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April 1, 1989AJP Cell Physiology

Doxyl stearic acids (16-DSA and 12-DSA) rapidly and reversibly reduced gap junctional conductance to unmeasurable levels in a dose- and time-dependent manner in neonatal rat heart cells.

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Population

Pairs of neonatal rat heart cells

Comparison

Doxyl stearic acids (16-DSA and 12-DSA) vs Control conditions, methyl esters of 16- and…

Design

Preclinical

Key result

Doxyl stearic acids (16-DSA and 12-DSA) rapidly and reversibly reduced gap junctional conductance to unmeasurable levels in a dose- and time-dependent manner in neonatal rat heart cells.

Authors

JBJanis M. Burt

Discussion

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Overview

Supports hypothesis that ischemia-induced fatty acids promote arrhythmias via gap junction uncoupling; animal data leave mechanism unproven in vivo.

Structured PICO

P
Population
Pairs of neonatal rat heart cells
I
Intervention
Doxyl stearic acids (16-DSA and 12-DSA)
C
Comparator
Control conditions, methyl esters of 16- and 12-DSA, stearic acid, and TEMPO
O
Outcome
Gap junctional conductance (gj)surrogate

Doxyl stearic acids uncouple cardiac cells by reducing gap junctional conductance, suggesting a mechanism by which ischemia-induced free fatty acids may cause arrhythmias.

Cite This Study

Janis M. Burt (1989) studied this question. Doxyl stearic acids (16-DSA and 12-DSA) vs. Methyl esters of 16- and 12-DSA, stearic acid, TEMPO, and control conditions was evaluated on Gap junctional conductance (gj). Doxyl stearic acids (16-DSA and 12-DSA) rapidly and reversibly reduced gap junctional conductance to unmeasurable levels in a dose- and time-dependent manner in neonatal rat heart cells.

synapsesocial.com/papers/6a9fdb223a35f4a2c890e166https://doi.org/10.1152/ajpcell.1989.256.4.c913
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