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William K. Milsom - One of the best experts on this subject based on the ideXlab platform.
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Developmental changes in cold tolerance and ability to autoresuscitate from hypothermic Respiratory Arrest are not linked in rats and hamsters
Respiratory physiology & neurobiology, 2012Co-Authors: Andrea E. Corcoran, Denis V. Andrade, Lieneke H. Marshall, William K. MilsomAbstract:Abstract In adult mammals, severe hypothermia leads to Respiratory and cardiac Arrest, followed by death. Neonatal rats and hamsters can survive much lower body temperatures and, upon artificial rewarming, spontaneously recover from Respiratory Arrest (autoresuscitate), typically suffering no long-term effects. To determine developmental and species differences in cold tolerance (defined here as the temperature of Respiratory Arrest) and its relation to the ability to autoresuscitate, we cooled neonatal and juvenile Sprague-Dawley rats and Syrian hamsters until respiration ceased, followed by rewarming. Ventilation and heartbeat were continuously monitored. In rats, cold tolerance did not change throughout development, however the ability to autoresuscitate from hypothermic Respiratory Arrest did (lost between postnatal days, P, 14 and 20), suggesting that the mechanisms for maintaining breathing at low temperatures was retained throughout development while those initiating breathing on rewarming were altered. Hamsters, however, showed increased cold tolerance until P26–28 and were able to autoresuscitate into adulthood (provided the heart kept beating throughout Respiratory Arrest). Also, hamsters were more cold tolerant than rats. We saw no evidence of gasping to initiate breathing following Respiratory Arrest, contributing to the hypothesis that hypothermic Respiratory Arrest does not lead to anoxia.
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Riluzole disrupts autoresuscitation from hypothermic Respiratory Arrest in neonatal hamsters but not rats.
Respiratory physiology & neurobiology, 2009Co-Authors: Angelina Y. Fong, Lieneke H. Marshall, William K. MilsomAbstract:Abstract We examined the effect of riluzole on expression of the central Respiratory rhythm and the ability of neonates to autoresuscitate from hypothermic Respiratory Arrest using in vitro brainstem-spinal cord preparations of rats and hamsters. At a constant temperature of 27 °C, riluzole (5–200 μM) decreased the burst amplitude of Respiratory-related motor discharge, but had little effect on the fictive Respiratory frequency in rat preparations. In contrast, in hamster preparations, riluzole reduced fictive Respiratory frequency, but had little effect on burst amplitude. Hamster preparations were more cold-tolerant than rat preparations, with Respiratory Arrest and autoresuscitation occurring at lower temperatures during cooling of the preparation. This difference was removed by incubation with riluzole (5 μM); riluzole significantly increased the temperature at which fictive respiration Arrested and restarted in hamster preparations, but had no effect in rat preparations. The species differences observed in this study may reflect fundamental differences in the relative role of riluzole-sensitive mechanisms in the expression of the Respiratory rhythm in early development of an altricial vs. a more precocial species.
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Hypothermia and recovery from Respiratory Arrest in a neonatal rat in vitro brain stem preparation.
American journal of physiology. Regulatory integrative and comparative physiology, 2002Co-Authors: Nm Mellen, William K. Milsom, Jack L. FeldmanAbstract:This study was designed to examine the possibility that Respiratory Arrest during hypothermia occurs at the level of premotor or motor neurons rather than at the level of the central rhythm generator itself. Specifically, we sought to determine the consequences of hypothermic cooling until Respiratory Arrest, and subsequent rewarming, on neurons in the pre-Botzinger Complex, as an indication of the output of the entire rhythmogenic network; and from cervical spinal (phrenic) ventral roots, as an indication of motor neuron output, in an in vitro neonatal rat brain stem-spinal cord preparation. We found that hypothermia led to a slowing of the Respiratory rhythm with little or no decrease in the magnitude of phrenic motor output or the field potential of pre-Botzinger Complex neurons. Ultimate Arrest occurred abruptly and simultaneously in recordings from both sites, indicating that the Arrest was due to failure of the central rhythm-generating network, primarily due to removal of a conditional excitation. On being rewarmed, the motor output recorded at both sites was usually fractionated, initially suggesting that changes occurred in network synchronization either during cooling or during reactivation following hypothermic Arrest.
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Hypothermia and recovery from Respiratory Arrest in a neonatal rat in-vitro brainstem preparation
Respiratory Research, 2001Co-Authors: Jl Feldman, Nm Mellen, William K. MilsomAbstract:In mammals, progressive hypothermia leads to loss of reflex responses, Respiratory Arrest, and finally, cardiac Arrest and death. Under acute conditions in neonatal mammals, if progressive rewarming occurs soon enough, both the heart beat and breathing will resume spontaneously and they will recover fully but in adult rats, once Respiratory Arrest occurs, the animals must be artificially resuscitated. The mechanistic basis of the initial Respiratory Arrest in hypothermia as well as the ontogenetic changes in tolerance and in the ability of the system to autoresuscitate on rewarming are poorly understood. Onimura and Homma [1], demonstrated that when temperature was lowered from 26 to 24°C in an en bloc brainstem-spinal cord preparation from newborn rats, Respiratory rate was depressed and bursts of activity in Pre-I neurons were not always followed by bursts of inspiratory activity in Respiratory motor neurons. This suggested that either the number of active Pre-I neurons decreased and were no longer sufficient to activate the motor neuron pools, or that the threshold for the generation of inspiratory-modulated efferent activity in the motor neuron pools was raised, or both. This in turn suggested that Respiratory Arrest might occur at the level of pre-motor or motor neurons rather than at the level of the rhythm generator itself. This study was designed to examine whether Respiratory Arrest during hypothermia occurs at the level of pre motor or motor neurons rather than at the level of the central rhythm generator itself. Specifically we sought to determine the consequences of hypothermic cooling until Respiratory Arrest, and subsequent re warming, on neurons in the preBotzinger Complex (via field potential recordings), as an indication of the output of the entire rhythmo-genic network; and from cervical spinal (phrenic) ventral roots (via suction electrode recording), as an indication of motor neuron output, in an in vitro neonatal rat brainstem-spinal cord preparation. With this preparation, progressive cooling slowed the frequency of fictive breathing with the cycle period increasing exponentially until Respiratory related rhythmic activity ceased. There was no decrease in the peak, integrated sum or duration of the field potential during this process; ie, while slowing was progressive, Arrest was not. The same was not completely true of the phrenic motor output. During progressive cooling there was a 14% fall in peak amplitude and a 32% fall in the integrated sum of the activity associated with each fictive burst. There were also rare instances at low temperature during both cooling and recovery where bursts of activity in the field potential were not accompanied by any increase in activity in the phrenic motor output. These data suggest that there must have been some increase in the threshold for generation of activity in the phrenic motor neuron pool relative to the neuron pool from which the field potential was recorded. Ultimate Arrest, however, appears to occur at the level of the central rhythm generating network giving rise to complete and abrupt cessation of activation of the motor neuron pool(s). On rewarming, the motor output often was fractionated suggesting that changes occurred in network synchronization either during cooling or during reactivation following hypothermic Arrest.
George B. Richerson - One of the best experts on this subject based on the ideXlab platform.
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Amygdala lesions reduce seizure-induced Respiratory Arrest in DBA/1 mice.
Epilepsy & behavior : E&B, 2019Co-Authors: Anthony Marincovich, Eduardo Bravo, Brian J. Dlouhy, George B. RichersonAbstract:Abstract Sudden unexpected death in epilepsy (SUDEP) is the most common cause of death in patients with refractory epilepsy. Human studies and animal models suggest that Respiratory Arrest is the initiating event leading to death in many cases of SUDEP. It has previously been reported that the onset of apnea can coincide with the spread of seizures to the amygdala, and apnea can be reproduced by electrical stimulation of the amygdala. The aim of the current work was to determine if the amygdala is required for seizure-induced Respiratory Arrest (S-IRA) in a mouse model of SUDEP. Experiments were performed on DBA/1 mice that have audiogenic seizures with a high incidence of fatal postictal Respiratory Arrest. Electrolytic lesions of the amygdala significantly reduced the incidence of S-IRA without altering seizures, baseline breathing, or the hypercapnic ventilatory response. These results indicate that the amygdala is a critical node in a pathway to the lower brainstem that is needed for seizures to cause Respiratory Arrest. Significance statement Sudden unexpected death in epilepsy is the most common cause of mortality in patients with refractory epilepsy, and S-IRA is thought to be important in the pathophysiology in many cases. In a patient with epilepsy, the onset of apnea has been shown to coincide with spread of seizures to the amygdala, and in multiple patients, apnea was induced by stimulation of the amygdala. Here, we show that lesions of the amygdala reduced the incidence of S-IRA and death in a mouse model of SUDEP. These results provide evidence that the amygdala may be a critical node in the pathway by which seizures influence the brainstem Respiratory network to cause apnea. This article is part of the Special Issue NEWroscience 2018
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amygdala lesions reduce seizure induced Respiratory Arrest in dba 1 mice
Epilepsy & Behavior, 2019Co-Authors: Anthony Marincovich, Eduardo Bravo, Brian J. Dlouhy, George B. RichersonAbstract:Abstract Sudden unexpected death in epilepsy (SUDEP) is the most common cause of death in patients with refractory epilepsy. Human studies and animal models suggest that Respiratory Arrest is the initiating event leading to death in many cases of SUDEP. It has previously been reported that the onset of apnea can coincide with the spread of seizures to the amygdala, and apnea can be reproduced by electrical stimulation of the amygdala. The aim of the current work was to determine if the amygdala is required for seizure-induced Respiratory Arrest (S-IRA) in a mouse model of SUDEP. Experiments were performed on DBA/1 mice that have audiogenic seizures with a high incidence of fatal postictal Respiratory Arrest. Electrolytic lesions of the amygdala significantly reduced the incidence of S-IRA without altering seizures, baseline breathing, or the hypercapnic ventilatory response. These results indicate that the amygdala is a critical node in a pathway to the lower brainstem that is needed for seizures to cause Respiratory Arrest. Significance statement Sudden unexpected death in epilepsy is the most common cause of mortality in patients with refractory epilepsy, and S-IRA is thought to be important in the pathophysiology in many cases. In a patient with epilepsy, the onset of apnea has been shown to coincide with spread of seizures to the amygdala, and in multiple patients, apnea was induced by stimulation of the amygdala. Here, we show that lesions of the amygdala reduced the incidence of S-IRA and death in a mouse model of SUDEP. These results provide evidence that the amygdala may be a critical node in the pathway by which seizures influence the brainstem Respiratory network to cause apnea. This article is part of the Special Issue NEWroscience 2018
Philip B. Cornish - One of the best experts on this subject based on the ideXlab platform.
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Respiratory Arrest after spinal anesthesia with lidocaine and fentanyl.
Anesthesia and analgesia, 1997Co-Authors: Philip B. CornishAbstract:Acase of postoperative Respiratory Arrest after spinal anesthesia using lidocaine and fentanyl is described. Possible causes are discussed, including cephalad spread of fentanyl, high spinal anesthesia, residual systemic sedation, or a combination of these. The use of fentanyl in this context is questioned.
Amy L. Dzierba - One of the best experts on this subject based on the ideXlab platform.
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Polymyxin Use Associated With Respiratory Arrest
Chest, 2012Co-Authors: Hannah Wunsch, Vivek K. Moitra, Mona Patel, Amy L. DzierbaAbstract:The polymyxins (polymyxin B and E) are bactericidal polypeptide antibiotics first discovered in 1947 and used for the treatment of gram-negative bacterial infections. Renal and neurologic toxicities coupled with the increasing availability of effective alternatives led to declining use in the 1960s. The emergence of multidrug-resistant organisms in the past decade has resulted in a resurgence in the use of polymyxins in critically ill patients, yet the side effects are not well known. We report two cases of Respiratory Arrest likely due to polymyxin B infusions in the context of a 10-fold increase in the use of polymyxin B in our institution over the past 10 years.
Nm Mellen - One of the best experts on this subject based on the ideXlab platform.
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Hypothermia and recovery from Respiratory Arrest in a neonatal rat in vitro brain stem preparation.
American journal of physiology. Regulatory integrative and comparative physiology, 2002Co-Authors: Nm Mellen, William K. Milsom, Jack L. FeldmanAbstract:This study was designed to examine the possibility that Respiratory Arrest during hypothermia occurs at the level of premotor or motor neurons rather than at the level of the central rhythm generator itself. Specifically, we sought to determine the consequences of hypothermic cooling until Respiratory Arrest, and subsequent rewarming, on neurons in the pre-Botzinger Complex, as an indication of the output of the entire rhythmogenic network; and from cervical spinal (phrenic) ventral roots, as an indication of motor neuron output, in an in vitro neonatal rat brain stem-spinal cord preparation. We found that hypothermia led to a slowing of the Respiratory rhythm with little or no decrease in the magnitude of phrenic motor output or the field potential of pre-Botzinger Complex neurons. Ultimate Arrest occurred abruptly and simultaneously in recordings from both sites, indicating that the Arrest was due to failure of the central rhythm-generating network, primarily due to removal of a conditional excitation. On being rewarmed, the motor output recorded at both sites was usually fractionated, initially suggesting that changes occurred in network synchronization either during cooling or during reactivation following hypothermic Arrest.
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Hypothermia and recovery from Respiratory Arrest in a neonatal rat in-vitro brainstem preparation
Respiratory Research, 2001Co-Authors: Jl Feldman, Nm Mellen, William K. MilsomAbstract:In mammals, progressive hypothermia leads to loss of reflex responses, Respiratory Arrest, and finally, cardiac Arrest and death. Under acute conditions in neonatal mammals, if progressive rewarming occurs soon enough, both the heart beat and breathing will resume spontaneously and they will recover fully but in adult rats, once Respiratory Arrest occurs, the animals must be artificially resuscitated. The mechanistic basis of the initial Respiratory Arrest in hypothermia as well as the ontogenetic changes in tolerance and in the ability of the system to autoresuscitate on rewarming are poorly understood. Onimura and Homma [1], demonstrated that when temperature was lowered from 26 to 24°C in an en bloc brainstem-spinal cord preparation from newborn rats, Respiratory rate was depressed and bursts of activity in Pre-I neurons were not always followed by bursts of inspiratory activity in Respiratory motor neurons. This suggested that either the number of active Pre-I neurons decreased and were no longer sufficient to activate the motor neuron pools, or that the threshold for the generation of inspiratory-modulated efferent activity in the motor neuron pools was raised, or both. This in turn suggested that Respiratory Arrest might occur at the level of pre-motor or motor neurons rather than at the level of the rhythm generator itself. This study was designed to examine whether Respiratory Arrest during hypothermia occurs at the level of pre motor or motor neurons rather than at the level of the central rhythm generator itself. Specifically we sought to determine the consequences of hypothermic cooling until Respiratory Arrest, and subsequent re warming, on neurons in the preBotzinger Complex (via field potential recordings), as an indication of the output of the entire rhythmo-genic network; and from cervical spinal (phrenic) ventral roots (via suction electrode recording), as an indication of motor neuron output, in an in vitro neonatal rat brainstem-spinal cord preparation. With this preparation, progressive cooling slowed the frequency of fictive breathing with the cycle period increasing exponentially until Respiratory related rhythmic activity ceased. There was no decrease in the peak, integrated sum or duration of the field potential during this process; ie, while slowing was progressive, Arrest was not. The same was not completely true of the phrenic motor output. During progressive cooling there was a 14% fall in peak amplitude and a 32% fall in the integrated sum of the activity associated with each fictive burst. There were also rare instances at low temperature during both cooling and recovery where bursts of activity in the field potential were not accompanied by any increase in activity in the phrenic motor output. These data suggest that there must have been some increase in the threshold for generation of activity in the phrenic motor neuron pool relative to the neuron pool from which the field potential was recorded. Ultimate Arrest, however, appears to occur at the level of the central rhythm generating network giving rise to complete and abrupt cessation of activation of the motor neuron pool(s). On rewarming, the motor output often was fractionated suggesting that changes occurred in network synchronization either during cooling or during reactivation following hypothermic Arrest.
