthetics; 0/Ethers; 0/Methyl Ethers; 28523-86-6/sevoflurane |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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