Linked Life Data

2688982

Source:http://linkedlifedata.com/resource/pubmed/id/2688982

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6 Suppl
pubmed:dateCreated
1990-1-29
pubmed:abstractText
Cardiac arrhythmias are generated as the result of disorders of automaticity or impulse conduction. Regardless of the mechanism, however, calcium is likely to be involved. The rate of Ca2+ flux across the membrane of automatic cells alters their firing rate. Myocardial cells that do not ordinarily initiate action potentials can do so when they are partially depolarized. Low extracellular Ca2+ concentrations or Ca2+ channel-blocking drugs can reduce or abolish such ectopic firing. Early afterdepolarizations are also induced in cardiac cells by partial depolarization, whereas delayed afterdepolarizations are induced by Ca2+ overloading. Early afterdepolarizations and delayed afterdepolarizations can both be suppressed by low external Ca2+ concentrations or by Ca2+ channel blockers. With respect to arrhythmias ascribable to disorders of conduction, Ca2+ channel blockers can aggravate conduction disturbances in the sinoatrial node or atrioventricular junction. Furthermore, these drugs can abolish those reentrant arrhythmias in which a cardiac impulse rotates around a loop in which nodal tissue is an integral element. Ca2+ channel blockers can also reduce the susceptibility for ventricular fibrillation to supervene in ischemic hearts, especially when the sympathetic nervous system is overactive.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0009-7322
pubmed:author
pubmed:issnType
Print
pubmed:volume
80
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
IV23-30
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Role of calcium in arrhythmogenesis.
pubmed:affiliation
Division of Investigative Medicine, Mount Sinai Medical Center, Cleveland, Ohio 44106.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review