Key result
Morphine at 0.1 microM significantly augmented L-type Ca2+ current by 23% (P<0.05) and increased inward rectifier K+ current by 27% (P<0.05) in isolated rabbit ventricular myocytes.
Why the study?
Does morphine alter cardiac action potential and membrane currents in isolated rabbit ventricular myocytes?
Population
Isolated rabbit ventricular myocytes
Comparison
Morphine at concentrations from 0.01 to 1 microM vs Control (no morphine)
Design
Preclinical
Authors
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May alter rabbit ventricular electrophysiology; leaves open translation to human cardiac effects or clinical practice.
Does morphine alter cardiac action potential and membrane currents in isolated rabbit ventricular myocytes?
Effect estimate: increased by 23%
Absolute Event Rate: 7.3% vs 5.9%
p-value: p=< 0.05
Morphine prolongs action potential duration by increasing L-type Ca2+ current via delta- and kappa-opioid receptors, and hyperpolarizes resting membrane potential by increasing inward rectifier K+ current independently of opioid receptors in rabbit ventricular myocytes.
Xiao et al. (2005) studied this question. Morphine vs. control was evaluated on L-type Ca2+ current (ICa.L) at +10 mV (increased by 23%, p=< 0.05). Morphine at 0.1 microM significantly augmented L-type Ca2+ current by 23% (P<0.05) and increased inward rectifier K+ current by 27% (P<0.05) in isolated rabbit ventricular myocytes.
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