Effect of five human anesthetics on respiratory control in cats

Younes, Magdy; Youssef, M.S.

doi:10.1152/jappl.1978.44.4.596

Cited by 29 publications

(4 citation statements)

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“…Younes and Youssef [20] reported that the phasic vagal influence was depressed markedly at 2% halothane, which equates to 2.3 MAC of halothane, supporting our results.…”

Section: Discussionsupporting

confidence: 91%

Effects of Halothane, Enflurane, Isoflurane, and Sevoflurane on Slowly Adapting Pulmonary Stretch Receptor Activity in Anesthetized Dogs

Mutoh

Tsubone

Nishimura

et al. 1998

Lung

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The aim of this study was to evaluate the effects of halothane, enflurane, isoflurane, and sevoflurane on slowly adapting pulmonary stretch receptor (SAR) activity in dogs. Eight beagles were anesthetized with an intravenous injection of a mixture of urethane and alpha-chloralose as a basal anesthesia, then vagotomized, artificially ventilated, and chest opened. Single afferent activities from SARs were recorded from the peripheral nerve cut end of the left vagus. Changes in SAR activities with inhalation of halothane, enflurane, isoflurane, and sevoflurane at 1, 1.5, and 2 times the minimal alveolar anesthetic concentration (MAC) were measured, and differences in the discharges within and among four anesthetics were evaluated. As a result, two different types of SARs, low threshold SARs and high threshold SARs, were detected in this study. In all anesthetics, expiratory discharges of low threshold SARs decreased significantly in a dose-dependent manner, whereas inspiratory discharges did not change significantly at any anesthetic level. Discharges of high threshold SARs tended to decrease with increasing anesthetic level; however, no statistical significance was observed at any anesthetic level. Only one exception to these changes was observed at 1 MAC of halothane where no significant decrease in the expiratory discharge of low threshold SARs or significant increase in the discharge of high threshold SARs was induced against a control value. In conclusion, recent inhalation anesthetics, except for halothane at the light anesthetic level, tended to decrease SAR activities depending on the anesthetic level, suggesting attenuation of the Hering-Breuer inflation reflex.

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“…Younes and Youssef [20] reported that the phasic vagal influence was depressed markedly at 2% halothane, which equates to 2.3 MAC of halothane, supporting our results.…”

Section: Discussionsupporting

confidence: 91%

Effects of Halothane, Enflurane, Isoflurane, and Sevoflurane on Slowly Adapting Pulmonary Stretch Receptor Activity in Anesthetized Dogs

Mutoh

Tsubone

Nishimura

et al. 1998

Lung

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“…This is because reflexes from the chest wall that have effects on TI are quite weak and tend to shorten TIn when the mechanical load is increased (21,22), whereas what we observed was a reduction in TIn as the mechanical load was decreased through an increase in ventilator flow.…”

Section: Response Of Neural Inspiratory Durationcontrasting

confidence: 67%

Effect of Ventilator Flow Rate on Respiratory Timing in Normal Humans

Fernández

Méndez

Younes

1999

Am J Respir Crit Care Med

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Respiratory rate (RR) increases as a function of ventilator flow rate (V). We wished to determine whether this is due to a decrease in neural inspiratory time (T In), neural expiratory time (TEn), or both. To accomplish this, we ventilated 15 normal subjects in the assist, volume cycled mode. Ventilator flow rate was varied at random, at four breaths with each step, over the flow range from 0.8 (Vmin) to 2.5 (Vmax) L/s. V T was kept constant. The pressure developed by respiratory muscles (Pmus) was calculated with the equation of motion (Pmus = V. R + V. E - Paw, where R = resistance, V = volume, E = elastance, and Paw = airway pressure). Electromyography of the diaphragm (Edi) was also done in five subjects. TIn and TEn were determined from the Pmus or Edi waveform. TIn decreased progressively as a function of V, from 1.44 +/- 0.34 s at Vmin to 0.62 +/- 0.26 s at Vmax (p < 0.00001). Changes in TEn were inconsistent and not significant. TIn/Ttot decreased significantly (0.30 +/- 0.06 at Vmin to 0.18 +/- 0.09 at Vmax; p < 0. 00001). We conclude that TI is highly sensitive to ventilator flow, and that the RR response to V is primarily related to this T In response. Because an increase in V progressively reduces T In/Ttot, and this variable is an important determinant of inspiratory muscle energetics, we further conclude that inspiratory muscle energy expenditure is quite sensitive to V over the range from 0.8 to 2.5 L/s.

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“…For example, opioids enhance HeringBreuer reflex-mediated slowing of respiration (5, 7, 9, 12, 21, Rhythmic membrane depolarization and hyperpolarization in the neuron, along with PNA, are slowed by fentanyl, and neuron input resistance is increased during all phases of the respiratory cycle. 61), but the effect is due solely to prolongation of the expiratory phase, and, in the present study, the reflex was eliminated by bilateral cervical vagotomy before fentanyl was tested. Respiration is also slowed when N-methyl-D-aspartate (NMDA) receptors are pharmacologically blocked and vagal pulmonary feedback to the central nervous system is prevented (13,57).…”

Section: Discussionmentioning

confidence: 39%

Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating neurons

Lalley¹

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Lalley, Peter M. Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating neurons. Am J Physiol Regul Integr Comp Physiol 290: R1387-R1396, 2006. First published November 10, 2005 doi:10.1152/ajpregu.00530.2005.-Opiates have effects on respiratory neurons that depress tidal volume and air exchange, reduce chest wall compliance, and slow rhythm. The most dose-sensitive opioid effect is slowing of the respiratory rhythm through mechanisms that have not been thoroughly investigated. An in vivo dose-response analysis was performed on medullary respiratory neurons of adult cats to investigate two untested hypotheses related to mechanisms of opioid-mediated rhythm slowing: 1) Opiates suppress intrinsic conductances that limit discharge duration in medullary inspiratory and expiratory neurons, and 2) opiates delay the onset and lengthen the duration of discharges postsynaptically in phase-regulating postinspiratory and late-inspiratory neurons. In anesthetized and unanesthetized decerebrate cats, a threshold dose (3 g/kg) of the -opioid receptor agonist fentanyl slowed respiratory rhythm by prolonging discharges of inspiratory and expiratory bulbospinal neurons. Additional doses (2-4 g/kg) of fentanyl also lengthened the interburst silent periods in each type of neuron and delayed the rate of membrane depolarization to firing threshold without altering synaptic drive potential amplitude, input resistance, peak action potential frequency, action potential shape, or afterhyperpolarization. Fentanyl also prolonged discharges of postinspiratory and late-inspiratory neurons in doses that slowed the rhythm of inspiratory and expiratory neurons without altering peak membrane depolarization and hyperpolarization, input resistance, or action potential properties. The temporal changes evoked in the tested neurons can explain the slowing of network respiratory rhythm, but the lack of significant, direct opioid-mediated membrane effects suggests that actions emanating from other types of upstream bulbar respiratory neurons account for rhythm slowing.fentanyl; medullary respiratory neurons; phrenic nerve activity; naloxonazine; naltrindole OPIATES ARE WELL KNOWN for their ability to depress ventilation by slowing breathing frequency and reducing tidal volume, gas exchange, upper airway patency, and chest wall compliance (3,4,36,39). They also blunt respiratory network responsiveness to hypoxia and CO 2 /acidosis (11,25,51,60).Opiate slowing of respiratory rhythm, leading to arrest of breathing after the highest doses, has been the topic of many experimental investigations (2,10,14,16,22,24,30,34,37,48,52,60). According to most recent studies, rhythm slowing seems to be principally related to depression of inspiratory interneurons in the pre-Bötzinger complex (PBC) (15, 34, 37), a region within the ventrolateral respiratory column (VRC) that seems to be critical for generation of respiratory rhythm (40, 52). However, endogenous opioid peptides are distributed throughout the bulbar respiratory ...

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Effect of five human anesthetics on respiratory control in cats

Cited by 29 publications

References 0 publications

Effects of Halothane, Enflurane, Isoflurane, and Sevoflurane on Slowly Adapting Pulmonary Stretch Receptor Activity in Anesthetized Dogs

Effects of Halothane, Enflurane, Isoflurane, and Sevoflurane on Slowly Adapting Pulmonary Stretch Receptor Activity in Anesthetized Dogs

Effect of Ventilator Flow Rate on Respiratory Timing in Normal Humans

Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating neurons

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