Key result
Dorsal spinal cord stimulation significantly blunted the capacity of middle cervical ganglion neurons to reflexly respond to regional ventricular ischemia (29.5 vs 111.0 impulses/min, p<0.01), but not to global cardiac stress.
Why the study?
Does spinal cord stimulation reduce the capacity of intrathoracic extracardiac neurons to transduce myocardial ischemia in anesthetized canines?
Does spinal cord stimulation reduce the capacity of intrathoracic extracardiac neurons to transduce myocardial ischemia in anesthetized canines?
Absolute Event Rate: 29.5% vs 111%
p-value: p=<0.01
Spinal cord stimulation reduces the reflex response of intrathoracic extracardiac neurons to regional myocardial ischemia, highlighting a potential neuromodulation target to minimize adverse adrenergic excitation.
Highlights spinal cord stimulation as potential ischemia-modulation target; leaves open human translation from this animal model.
Populations of intrathoracic extracardiac neurons transduce myocardial ischemia, thereby contributing to sympathetic control of regional cardiac indices during such pathology. Our objective was to determine whether electrical neuromodulation using spinal cord stimulation (SCS) modulates such local reflex control. In 10 anesthetized canines, middle cervical ganglion neurons were identified that transduce the ventricular milieu. Their capacity to transduce a global (rapid ventricular pacing) vs. regional (transient regional ischemia) ventricular stress was tested before and during SCS (50 Hz, 0.2 ms duration at 90% MT) applied to the dorsal aspect of the T1 to T4 spinal cord. Rapid ventricular pacing and transient myocardial ischemia both activated cardiac-related middle cervical ganglion neurons. SCS obtunded their capacity to reflexly respond to the regional ventricular ischemia, but not rapid ventricular pacing. In conclusion, spinal cord inputs to the intrathoracic extracardiac nervous system obtund the latter's capacity to transduce regional ventricular ischemia, but not global cardiac stress. Given the substantial body of literature indicating the adverse consequences of excessive adrenergic neuronal excitation on cardiac function, these data delineate the intrathoracic extracardiac nervous system as a potential target for neuromodulation therapy in minimizing such effects.
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Ardell et al. (2009) studied Myocardial ischemia (animal model) (n=10). Dorsal spinal cord stimulation (SCS) vs. No spinal cord stimulation (baseline/control states) was evaluated on Middle cervical ganglion neuronal activity (impulses/min) in response to regional ventricular ischemia (p=<0.01). Dorsal spinal cord stimulation significantly blunted the capacity of middle cervical ganglion neurons to reflexly respond to regional ventricular ischemia (29.5 vs 111.0 impulses/min, p<0.01), but not to global cardiac stress.
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