Elevated body temperature enhances the laryngeal chemoreflex in decerebrate piglets

Curran, Aidan K.; Xia, Luxi; Leiter, James C.; Bartlett, D.

doi:10.1152/japplphysiol.00906.2004

Cited by 41 publications

(59 citation statements)

References 39 publications

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“…Another aspect of our experimental LCR maneuvers that distinguish them from naturally occurring apneas is that the animals are continuously ventilated and so do not become hypoxic or hypercapnic during the periods of phrenic “apnea”. We found in this study and have found in previous studies somewhat variable effects of drug or changes in body temperature on respiratory frequency (Curran et al, 2005; Xia et al, 2007a, b). It is worth noting that, to the extent an increased respiratory frequency represents an increased respiratory drive, such an increase in frequency would tend to decrease, rather than increase the duration of apnea and the LCR.…”

Section: Discussionsupporting

confidence: 82%

“…These five breaths did not need to have the same frequency or amplitude as the control breaths; we simply required that they be regular (Curran et al, 2005; van der Velde et al, 2003; Xia et al, 2007b). The respiratory disruption measured in this way included both periods of unstable respiratory activity and apneas.…”

Section: Methodsmentioning

confidence: 99%

“…The apnea and LCR durations were not normally distributed, and the variances among treatments were not homogenous; both of which violate the assumptions upon which the ANOVA is based. Therefore, apnea and LCR durations were log-transformed for the statistical analysis, as we have done previously (Curran et al, 2005; Duy et al, 2010), and the ANOVA was performed on the log-transformed data. Data are presented in the text and figures as the mean ± the standard error of the mean of the untransformed values of each variable.…”

Section: Methodsmentioning

confidence: 99%

“…For example, thermal stress (elevated room temperature, increased covering with bed clothes, etc.) is a risk factor for SIDS, and elevated body temperature enhanced laryngeal adduction induced by superior laryngeal nerve stimulation in dogs (Haraguchi et al, 1983) and prolonged the LCR elicited by injection small volumes of water into the larynx in decerebrate piglets (Curran et al, 2005). The effect of elevated body temperature on the LCR depends on activation of TRPV1 receptors within the nucleus of the tractus solitarius (NTS) (Xia et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Interleukin-1β and interleukin-6 enhance thermal prolongation of the LCR in decerebrate piglets

Xia

Bartlett

Leiter

2016

Respiratory Physiology & Neurobiology

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Thermal stress and prior upper respiratory tract infection are risk factors for the Sudden Infant Death Syndrome. The adverse effects of prior infection are likely mediated by interleukin-1β (IL-1β). Therefore, we examined the single and combined effects of IL-1β and elevated body temperature on the duration of the Laryngeal Chemoreflex (LCR) in decerebrate neonatal piglets ranging in age from post-natal day (P) 3 to P7. We examined the effects of intraperitoneal (I.P.) injections of 0.3 mg/Kg IL-1β with or without I.P. 10 mg/Kg indomethacin pretreatment on the duration of the LCR, and in the same animals we also examined the duration of the LCR when body temperature was elevated approximately 2 °C. We found that IL-1β significantly increased the duration of the LCR even when body temperature was held constant. There was a significant multiplicative effect when elevated body temperature was combined with IL-1β treatment: prolongation of the LCR was significantly greater than the sum of independent thermal and IL-1β-induced prolongations of the LCR. The effects of IL-1β, but not elevated body temperature, were blocked by pretreatment with indomethacin alone. We also tested the interaction between IL-6 given directly into the nucleus of the solitary tract (NTS) bilaterally in 100 ngm microinjections of 50 μL and pre-treatment with indomethacin. Here again, there was a multiplicative effect of IL-6 treatment and elevated body temperature, which significantly prolonged the LCR. The effect of IL-6 on the LCR, but not elevated body temperature, was blocked by pretreatment with indomethacin. We conclude that cytokines interact with elevated body temperature, probably through direct thermal effects on TRPV1 receptors expressed pre-synaptically in the NTS and through cytokine-dependent sensitization of the TRPV1 receptor. This sensitization is likely initiated by cyclo-oxygenase-2 dependent synthesis of prostaglandin E2, which is stimulated by elevated levels of IL-1β or IL-6. Inflammatory sensitization of the LCR coupled with thermal prolongation of the LCR may increase the propensity for apnea and Sudden Infant Death Syndrome.

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Section: Discussionsupporting

confidence: 82%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Interleukin-1β and interleukin-6 enhance thermal prolongation of the LCR in decerebrate piglets

Xia

Bartlett

Leiter

2016

Respiratory Physiology & Neurobiology

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“…Indeed, temperature has been shown to have significant effects on the activity of the carotid and aortic chemoreceptors, at least in adults (25,34,44). An alternative explanation is that T B has an independent effect on central chemoreceptors (28) or enhances the peripheral chemoreflex through a central action (e.g., nucleus of the solitary tract), similar to the effect of temperature on other chemoreflexes in newborns (18).…”

Section: Discussionmentioning

confidence: 99%

Breath-to-breath hypercapnic response in neonatal rats: temperature dependency of the chemoreflexes and potential implications for breathing stability

Cummings

Frappell²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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The breathing of newborns is destabilized by warm temperatures. We hypothesized that in unanesthetized, intact newborn rats, body temperature (T(B)) influences the peripheral chemoreflex response (PCR response) to hypercapnia. To test this, we delivered square-wave challenges of 8% CO(2) in air to postnatal day 4-5 (P4-P5) rats held at a T(B) of 30 degrees C (Cold group, n = 11), 33 degrees C (Cool group, n = 10), and 35 degrees C thermoneutral zone group [thermoneutral zone (TNZ) group, n = 11], while measuring ventilation (Ve) directly with a pneumotach and mask. Cool animals were challenged with 8% CO(2) balanced in either air or hyperoxia (n = 10) to identify the PCR response. Breath-to-breath analysis was performed on 30 room air breaths and every breath of the 1-min CO(2) challenge. As expected, warmer T(B) was associated with an unstable breathing pattern in room air: TNZ animals had a coefficient of variation in Ve (Ve CV%) that was double that of animals held at cooler T(B) (P < 0.001). Hyperoxia markedly suppressed the hypercapnic ventilatory response over the first 10 breaths (or approximately 4 s), suggesting that this domain is dominated by the PCR response. The PCR response (P = 0.03) and total response (P = 0.04) were significantly greater in TNZ animals compared with hypothermic animals. The total response had a significant, negative relationship with Vco(2) (R(2) = 0.53; P < 0.001). Breathing stability was positively related to the total response (R(2) = 0.36; P < 0.001) and to a lesser extent, the PCR response (R(2) = 0.19; P = 0.01) and was negatively related to Vco(2) (R(2) = 0.34; P < 0.001). ANCOVA confirmed a significant effect of T(B) alone on breathing stability (P < 0.01), with no independent effects of Vco(2) (P = 0.41), the PCR response (P = 0.82), or the total Ve response (P = 0.08). Our data suggest that in early postnatal life, the chemoreflex responses to CO(2) are highly influenced by T(B), and while related to breathing stability, are not predictors of stability after accounting for the independent effect of T(B).

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Potential Central Nervous System Involvement in Sudden Unexpected Infant Deaths and the Sudden Infant Death Syndrome

Thach

2015

Comprehensive Physiology

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Sudden unexpected infant death (SUID) in infancy which includes Sudden Infant Death Syndrome (SIDS) is the commonest diagnosed cause of death in the United States for infants 1 month to 1 year of age. Central nervous system mechanisms likely contribute to many of these deaths. We discuss some of these including seizure disorders, prolonged breath holding, arousal from sleep and its habituation, laryngeal reflex apnea potentiated by upper airway infection, and failure of brainstem-mediated autoresuscitation. In the conclusions section, we speculate how lives saved through back sleeping might result in later developmental problems in certain infants who otherwise might have died while sleeping prone.

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Elevated body temperature enhances the laryngeal chemoreflex in decerebrate piglets

Abstract: Elevated body temperature enhances the laryngeal chemoreflex in decerebrate piglets.

Cited by 41 publications

References 39 publications

Interleukin-1β and interleukin-6 enhance thermal prolongation of the LCR in decerebrate piglets

Interleukin-1β and interleukin-6 enhance thermal prolongation of the LCR in decerebrate piglets

Breath-to-breath hypercapnic response in neonatal rats: temperature dependency of the chemoreflexes and potential implications for breathing stability

Potential Central Nervous System Involvement in Sudden Unexpected Infant Deaths and the Sudden Infant Death Syndrome

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