▪ Abstract Breathing is a vital behavior that is particularly amenable to experimental investigation. We review recent progress on three problems of broad interest. (i) Where and how is respiratory rhythm generated? The preBotzinger Complex is a critical site, whereas pacemaker neurons may not be essential. The possibility that coupled oscillators are involved is considered. (ii) What are the mechanisms that underlie the plasticity necessary for adaptive changes in breathing? Serotonin-dependent long-term facilitation following intermittent hypoxia is an important example of such plasticity, and a model that can account for this adaptive behavior is discussed. (iii) Where and how are the regulated variables CO2 and pH sensed? These sensors are essential if breathing is to be appropriate for metabolism. Neurons with appropriate chemosensitivity are spread throughout the brainstem; their individual properties and collective role are just beginning to be understood.

Breathing: Rhythmicity, plasticity, chemosensitivity

Recent experiments in vivo and in vitro have advanced our understanding of the sites and mechanisms involved in mammalian respiratory rhythm generation. Here we evaluate and interpret the new evidence for two separate brainstem respiratory oscillators and for the essential role of emergent network properties in rhythm generation. Lesion studies suggest that respiratory cell death might explain morbidity and mortality associated with neurodegenerative disorders and ageing.

/pdf/looking-for-inspiration-new-perspectives-on-respiratory-39nub9tzg7.pdf

Looking for inspiration: new perspectives on respiratory rhythm.

In this review, we summarize the clinical implications of residual neuromuscular block. Data suggest that residual neuromuscular block is a common complication in the postanesthesia care unit, with approximately 40% of patients exhibiting a train-of-four ratio <0.9. Volunteer studies have demonstrated that small degrees of residual paralysis (train-of-four ratios 0.7-0.9) are associated with impaired pharyngeal function and increased risk of aspiration, weakness of upper airway muscles and airway obstruction, attenuation of the hypoxic ventilatory response (approximately 30%), and unpleasant symptoms of muscle weakness. Clinical studies have also identified adverse postoperative events associated with intraoperative neuromuscular management. Large databased investigations have identified intraoperative use of muscle relaxants and residual neuromuscular block as important risk factors in anesthetic-related morbidity and mortality. Furthermore, observational and randomized clinical trials have demonstrated that incomplete neuromuscular recovery during the early postoperative period may result in acute respiratory events (hypoxemia and airway obstruction), unpleasant symptoms of muscle weakness, longer postanesthesia care unit stays, delays in tracheal extubation, and an increased risk of postoperative pulmonary complications. These recent data suggest that residual neuromuscular block is an important patient safety issue and that neuromuscular management affects postoperative outcomes.

http://rusanesth.com/assets/files/airlin2/NMB%20Part%201.pdf

Residual neuromuscular block: lessons unlearned. Part I: definitions, incidence, and adverse physiologic effects of residual neuromuscular block.

Background:Sugammadex (Org 25969) forms a complex with steroidal neuromuscular blocking agents, thereby reversing neuromuscular block. This study investigated the dose–response relation, safety, and pharmacokinetics of sugammadex to reverse rocuronium-induced block.Methods:Twenty-seven male surgical

Reversal of rocuronium-induced neuromuscular block by the selective relaxant binding agent sugammadex: a dose-finding and safety study.

Collapsible pharyngeal airway size is determined by interaction between structural properties of the pharyngeal airway and neural regulation of the pharyngeal dilating muscles. Obesity seems to have two distinct mechanical influences on the pharyngeal airway collapsibility. First, obesity increases soft tissue surrounding the pharyngeal airway within limited maxillomandible enclosure occupying and narrowing its space (pharyngeal anatomical imbalance). Second, obesity, particularly central obesity, increases visceral fat volume decreasing lung volume. Pharyngeal wall collapsibility is increased by the lung volume reduction, possibly through decreased longitudinal tracheal traction (lung volume hypothesis). Neural compensation for functioning structural abnormalities operating during wakefulness is lost during sleep, leading to pharyngeal obstruction. Instability of the negative feedback of the respiratory system may accelerate cycling of pharyngeal closure and opening. Improvement of the pharyngeal anatomical imbalance and maintenance of lung volume are the keys for safe perioperative airway managements of obese patients with obstructive sleep apnea.

/pdf/obstructive-sleep-apnea-of-obese-adults-pathophysiology-and-15xfqaheez.pdf

Obstructive sleep apnea of obese adults: pathophysiology and perioperative airway management.

Background Underlying mechanisms behind opioid-induced respiratory depression are not fully understood. The authors investigated changes in burst rate, intraburst firing frequency, membrane properties, as well as presynaptic and postsynaptic events of respiratory neurons in the isolated brainstem after administration of opioid receptor agonists. Methods Newborn rat brainstem-spinal cord preparations were used and superfused with mu-, kappa-, and delta-opioid receptor agonists. Whole cell recordings were performed from three major classes of respiratory neurons (inspiratory, preinspiratory, and expiratory). Results Mu- and kappa-opioid receptor agonists reduced the spontaneous burst activity of inspiratory neurons and the C4 nerve activity. Forty-two percent of the inspiratory neurons were hyperpolarized and decreased in membrane resistance during opioid-induced respiratory depression. Furthermore, under synaptic block by tetrodotoxin perfusion, similar changes of inspiratory neuronal membrane properties occurred after application of mu- and kappa-opioid receptor agonists. In contrast, resting membrane potential and membrane resistance of preinspiratory and majority of expiratory neurons were unchanged by opioid receptor agonists, even during tetrodotoxin perfusion. Simultaneous recordings of inspiratory and preinspiratory neuronal activities confirmed the selective inhibition of inspiratory neurons caused by mu- and kappa-opioid receptor agonists. Application of opioids reduced the slope of rising of excitatory postsynaptic potentials evoked by contralateral medulla stimulation, resulting in a prolongation of the latency of successive first action potential responses. Conclusions Mu- and kappa-opioid receptor agonists caused reduction of final motor outputs by mainly inhibiting medullary inspiratory neuron network. This inhibition of inspiratory neurons seems to be a result of both a presynaptic and postsynaptic inhibition. The central respiratory rhythm as reflected by the preinspiratory neuron burst rate was essentially unaltered by the agonists.

Opioid action on respiratory neuron activity of the isolated respiratory network in newborn rats

Background: Neuromuscular blocking agents reduce the human ventilatory response to hypoxia at partial neuromuscular block. It was hypothesized that vecuronium impairs carotid body chemoreceptor function during hypoxia. Method: The effect of systemic administration of vecuronium on single chemoreceptor activity during hypoxia, as recorded from a single nerve fiber preparation of the carotid sinus nerve, was studied in seven mechanically ventilated New Zealand White rabbits during continuous thiopental anesthesia. During normoventilation, the isocapnic hypoxic chemosensitivity of the single carotid body chemoreceptor was measured at four levels of oxygenation; these measurements were repeated at six separate occasions: control recording before injection, after intravenous administrations of 0.1 mg and 0.5 mg of vecuronium, and then at three occasions during a 90-min recovery period. Chemoreceptor chemosensitivity during isocapnic hypoxia was expressed as a hyperbolic function: Chemoreceptor output (Hz) = a + b × Pa O2 -1 (mmHg). Results: Chemosensitivity was reduced after both 0.1 mg and 0.5 mg vecuronium intravenous administration compared with control measurements; the hypoxic response curve was significantly depressed after both doses (P < 0.05). Notably, there was variation in the effect of vecuronium; some chemoreceptor preparations showed only minimal impairment, whereas some showed an almost abolished response to hypoxia. The chemosensitivity remained significantly depressed at 30 and 60 min but had recovered spontaneously at 90 min after 0.5 mg vecuronium. Discussion: It is concluded that vecuronium depresses carotid body chemoreceptor function to a varying extent during hypoxia and that the depression recovers spontaneously.

Carotid Body Chemoreceptor Function Is Impaired by Vecuronium during Hypoxia

UNLABELLED Whether volatile anesthetics have an effect on the peripheral chemoreceptors is controversial, possibly because of differences in end-tidal CO(2) concentrations. We studied the effect of isoflurane on the hypoxic chemosensitivity of carotid body chemoreceptors at three different PaCO(2) levels before and during the administration of 1.0% isoflurane (0.5 minimum alveolar anesthetic concentration) in six normothermic New Zealand white rabbits anesthetized with thiopental. The response of the chemoreceptors was fitted to the equation: Frequency (Hz) = a + b x PaCO(2) + c x (1/PaO(2)) + Dx (1/PaO(2))(2). Mean values for the coefficients a, b, c and d for the control state were -4.5, 0.13, 771, and 6332, respectively. This relationship was not changed by addition of isoflurane at 1.0% end-tidal concentration (P = 0.40, analysis of variance). We conclude that isoflurane at 1.0% end-tidal concentration does not depress the hypoxic response of rabbit carotid body chemoreceptors during either hypo-, normo-, or hypercapnia. IMPLICATIONS By measuring single-fiber chemoreceptor activity in anesthetized rabbits, we showed that isoflurane at 1.0% end-tidal concentration does not depress the hypoxic chemosensitivity of peripheral chemoreceptors during either hypo-, normo-, or hypercapnia in this species.

Isoflurane does not depress the hypoxic response of rabbit carotid body chemoreceptors.

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Opioid action on respiratory neuron activity of the isolated respiratory network in newborn rats

Carotid Body Chemoreceptor Function Is Impaired by Vecuronium during Hypoxia

Isoflurane does not depress the hypoxic response of rabbit carotid body chemoreceptors.