| Coronary venous hypertension prevents the formation of the electrophysiological arrhythmogenic substrate of acute ischemia in the dog: salutary effects of preserved myocardial hydration. | |
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MedLine Citation:
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PMID: 9515002 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Coronary venous hypertension induced by partial coronary sinus obstruction (CSO) in the dog, prevents or delays the predictable ventricular fibrillation (VF) of the early phase of acute ischemia. Also, CSO acting presumably through enhanced myocardial hydration, normalizes the inhomogenous extracellular potassium ([K+]o) accumulation, a major factor in producing the electrophysiological disparities, characteristic of arrhythmogenic substrate. To further clarify the mechanism of early ischemic VF prevention in dogs, radioactive microspheres were used to evaluate regional perfusion changes, resulting from CSO sufficient to raise the coronary sinus pressure to 40 mmHg, before and during ischemia induced by double coronary artery occlusion (CAO) (n=5). Also, global or regional unipolar electrogram mapping was used to assess changes of epicardial ventricular activation times (AT) and sequence and activation recovery intervals (ARI) during CSO, CAO and combined CSO and CAO, induced in random order (n=8). CSO did not affect regional perfusion nor improved collateral blood flow during ischemia. With CSO, AT shortened modestly over time (0.41+/-1.1 ms/min, r=0.85, P<0. 05) and ARI transiently decreased by up to 5.5%. With CAO, AT became variably delayed and isochrone map distortions were indicative of localized conduction delays or blocks, consistent with elevated [K+]o. In contrast, when CAO was preceded by CSO, AT delays were homogenous and normal activation sequence was preserved. Also, whereas with CAO, ARI shortened unequally over the ischemic region by as much as 43% at individual sites (average of 38.3+/-6.8 ms, P<0. 001), with combined CSO and CAO, ARI shortening was less pronounced and more homogenous (26.1+/-5.6 ms, P<0.05), not exceeding 29% at any site. Thus, in accordance with previous findings of enhanced [K+]o homogeneity, coronary venous hypertension reduces the disparities of activation and refractoriness of ischemia attributable, at least in part, to disparate [K+]o accumulation. Since no collateral blood flow improvement could be identified, the salutary electrophysiological effects of CSO may reflect a more homogenous extracellular environment, due to preservation of normal microvascular pressure (Pmv) and sustained filtration and lymph flow. |
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Authors:
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A C Kralios; F A Kralios; F L Anderson; M Leonard |
Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, Non-P.H.S. |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 30 ISSN: 0022-2828 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 1998 Feb |
Date Detail:
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Created Date: 1998-05-28 Completed Date: 1998-05-28 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 255-68 Citation Subset: IM |
Copyright Information:
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Copyright 1998 Academic Press Limited. |
Affiliation:
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Department of Veterans Affairs Medical Center, Cardiology Section, University of Utah, Salt Lake City 84148, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acute Disease Animals Body Water / metabolism Constriction Coronary Vessels / physiopathology* Dogs Electrophysiology Extracellular Space / metabolism Hypertension / physiopathology* Myocardial Ischemia / complications*, physiopathology* Potassium / metabolism Ventricular Fibrillation / etiology, physiopathology, prevention & control* |
| Chemical | |
Reg. No./Substance:
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7440-09-7/Potassium |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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