Molecular mechanisms of the reversal of imipramine-induced sodium channel blockade by alkalinization in human cardiac myocytes
Why the study?
Does alkalinization reverse imipramine-induced sodium channel blockade in isolated human atrial myocytes?
Population
Isolated human atrial myocytes
Comparison
Alkalinization in the presence of imipramine vs Imipramine alone (absence of alkalinization)
Design
Preclinical
Authors
Discussion
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Member takes
Implication
May support pH modulation in TCA Na-channel toxicity; hypothesis-generating from animal data, human validation required.
Structured PICO
Does alkalinization reverse imipramine-induced sodium channel blockade in isolated human atrial myocytes?
P
Population
Isolated human atrial myocytes
I
Intervention
Alkalinization (intracellular and extracellular) in the presence of imipramine (1 and 5 microM)
C
Comparator
Imipramine alone (absence of alkalinization)
O
Outcome
Sodium current (INa) and state-dependent INa block (dissociation constant Kd)surrogate
Alkalinization reverses imipramine-induced sodium channel blockade primarily by promoting unbinding from the receptor, with intracellular alkalosis playing a key role in activated-state interaction.
Cite This Study
Bou‐Abboud et al. (1998) studied this question.