Autonomic dysfunction with early respiratory syncytial virus-related infection

Stock, Claire; Teyssier, G; Pichot, Vincent; Goffaux, Philippe; Barthélémy, Jean‐Claude; Patural, Hugues

doi:10.1016/j.autneu.2010.03.012

Cited by 35 publications

(23 citation statements)

References 38 publications

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“…Apnea is a common presenting sign of both local and systemic infection [39, 84]. Apnea can be triggered by a number of central nervous system diseases, including intracranial hemorrhage, hypoxic-ischemic encephalopathy, and seizures.…”

Section: Factors Involved In Apneamentioning

confidence: 99%

Apnea of prematurity: from cause to treatment

2011

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Apnea of prematurity (AOP) is a common problem affecting premature infants, likely secondary to a “physiologic” immaturity of respiratory control that may be exacerbated by neonatal disease. These include altered ventilatory responses to hypoxia, hypercapnia, and altered sleep states, while the roles of gastroesophageal reflux and anemia remain controversial. Standard clinical management of the obstructive subtype of AOP includes prone positioning and continuous positive or nasal intermittent positive pressure ventilation to prevent pharyngeal collapse and alveolar atelectasis, while methylxanthine therapy is a mainstay of treatment of central apnea by stimulating the central nervous system and respiratory muscle function. Other therapies, including kangaroo care, red blood cell transfusions, and CO2 inhalation, require further study. The physiology and pathophysiology behind AOP are discussed, including the laryngeal chemoreflex and sensitivity to inhibitory neurotransmitters, as are the mechanisms by which different therapies may work and the potential long-term neurodevelopmental consequences of AOP and its treatment.

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Section: Factors Involved In Apneamentioning

confidence: 99%

Apnea of prematurity: from cause to treatment

2011

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“…In addition to inflammatory stimuli, anoxia itself induces PGE 2 synthesis (15) and might lead to deleterious brain damage in postnatal rats (16). We and others have suggested that PGE 2 may serve as a critical mediator between infection and apnea (1,2,8,17). …”

mentioning

confidence: 94%

“…Respiratory syncytial virus infection and subsequent inflammation may induce autonomic dysfunction in preterm as well as young term infants (2). Moreover, infection often precedes episodes of sudden infant death syndrome (3).…”

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confidence: 99%

mPGES-1 and prostaglandin E2: vital role in inflammation, hypoxic response, and survival

Siljehav¹,

Hofstetter²,

Jakobsson

et al. 2012

Pediatr Res

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BackGround: apnea associated with infection and inflammation is a major medical concern in preterm infants. Prostaglandin e 2 (PGe 2 ) serves as a critical mediator between infection and apnea. We hypothesize that alteration of the microsomal PGe synthase-1 (mPGes-1) PGe 2 pathway influences respiratory control and response to hypoxia. MEthodS: Nine-d-old wild-type (WT) mice, mPGes-1 heterozygote (mPGes-1 +/-), and mPGes-1 knockout (mPGes-1 -/-) mice were used. Respiration was investigated in mice using flow plethysmography after the mice received either interleukin-1β (IL-1β) (10 µg/kg) or saline. Mice were subjected to a period of normoxia, subsequent exposure to hyperoxia, and finally either moderate (5 min) or severe hypoxia (until 1 min after last gasp). rESultS: IL-1β worsened survival in WT mice but not in mice with reduced or no mPGes-1. Reduced expression of mPGes-1 prolonged gasping duration and increased the number of gasps during hypoxia. Response to intracerebroventricular PGe 2 was not dependent on mPGes-1 expression. concluSion: activation of mPGes-1 is involved in the rapid and vital response to severe hypoxia as well as inflammation. attenuation of mPGes-1 appears to have no detrimental effects, yet prolongs autoresuscitation efforts and improves survival. consequently, inhibition of the mPGes-1 pathway may serve as a potential therapeutic target for the treatment of apnea and respiratory disorders.

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“…PGE 2 depresses breathing in fetal and newborn sheep, mice, and in humans in vivo (25,30,51), and also inhibits respiration-related neurons in vitro (23,25,39). Others and we have suggested that PGE 2 serves as a critical mediator of inflammation and apnea (22,24,25,48).In addition to an inflammatory stimulus, hypoxia itself induces PGE 2 synthesis (31) that depresses respiration (43) and might lead to deleterious brain damage (32). During perinatal hypoxia PGE 2 metabolite levels in cerebrospinal fluid are increased and directly correlate with the severity of perinatal asphyxia in human neonates (3).…”

mentioning

confidence: 94%

Il-1β and prostaglandin E₂attenuate the hypercapnic as well as the hypoxic respiratory response via prostaglandin E receptor type 3 in neonatal mice

Siljehav

Shvarev

Herlenius

2014

Journal of Applied Physiology

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Prostaglandin E2 (PGE2) serves as a critical mediator of hypoxia, infection, and apnea in term and preterm babies. We hypothesized that the prostaglandin E receptor type 3 (EP3R) is the receptor responsible for PGE2-induced apneas. Plethysmographic recordings revealed that IL-1β (ip) attenuated the hypercapnic response in C57BL/6J wild-type (WT) but not in neonatal (P9) EP3R(-/-) mice (P < 0.05). The hypercapnic responses in brain stem spinal cord en bloc preparations also differed depending on EP3R expression whereby the response was attenuated in EP3R(-/-) preparations (P < 0.05). After severe hypoxic exposure in vivo, IL-1β prolonged time to autoresuscitation in WT but not in EP3R(-/-) mice. Moreover, during severe hypoxic stress EP3R(-/-) mice had an increased gasping duration (P < 0.01) as well as number of gasps (P < 0.01), irrespective of intraperitoneal treatment, compared with WT mice. Furthermore, EP3R(-/-) mice exhibited longer hyperpneic breathing efforts when exposed to severe hypoxia (P < 0.01). This was then followed by a longer period of secondary apnea before autoresuscitation occurred in EP3R(-/-) mice (P < 0.05). In vitro, EP3R(-/-) brain stem spinal cord preparations had a prolonged respiratory burst activity during severe hypoxia accompanied by a prolonged neuronal arrest during recovery in oxygenated medium (P < 0.05). In conclusion, PGE2 exerts its effects on respiration via EP3R activation that attenuates the respiratory response to hypercapnia as well as severe hypoxia. Modulation of the EP3R may serve as a potential therapeutic target for treatment of inflammatory and hypoxic-induced detrimental apneas and respiratory disorders in neonates.

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Autonomic dysfunction with early respiratory syncytial virus-related infection

Cited by 35 publications

References 38 publications

Apnea of prematurity: from cause to treatment

Apnea of prematurity: from cause to treatment

mPGES-1 and prostaglandin E2: vital role in inflammation, hypoxic response, and survival

Il-1β and prostaglandin E₂attenuate the hypercapnic as well as the hypoxic respiratory response via prostaglandin E receptor type 3 in neonatal mice

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Autonomic dysfunction with early respiratory syncytial virus-related infection

Cited by 35 publications

References 38 publications

Apnea of prematurity: from cause to treatment

Apnea of prematurity: from cause to treatment

mPGES-1 and prostaglandin E2: vital role in inflammation, hypoxic response, and survival

Il-1β and prostaglandin E2attenuate the hypercapnic as well as the hypoxic respiratory response via prostaglandin E receptor type 3 in neonatal mice

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Il-1β and prostaglandin E₂attenuate the hypercapnic as well as the hypoxic respiratory response via prostaglandin E receptor type 3 in neonatal mice