Minimal force‐frequency modulation of inotropy and relaxation of in situ murine heart
Population
Open-chest mice of various strains (n = 16) under etomidate/urethane anaesthesia
Comparison
Heart rate modulation (slowing with ULFS-49 to <… vs Different heart rates within the same subjects
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Caution advised extrapolating murine contractility to humans; leaves open accurate phenotyping of genetically engineered cardiac disease models.
Structured PICO
P
Population
Open-chest mice of various strains (n = 16) under etomidate/urethane anaesthesia
I
Intervention
Heart rate modulation (slowing with ULFS-49 to < 400 beats min(-1) and atrial or ventricular pacing via intra-oesophageal catheter)
C
Comparator
Different heart rates within the same subjects (e.g., resting HR vs paced HRs)
O
Outcome
Cardiac-specific contractile indexes (dP/dt(max), relaxation time constant) across different heart ratessurrogate
The in situ murine heart exhibits minimal force-frequency reserve at physiological heart rates, which is important for interpreting genetically engineered mouse models of cardiac disease.
Cite This Study
Georgakopoulos et al. (2001) studied this question.