Selective Sinoatrial Node Optical Mapping and the Mechanism of Sinus Rate Acceleration
View Full Paper
Ask AI
Bookmark
Share
Population
12 male mongrel dogs weighing 22-28 kg
Comparison
High-potassium Tyrode's solution to suppress… vs Baseline and/or pre-isoproterenol state
Design
Preclinical
Authors
Discussion
Loading...
Member takes
Implication
Supports Ca clock in sympathetic SAN acceleration in animals; hypothesis-generating for human sinus node therapies.
Structured PICO
P
Population
12 male mongrel dogs weighing 22-28 kg (10 used for isolated, Langendorff-perfused right atria optical mapping, 2 for microelectrode recording)
I
Intervention
High-potassium Tyrode's solution (10 mmol/L) to suppress right atrial excitability, followed by isoproterenol (0.01-0.1 µmol/L) with or without ryanodine (3 µmol/L) or ZD7288 (3 µmol/L)
C
Comparator
Baseline (normal potassium 4.5 mmol/L) and/or pre-isoproterenol state
O
Outcome
Cycle length of sinus beats, shift of leading pacemaker site, and lead time of intracellular calcium (Cai) upstroke to membrane potential (Vm) upstrokesurrogate
Selective optical mapping of the intact sinoatrial node using high extracellular potassium confirms that acceleration of calcium cycling (Ca clock) underlies sinus tachycardia during sympathetic stimulation.
Limitations
- High-potassium concentration is not a physiological state, and may affect SAN function.
Cite This Study
Shinohara et al. (2011) studied this question.
View Full Paper
Ask AI
Bookmark
Share