Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 7-Day Trial for You or Your Team.

Learn More →

Myocardial gap junction organization in ischemia and infarction

Myocardial gap junction organization in ischemia and infarction Ischemia causes an increase in myocardial resistivity and a decrease in conduction velocity, thereby enhancing cardiac contractile dysfunction and arrhythmic tendency. Myocardial gap junctions, as principal determinants of conduction velocity, may, therefore, be expected to be deranged in ischemia. Despite a lack of consensus, attempts at correlating gap junction ultrastructural morphology with functional state have revealed the component connexons of gap junctions in freeze‐fractured myocardium to be in multiple small hexagonal arrays, tending to become randomly distributed and compacted under uncoupling conditions. Further hypoxic uncoupling causes ultrastructural damage and a reduction in gap‐junctional surface area. Immunohistochemical detection of connexin43 gap junctions in chronically ischemic non‐infarcted human myocardium demonstrates a reduction in junctional surface area within a normal number of intercalated disks per myocyte, and with a normal distribution of junction sizes. In healed canine infarction there are smaller and fewer gap junctions in the fibrotic myocardium adjacent to infarcts, with reductions in overall gap‐junctional content and the proportion of side‐to‐side vs. end‐to‐end intercellular connections. Immunohistochemical examination of intact human ventricular myocardium shows the myocytes immediately abutting healed infarcts to hve connexin43 gap junctions spread longitudinally over the cell surfaces, and not in discrete transversely orienated intercalated disks as in normal myocardium. Early after canine infarction, and before fibrotic healing, the connexin43 gap junctions in myocytes abutting the infarct show disorganization similar to that described in healed human infarcts, suggesting that this disturbance is an early pathophysiological cellular response, and not simply due to later fibrotic distortion. Such changes in gap‐junctional organization in myocardial ischemia and infarction may be implicated in the elusive link between subcellular structure, contractile dysfunction and arrhythmogenesis. © 1995 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Microscopy Research and Technique Wiley

Myocardial gap junction organization in ischemia and infarction

Peters, Nicholas S.
Microscopy Research and Technique , Volume 31 (5) – Jan 1, 1995
Download PDF
12 pages

Loading next page...
 
/lp/wiley/myocardial-gap-junction-organization-in-ischemia-and-infarction-H5Z0ITrhb8

References (114)

Publisher
Wiley
Copyright
Copyright © 1995 Wiley Subscription Services, Inc., A Wiley Company
ISSN
1059-910X
eISSN
1097-0029
DOI
10.1002/jemt.1070310507
pmid
8534899
Publisher site
See Article on Publisher Site

Abstract

Ischemia causes an increase in myocardial resistivity and a decrease in conduction velocity, thereby enhancing cardiac contractile dysfunction and arrhythmic tendency. Myocardial gap junctions, as principal determinants of conduction velocity, may, therefore, be expected to be deranged in ischemia. Despite a lack of consensus, attempts at correlating gap junction ultrastructural morphology with functional state have revealed the component connexons of gap junctions in freeze‐fractured myocardium to be in multiple small hexagonal arrays, tending to become randomly distributed and compacted under uncoupling conditions. Further hypoxic uncoupling causes ultrastructural damage and a reduction in gap‐junctional surface area. Immunohistochemical detection of connexin43 gap junctions in chronically ischemic non‐infarcted human myocardium demonstrates a reduction in junctional surface area within a normal number of intercalated disks per myocyte, and with a normal distribution of junction sizes. In healed canine infarction there are smaller and fewer gap junctions in the fibrotic myocardium adjacent to infarcts, with reductions in overall gap‐junctional content and the proportion of side‐to‐side vs. end‐to‐end intercellular connections. Immunohistochemical examination of intact human ventricular myocardium shows the myocytes immediately abutting healed infarcts to hve connexin43 gap junctions spread longitudinally over the cell surfaces, and not in discrete transversely orienated intercalated disks as in normal myocardium. Early after canine infarction, and before fibrotic healing, the connexin43 gap junctions in myocytes abutting the infarct show disorganization similar to that described in healed human infarcts, suggesting that this disturbance is an early pathophysiological cellular response, and not simply due to later fibrotic distortion. Such changes in gap‐junctional organization in myocardial ischemia and infarction may be implicated in the elusive link between subcellular structure, contractile dysfunction and arrhythmogenesis. © 1995 Wiley‐Liss, Inc.

Journal

Microscopy Research and Technique – Wiley

Published: Jan 1, 1995

Keywords: ; ; ; ; ; ;

There are no references for this article.