Is carotid body clenervation the silver bullet for heart failure?

摘要

The carotid body chemoreceptors are traditionally viewed as the body's primary oxygen sensors. Activation of the carotid body chemoreceptors in response to a fall in arterial oxygen levels results in reflex increases in both ventilation and sympathetic nervous system activity. Additionally, a growing body of experimental evidence in both animals and humans supports a role for the carotid body chemoreceptors in the pathophysiology of several sympafhoexcitatory conditions such as hypertension, sleep apnoea and congestive heart failure (CHF). Consistent with this idea, in a recent issue of The Journal Physiology, Marcus and colleagues (Marcus et al. 2013) confirmed that the carotid body chemoreceptors play a central role in CHF pathophysiology. Expanding on their previous experiments in rats (Del Rio et al. 2013), Marcus et al. induced CHF in a group of rabbits through ventricular pacing and examined the effect of carotid body denervation on ventilation, autonomic nervous system activity and markers of cardiac function. Remarkably, only 9 days after denervation, a number of ventilatory, autonomic and cardiac function variables commonly impaired in CHF were improved. These results raise several important questions regarding the contribution of the carotid body chemoreceptors to CHF pathophysiology: how does carotid body denervation initiate improvements in CHF; what is the link between the carotid body chemoreceptors and cardiac function in CHF; could carotid body denervation replace traditional therapeutic strategies for CHF?