Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
|
pubmed:dateCreated |
1993-4-15
|
pubmed:abstractText |
These experiments analyse the phase-dependent properties of spontaneous oscillations of the sarcoplasmic reticulum (SR) induced by Ca2+ overload. Right atrial tissue was loaded with intracellular Ca2+ by exposure to a modified Tyrode solution containing 50% of normal Na+ and 0.5 mM K+. Verapamil (2 microM) was added to block regenerative activity. Intracellular Ca2+ overload elicited spontaneous, rhythmic voltage and tension oscillations that were phase locked 1:1. Voltage and tension oscillations were abolished by exposure to low (0.9 mM) external Ca2+, 1 microM ryanodine, or 10 mM caffeine, indicating that both voltage and tension oscillations resulted from spontaneous oscillations in SR Ca2+ release. Single pulses of nerve-stimulated ACh release elicited phase shifts in both voltage and tension oscillations. Sinusoidal current was used as a periodic stimulus to drive membrane voltage and elicit periodic voltage oscillations. Stimulated voltage oscillations entrained spontaneous tension oscillations 1:1 in a range of frequencies close to the basic spontaneous SR oscillatory cycle length, or 2:1 at frequencies close to one-half the spontaneous SR oscillatory cycle length. Stimulation frequencies between these two regions entrained tension oscillations in predictable fixed coupled ratios (4:3, 3:2) and resulted in Wenckeback-like voltage patterns. Stimulation frequencies between phase-locked regions resulted in complex coupling relationships and irregular voltage patterns. Exposure to 1 microM ryanodine, 0.9 mM external Ca2+, or 10 mM caffeine abolished irregular voltage patterns and tension. We conclude that the SR oscillator exhibits phase-dependent sensitivity to perturbations at the surface membrane. As a result, external perturbations can elicit phase differences between spontaneous SR oscillations and membrane voltage that cause either phase-locked or irregular voltage patterns. These findings identify an intracellular mechanism that may contribute to the development of cardiac dysrhythmias resulting from intracellular Ca2+ overload.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Jan
|
pubmed:issn |
0958-0670
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
78
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
79-93
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:8383504-Acetylcholine,
pubmed-meshheading:8383504-Action Potentials,
pubmed-meshheading:8383504-Animals,
pubmed-meshheading:8383504-Arrhythmias, Cardiac,
pubmed-meshheading:8383504-Calcium,
pubmed-meshheading:8383504-Calcium Channels,
pubmed-meshheading:8383504-Cats,
pubmed-meshheading:8383504-Electric Stimulation,
pubmed-meshheading:8383504-Female,
pubmed-meshheading:8383504-Heart Atria,
pubmed-meshheading:8383504-Male,
pubmed-meshheading:8383504-Membrane Potentials,
pubmed-meshheading:8383504-Myocardial Contraction,
pubmed-meshheading:8383504-Periodicity,
pubmed-meshheading:8383504-Sarcoplasmic Reticulum
|
pubmed:year |
1993
|
pubmed:articleTitle |
Phase-dependent properties of the cardiac sarcoplasmic reticulum oscillator in cat right atrium: a mechanism contributing to dysrhythmias induced by Ca2+ overload.
|
pubmed:affiliation |
Department of Physiology, Loyola University of Chicago, Stritch School of Medicine, Maywood, IL 60153.
|
pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.
|