Respiratory Sinus Arrhythmia

Abstract

Abstract-The heart rate increases during inspiration and decreases during expiration. This respiratory sinus arrhythmia (RSA) occurs by modulation of premotor cardioinhibitory parasympathetic neuron (CPN) activity. However, RSA has not been fully characterized in rats, and despite the critical role of CPNs in the generation of RSA, little is known about the mechanisms that mediate this cardiorespiratory interaction. This study demonstrates that RSA in conscious rats is similar to that in other species. The mechanism of RSA was then examined in vitro. Rhythmic inspiratory-related activity was recorded from the hypoglossal rootlet of 700-to 800-m medullary sections. CPNs were identified by retrograde fluorescent labeling, and neurotransmission to CPNs was examined using patch-clamp electrophysiological techniques. During inspiratory bursts, the frequency of both spontaneous ␥-aminobutyric acidergic (GABAergic) and spontaneous glycinergic synaptic events in CPNs was significantly increased. Focal application of the nicotinic antagonist dihydro-␤-erythroidine in an ␣ 4 ␤ 2 -selective concentration (3 mol/L) abolished the respiratory-evoked increase in GABAergic frequency. In contrast, the increase in glycinergic frequency during inspiration was not altered by nicotinic antagonists. Prenatal nicotine exposure exaggerated the increase in GABAergic frequency during inspiration and enhanced GABAergic synaptic amplitude both between and during inspiratory events. Glycinergic synaptic frequency and amplitude were unchanged by prenatal nicotine exposure. This study establishes a neurochemical link between neurons essential for respiration and CPNs, reveals a functional role for endogenous acetylcholine release and the activation of nicotinic receptors in the generation of RSA, and demonstrates that this cardiorespiratory interaction is exaggerated in rats prenatally exposed to nicotine. Key Words: nucleus ambiguus Ⅲ vagal activity Ⅲ respiratory sinus arrhythmia Ⅲ prenatal nicotine Ⅲ sudden infant death syndrome T he heart rate increases during inspiration and decreases during the post-inspiration/expiration period. This respiratory-related change in heart rate, respiratory sinus arrhythmia (RSA), helps to match pulmonary blood flow to lung inflation and to maintain an appropriate diffusion gradient for oxygen in the lungs.

Regulation of Breathing and Autonomic Outflows by Chemoreceptors

“…Some of the inputs of presumptive CVPGNs are also known from experiments in which PRV was introduced in the heart muscle or the pericardial fat pads which contain the cardiac parasympathetic ganglia. More recently, investigators have injected a retrogradely transported dye into the pericardiac sac of neonate rats to visualize and record from putative cardiovagal parasympathetic preganglionic neurons in slices (321). Attractive in principle, this method may not be as specific as originally presumed because it seems to also label esophageal MNs located in the compact portion of nucleus ambiguus (150).…”

Methods of assessing vagus nerve activity and reflexes

“…Furthermore, the anesthetic agents often needed for animal studies alter autonomic and cardiovascular functions with parasympathetic nerve activity being notably susceptible. Examples of decerebrate and in vitro preparations that overcome these limitations include decerebrate animals [94, 95], the working heart-brain stem preparation [122–124], innervated heart-ganglia preparations [125, 126], medullary brain slice preparations (e.g., NA) [127, 128], and intact whole-mount cardiac ganglia preparations and neurons dissociated from ganglia [129]. The working heart - brain stem preparation is illustrated in Fig.…”

Prenatal nicotine exposure alters postnatal cardiorespiratory integration in young male but not female rats

“…The coupling between respiratory and cardiovascular control systems can also be identified by the relationship between respiratory frequency and the mean spectral frequency within the HF band following HR spectral analysis (Bernardi et al, 1989, Hirsch and Bishop, 1981). In the rodent RSA is not fully established until late postnatal development (postnatal day 21–30) (Kelly and Richards, 1997, Adolph, 1967, Adolph, 1971, Tucker and Johnson, 1984, Seidler and Slotkin, 1979), yet data from the neonatal rat in vitro suggest the neural circuitry involved in coordinating RSA-related modulation of parasympathetic drive is present as early as postnatal day 5 (P5) and is mediated by increases in inhibitory neurotransmission to cardiac vagal motoneurons during fictive inspiration (Neff et al, 2003). Moreover, this in vitro work suggests that this respiratory-related inhibitory input is selectively modulated by nicotinic receptors (Neff et al, 2003).…”