Respiratory modulation of premotor cardiac vagal neurons in the brainstem

Abstract

The respiratory and cardiovascular systems are highly intertwined, both anatomically and physiologically. Respiratory and cardiovascular neurons are often co-localized in the same brainstem regions, and this is particularly evident in the ventral medulla which contains pre-sympathetic neurons in the rostral ventrolateral medulla, premotor parasympathetic cardioinhibitory neurons in the nucleus ambiguus, and the ventral respiratory group, which includes the pre-Botzinger complex. Anatomical studies of respiratory and cardiovascular neurons have demonstrated that many of these neurons have projections and axon collateral processes which extend into their neighboring cardiorespiratory regions providing an anatomical substrate for cardiorespiratory interactions. As other reports in this Special Issue of Respiratory Physiology & Neurobiology focus on interactions between the respiratory network and baroreceptors, neurons in the nucleus tractus solitarius, presympathetic neurons and sympathetic activity, this report will focus on the respiratory modulation of parasympathetic activity and the neurons that generate parasympathetic activity to the heart, cardiac vagal neurons.

Proposal for mechanisms of protection of supine sleep against sudden infant death syndrome: an integrated mechanism review

“…The ventrolateral PAG (vlPAG) is the most caudal and ventral (hence the most primitive), expressing a passive coping strategy comprising quiescence, hyporeactivity, hypotension, and bradycardia (46). This is also described as a "co-ordinated immobilization and dissociation defence response" (47), akin to the primitive reptilian defense response (48). In adults, the vlPAG mediates panic and anxiety (49), as a most extreme and severe response to threat.…”

“…In adults, the vlPAG mediates panic and anxiety (49), as a most extreme and severe response to threat. The vlPAG outflow is intensely and purely parasympathetic (47). The above, and aspects of it, are described in various terms: neurocardiogenic syncope (50), vagal bradycardia (51), loss of cardiovagal baroreflex during vasovagal syncope (52), hypotension from decreased renal, and iliac vascular resistance (53).…”

“…The rebound expiration that follows allows for coronary perfusion of blood with some oxygenation, which allows for safe increase in heart rate (56). Increased heart rate and coronary perfusion without oxygenation increases cardiomyocyte damage and mortality (47). A period of compensatory tachycardia usually follows successful autoresuscitation.…”

“…The gasp therefore may be inadequate to achieve venous return, maintaining coronary hypoxia and reflex vagal bradycardia. The hypoxic induced bradycardia, mediated by the vagal nerve from nucleus ambiguous and the dorsal motor complex is protective for the heart, blocking the vagus decreases survival (47). Failure to inhibit the dorsal motor complex may be underlying QT syndromes identified as contributing to some cases of SIDS (7).…”

“…Though protective to the heart, the hypoxia is lethal to the brain. The AAE and failure to autoresuscitate can be augmented by nicotine and other factors; Dergecheva et al (47) state "exaggeration of protective response to hypoxia could be detrimental … fatal events are augmented cardiorespiratory responses" (page 9). Note that serotonin defects may both predispose to AAE, and contribute to failure to recover from them.…”