October 1, 1991Circulation
Cellular electrophysiological basis for oxygen radical-induced arrhythmias. A patch-clamp study in guinea pig ventricular myocytes.
Why the study?
Do oxygen radicals alter action potential parameters and ionic currents in guinea pig ventricular myocytes?
Population
Patch-clamped guinea pig ventricular myocytes
Comparison
Oxygen radicals generated by dihydroxyfumarate vs Presence of oxygen radical scavengers superoxide…
Design
Preclinical
Follow-up
Up to 5 minutes of exposure
Authors
Discussion
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Member takes
Implication
May contribute to reperfusion arrhythmias via myocyte electrophysiology; leaves open translation beyond isolated guinea pig cells.
Structured PICO
Do oxygen radicals alter action potential parameters and ionic currents in guinea pig ventricular myocytes?
P
Population
Patch-clamped guinea pig ventricular myocytes
I
Intervention
Oxygen radicals generated by dihydroxyfumarate (DHF, 5 mM)
C
Comparator
Presence of oxygen radical scavengers superoxide dismutase (SOD) and catalase (CAT), or intracellular calcium kept low by EGTA
O
Outcome
Action potential (AP) parameters and ionic currents (IK, ICa, IK1)surrogate
Oxygen radicals induce major electrophysiological alterations in isolated myocytes, including AP prolongation and EADs, providing a cellular basis for reperfusion arrhythmias.
Cite This Study
Cerbai et al. (1991) studied this question.