| Effect of cellular uncoupling by heptanol on conduction in infarcted myocardium. | |
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MedLine Citation:
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PMID: 2295139 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Experiments were performed in vitro on six normal thin ventricular epicardial tissue strips and 10 strips removed from the infarcted regions of dogs 21-60 days after experimental myocardial infarction. Conduction was evaluated by mapping activation sequences at 40-45 sites over an area of 1 x 2 cm during pacing at a basic cycle length of 2,000 msec. The amplitude and length of recorded electrograms were also determined at each site. After control recordings, heptanol, which increases gap junctional resistance, was added to the tissue bath at concentrations ranging between 0.2 and 1.0 mM. In contrast to its effect on normal tissues, heptanol caused 75 of 260 previously active sites in the infarcted tissues to become inactive. The affected sites were located in areas of very slow conduction and/or adjacent to areas of preexisting conduction block. In addition, heptanol decreased the length and degree of fractionation of electrograms recorded in slowly conducting regions of the infarcted tissues. The magnitude of the decrease in electrogram length following heptanol was related to the degree of electrogram abnormality during control as reflected in the ratio of electrogram length to amplitude. Heptanol shortened electrograms by causing local conduction block, which eliminated some components of the fractionated electrograms. In an additional eight epicardial strips removed from the infarcted region, 0.5 mM heptanol had only a slight effect (10.7% decrease) on the maximum rate of membrane depolarization. Thus, heptanol does not act primarily by way of depressing the fast inward current. We conclude from heptanol's effects on conduction and electrogram characteristics that slow and dissociated conduction in the infarcted region is due to an abnormality in gap junctional distribution between surviving cells and/or an abnormality in individual gap junctional function. |
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Authors:
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J F Spear; C W Balke; M D Lesh; A H Kadish; J L Levine; E N Moore |
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Publication Detail:
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Type: Comparative Study; 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: Circulation research Volume: 66 ISSN: 0009-7330 ISO Abbreviation: Circ. Res. Publication Date: 1990 Jan |
Date Detail:
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Created Date: 1990-02-15 Completed Date: 1990-02-15 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 202-17 Citation Subset: IM |
Affiliation:
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Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Action Potentials Alcohols / pharmacology* Animals Dogs Electrophysiology Heart Conduction System / drug effects*, physiopathology Heptanol Myocardial Infarction / pathology, physiopathology* Myocardium / pathology* Uncoupling Agents / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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HL-07346/HL/NHLBI NIH HHS; HL-25213/HL/NHLBI NIH HHS; HL-28393/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Alcohols; 0/Uncoupling Agents; 111-70-6/Heptanol |
| Comments/Corrections | |
Comment In:
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Circ Res. 1990 Nov;67(5):1299-300
[PMID:
2225362
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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