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Respiratory Drive (respiratory + drive)
Selected AbstractsDescending respiratory polysynaptic inputs to cervical and thoracic motoneurons diminish during early postnatal maturation in rat spinal cordEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2005Laurent Juvin Abstract Isolated brainstem-spinal cord preparations were used to explore the coexistence of a direct and an indirect descending drive from the brainstem respiratory centre to cervical and thoracic respiratory motoneurons in the neonatal Sprague,Dawley rat. Polysynaptic spinal relay pathways from the respiratory centre were suppressed by selectively perfusing the cord with mephenesin (1 mm) or a solution enriched with Ca2+ and Mg2+. At birth, both direct and spinally relayed pathways are functional and contribute equally to the global descending respiratory drive. However, during the first postnatal week, significant maturational changes appear in the way the respiratory centre controls its target respiratory motoneurons in the cervical and thoracic spinal cord, with the direct respiratory drive becoming progressively predominant with maturation (from 50% to around 75% of the global descending command). The relative contributions of the monosynaptic and the polysynaptic spinal pathways may therefore have important implications for effective respiratory control during early postnatal development. [source] Death of a 10-Month-Old Boy After Exposure to EthylmorphineJOURNAL OF FORENSIC SCIENCES, Issue 2 2010Arne Helland M.D. Abstract:, Ethylmorphine, an opiate that is partially metabolized to morphine, is a common ingredient in antitussive preparations. We present a case where a 10-month-old boy was administered ethylmorphine in the evening and found dead in bed the following morning. Postmortem toxicological analyses of heart blood by gas chromatography-mass spectrometry and liquid chromatography-mass spectrometry revealed the presence of ethylmorphine and morphine at concentrations of 0.17 ,M (0.054 mg/L) and 0.090 ,M (0.026 mg/L), respectively. CYP2D6 genotyping showed that the deceased had an extensive metabolizer genotype, signifying a "normal" capacity for metabolizing ethylmorphine to morphine. The autopsy report concluded that death was caused by a combination of opiate-induced sedation and weakening of respiratory drive, a respiratory infection, and a sleeping position that could have impeded breathing. This is the first case report where the death of an infant has been linked to ethylmorphine ingestion. [source] The neurophysiology of dyspneaJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 6 2008Matthew Scott Mellema DVM Abstract Objective , To review the human and veterinary literature regarding the neurophysiology of dyspnea and to provide evidence for the beneficial effects of several novel therapies aimed at the alleviation of dyspneic sensations. Data Sources , Data sources included scientific reviews, case reports, original research publications, and recent research conference proceedings. Human Data Synthesis , The use of blood oxygenation level-dependent functional magnetic resonance imaging technology has revealed that the brain regions activated by air hunger in humans are also those activated by fear, pain, and thirst perception. In human subjects, it has been found that agents known to enhance the firing of pulmonary slowly adapting receptors (SARs) can alleviate the sensation of dyspnea without altering central respiratory drive. Several small studies have also shown that nebulized opioids can reduce the sensation of dyspnea apparently via activation of peripheral opioid receptors in the lung. Veterinary Data Synthesis , There are several animal models relevant to both small and large animal clinical patient populations. Treatment of rats with a nebulized SAR sensitizing agent (furosemide) enhances SAR firing in response to lung inflation. Behavioral escape responses to airway occlusion are reduced in lightly anesthetized cats when treated with nebulized furosemide. Opioid agonists have been shown to inhibit the release of acetylcholine and other mediators from the airways of dogs and guinea pigs. Studies using a goat model with bilateral destruction of the pre-Bötzinger Complex do not support current paradigms of air hunger origination. Conclusions , Veterinary patients may benefit from an approach to dyspnea that incorporates an understanding of the origins of the unpleasant sensations associated with the condition. Several novel therapies have shown promise in alleviating dyspneic sensations without altering respiratory drive. Further study is needed to determine the safety and efficacy of these therapies in veterinary patients. [source] Pontine respiratory-modulated activity before and after vagotomy in decerebrate catsTHE JOURNAL OF PHYSIOLOGY, Issue 17 2008Thomas E. Dick The dorsolateral (DL) pons modulates the respiratory pattern. With the prevention of lung inflation during central inspiratory phase (no-inflation (no-I or delayed-I) tests), DL pontine neuronal activity increased the strength and consistency of its respiratory modulation, properties measured statistically by the ,2 value. This increase could result from enhanced respiratory-modulated drive arising from the medulla normally gated by vagal activity. We hypothesized that DL pontine activity during delayed-I tests would be comparable to that following vagotomy. Ensemble recordings of neuronal activity were obtained before and after vagotomy and during delayed-I tests in decerebrate, paralysed and ventilated cats. In general, changes in activity pattern during the delayed-I tests were similar to those after vagotomy, with the exception of firing-rate differences at the inspiratory,expiratory phase transition. Even activity that was respiratory-modulated with the vagi intact became more modulated while withholding lung inflation and following vagotomy. Furthermore, we recorded activity that was excited by lung inflation as well as changes that persisted past the stimulus cycle. Computer simulations of a recurrent inhibitory neural network model account not only for enhanced respiratory modulation with vagotomy but also the varied activities observed with the vagi intact. We conclude that (a) DL pontine neurones receive both vagal-dependent excitatory inputs and central respiratory drive; (b) even though changes in pontine activity are transient, they can persist after no-I tests whether or not changes in the respiratory pattern occur in the subsequent cycles; and (c) models of respiratory control should depict a recurrent inhibitory circuitry, which can act to maintain the stability and provide plasticity to the respiratory pattern. [source] Hypoxia-sensing properties of the newborn rat ventral medullary surface in vitroTHE JOURNAL OF PHYSIOLOGY, Issue 1 2006N. Voituron The ventral medullary surface (VMS) is a region known to exert a respiratory stimulant effect during hypercapnia. Several studies have suggested its involvement in the central inhibition of respiratory rhythm caused by hypoxia. We studied brainstem,spinal cord preparations isolated from newborn rats transiently superfused with a very low O2 medium, causing reversible respiratory depression, to characterize the participation of the VMS in hypoxic respiratory adaptation. In the presence of 0.8 mm Ca2+, very low O2 medium induced an increase in c-fos expression throughout the VMS. The reduction of synaptic transmission and blockade of the respiratory drive by 0.2 mm Ca2+,1.6 mm Mg2+ abolished c-fos expression in the medial VMS (at the lateral edge of the pyramidal tract) but not in the perifacial retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) VMS, suggesting the existence of perifacial RTN/pFRG hypoxia-sensing neurons. In the presence of Ca2+ (0.8 mm), lesioning experiments suggested a physiological difference in perifacial RTN/pFRG VMS between the lateral VMS (beneath the ventrolateral part of the facial nucleus) and the middle VMS (beneath the ventromedial part of the facial nucleus), at least in newborn rats. The lateral VMS lesion, corresponding principally to the most rostral part of the pFRG, produced hypoxia-induced stimulation, whereas the middle VMS lesion, corresponding to the main part of the RTN, abolished hypoxic excitation. This may involve relay via the medial VMS, which is thought to be the parapyramidal group. [source] Interventions for apnoea of prematurity: a personal viewACTA PAEDIATRICA, Issue 2 2010CF Poets Abstract Aim:, To review treatments for apnoea of prematurity (AOP). Methods:, Literature Review and description of personal practice. Results:, Provided that symptomatic apnoea has been ruled out, interventions to improve AOP can be viewed as directed at one of three underlying mechanisms: (i) a reduced work of breathing [e.g. prone positioning, nasal continuous positive airway pressure (CPAP)], (ii) an increased respiratory drive (e.g. caffeine), and (iii) an improved diaphragmatic function (e.g. branched-chain amino acids). Most options currently applied, however, have not yet been shown to be effective and/or safe, except for prone, head-elevated positioning, synchronized nasal ventilation/CPAP, and caffeine. Conclusion:, Treatment usually follows an incremental approach, starting with positioning, followed by caffeine (which should be started early, at least in infants <1250 g), and nasal ventilation or CPAP via variable flow systems that reduce work of breathing. From a research point of view, we most urgently need data on the frequency and severity of bradycardia and intermittent hypoxia that can yet be tolerated without putting an infant at risk of impaired development or retinopathy of prematurity. [source] Remifentanil for INSURE in preterm infants: a pilot study for evaluation of efficacy and safety aspectsACTA PAEDIATRICA, Issue 9 2009L Welzing Abstract Aim:, To evaluate intubating conditions, extubation times and outcome in preterm infants receiving remifentanil as induction agent for the INSURE procedure. Methods:, In twenty-one preterm infants of 29 to 32 weeks gestation and signs of respiratory distress, we utilized remifentanil as induction agent for the INSURE procedure. Following intubation and surfactant application, the infants were mechanically ventilated until respiratory drive was judged to be satisfactory for continuing CPAP therapy. Intubating conditions were classified by our own scoring system by rating limb movements, coughing and breathing. Heart rate, blood pressure and oxygen saturation were recorded during the entire INSURE procedure. Results:, Remifentanil provided excellent or good intubating conditions in all patients. We observed no serious side effects after remifentanil infusion, in particular, no thorax rigidity, clinically significant bradycardia or arterial hypotension. Average extubation time after surfactant administration was 16.9 min (1,45 min); none of the infants had to be reintubated. Following extubation, the infants required only 3.3 days (1,8 days) of CPAP therapy. None exhibited serious complications of prematurity like periventricular leucomalacia, intraventricular haemorrhage >I°, necrotizing enterocolitis or retinopathy. Conclusion:, In this pilot study, INSURE with remifentanil was associated with good intubating conditions and early extubation resulting in an excellent neonatal outcome. [source] Respiratory muscle strength and muscle endurance are not affected by acute metabolic acidemiaCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2009Tessa A. C. Nizet Summary Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilatory failure and hypercapnia. On the other hand, it is known that acute metabolic acidosis can also negatively affect (respiratory) muscle function and, therefore, could lead to a deterioration of respiratory failure. Moreover, we reasoned that the impact of metabolic acidosis on respiratory muscle strength and respiratory muscle endurance could be more pronounced in COPD patients as compared to asthma patients and healthy subjects, due to already impaired respiratory muscle function. In this study, the effect of metabolic acidosis was studied on peripheral muscle strength, peripheral muscle endurance, airway resistance, and on arterial carbon dioxide tension (PaCO2). Acute metabolic acidosis was induced by administration of ammonium chloride (NH4Cl). The effect of metabolic acidosis was studied on inspiratory and expiratory muscle strength and on respiratory muscle endurance. Effects were studied in a randomized, placebo-controlled cross-over design in 15 healthy subjects (4 male; age 33·2 ± 11·5 years; FEV1 108·3 ± 16·2% predicted), 14 asthma patients (5 male; age 48·1 ± 16·1 years; FEV1 101·6 ± 15·3% predicted), and 15 moderate to severe COPD patients (9 male; age 62·8 ± 6·8 years; FEV1 50·0 ± 11·8% predicted). An acute metabolic acidemia of BE ,3·1 mmol.L,1 was induced. Acute metabolic acidemia did not significantly affect strength or endurance of respiratory and peripheral muscles, respectively. In all subjects airway resistance was significantly decreased after induction of metabolic acidemia (mean difference ,0·1 kPa.sec.L,1 [95%-CI: ,0·1 ,,0·02]. In COPD patients PaCO2 was significantly lowered during metabolic acidemia (mean difference ,1·73 mmHg [,3·0 ,,0·08]. In healthy subjects and in asthma patients no such effect was found. Acute metabolic acidemia did not significantly decrease respiratory or peripheral muscle strength, respectively muscle endurance in nomal subjects, asthma, or COPD patients. Metabolic acidemia significantly decreased airway resistance in asthma and COPD patients, as well as in healthy subjects. Moreover, acute metabolic acidemia slightly improved blood gas values in COPD patients. The results suggest that stimulation of ventilation in respiratory failure, by induction of metabolic acidemia will not lead to deterioration of the respiratory failure. [source] | |||||||||||||