Effects of phrenicotomy and exercise on hypoxia-induced changes in phrenic motor output

Bach, Karen B.; Mitchell, Gordon S.

doi:10.1152/jappl.2000.89.5.1884

Cited by 10 publications

(3 citation statements)

References 29 publications

(37 reference statements)

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“…However, stimulation of these fibers alters c-Fos expression in neurons located in regions of the brainstem associated with respiratory pattern generation (Malakhova and Davenport, 2001). In addition, acute phrenicotomy alters the respiratory rate response to hypoxia in anesthetized rats (Bach and Mitchell, 2000). Interestingly, ipsilateral phrenicotomy increased baseline burst frequency in C 2 injured rats, suggesting that an inhibitory element had been removed.…”

Section: Altered Supraspinal Control Of Breathingmentioning

confidence: 95%

Respiratory Motor Recovery after Unilateral Spinal Cord Injury: Eliminating Crossed Phrenic Activity Decreases Tidal Volume and Increases Contralateral Respiratory Motor Output

Golder¹,

Fuller

Davenport³

et al. 2003

J. Neurosci.

103

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By 2 months after unilateral cervical spinal cord injury (SCI), respiratory motor output resumes in the previously quiescent phrenic nerve. This activity is derived from bulbospinal pathways that cross the spinal midline caudal to the lesion (crossed phrenic pathways). To determine whether crossed phrenic pathways contribute to tidal volume in spinally injured rats, spontaneous breathing was measured in anesthetized C2 hemisected rats at 2 months after injury with an intact ipsilateral phrenic nerve, or with ipsilateral phrenicotomy performed at the time of the SCI (i.e., crossed phrenic pathways rendered ineffective) (dual injury). Ipsilateral phrenicotomy did not alter the rapid shallow eupneic breathing pattern in C2 injured rats. However, the ability to generate large inspiratory volumes after either vagotomy or during augmented breaths was impaired if crossed phrenic activity was abolished. We also investigated whether compensatory plasticity in contralateral motoneurons would be affected by eliminating crossed phrenic activity. Thus, contralateral phrenic motor output was recorded in anesthetized, vagotomized, and mechanically ventilated rats with dual injury during chemoreceptor stimulation. Hypercapnia, hypoxia, and asphyxia increased contralateral phrenic burst amplitude in the dual injury group more than in rats with SCI alone. Dual injury rats also had elevated baseline burst frequency. Together, these results demonstrate a functional role of crossed phrenic activity after SCI. Moreover, by preventing ipsilateral phrenic motor recovery in rats with unilateral SCI, segmental and supraspinal changes could be induced in contralateral respiratory motor output beyond that seen with SCI alone.

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Section: Altered Supraspinal Control Of Breathingmentioning

confidence: 95%

Respiratory Motor Recovery after Unilateral Spinal Cord Injury: Eliminating Crossed Phrenic Activity Decreases Tidal Volume and Increases Contralateral Respiratory Motor Output

Golder¹,

Fuller

Davenport³

et al. 2003

J. Neurosci.

103

View full text Add to dashboard Cite

show abstract

“…Yes/No indicates that LTF was present in some control groups, but not others within the same study. Mahamed and Mitchell, 2008 Anesth Yes Yes >60 min Julien et al, 2008 Unanesth No Yes >60 min Hsieh et al, 2008 Anesth Not reported Yes >60 min Macfarlane and Mitchell, 2007b Anesth Ling et al, 2001 Anesth Not reported Yes >60 min Anesth No Yes >60 min Zabka et al, 2001a Anesth Yes Yes >60 min Anesth No Yes >60 min Baker and Mitchell, 2000 Anesth Yes Yes >60 min Bach and Mitchell, 2000 Anesth Yes Yes >60 min Janssen and Fregosi, 2000 Anesth No No Kinkead and Mitchell, 1999 Anesth No Yes >60 min Kinkead et al, 1998 Anesth No Yes >60 min Bach and Mitchell, 1996 Anesth Yes Yes >60 min Hayashi et al, 1993 Anesth No Yes >60 min…”

mentioning

confidence: 99%

Determinants of frequency long-term facilitation following acute intermittent hypoxia in vagotomized rats

Baker-Herman

Mitchell

2008

Respiratory Physiology & Neurobiology

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Acute intermittent (AIH), but not acute sustained hypoxia (ASH) elicits a form of respiratory plasticity known as long-term facilitation (LTF). In anesthetized rats, LTF is expressed as increased respiratory-related nerve burst amplitude, with variable effects on burst frequency. We analyzed a large data set from multiple investigators using the same experimental protocol to determine factors influencing frequency LTF. Our meta-analysis revealed that AIH elicits both phrenic amplitude and frequency LTF in anesthetized and vagotomized rats, but frequency LTF is small in comparison with amplitude LTF (12% versus 60%, respectively). ASH elicits a small, but significant frequency and amplitude LTF (8% and 10%, respectively) that is not significantly different than controls. Similar to all published reports, analysis of this large data set confirms that phrenic amplitude LTF following AIH is significantly greater than ASH. Multiple regression analysis revealed a strong correlation between baseline burst frequency and frequency LTF. Variations in baseline burst frequency may contribute to variation in frequency LTF and may underlie the apparent effects of some drug treatments.

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“…Originally, significant phrenic and hypoglossal (XII) LTF was consistently observed (1). In subsequent studies, phrenic LTF appeared somewhat smaller and XII LTF was not detectable (3,17). The only apparent difference between these studies is that SD rats were initially obtained from Sasco (S) and subsequently from Harlan (H).…”

mentioning

confidence: 99%

Expression of hypoglossal long-term facilitation differs between substrains of Sprague-Dawley rat

Fuller

Baker

Behan

et al. 2001

Physiological Genomics

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Long-term facilitation (LTF) is a prolonged, serotonin-dependent augmentation of respiratory motor output following episodic hypoxia. Previous observations lead us to hypothesize that LTF is subject to genetic influences and, as a result, differs between Sprague-Dawley (SD) rats from two vendors, Harlan (H) and Charles River Laboratories/Sasco (CRL/S). Using a blinded experimental design, we recorded integrated phrenic (integralPhr) and hypoglossal neurograms in anesthetized, vagotomized, paralyzed, and ventilated rats. At 60 min following three 5-min hypoxic episodes (Pa(O(2)) = 40 +/- 1 Torr; 5-min hyperoxic intervals), integralPhr was elevated from baseline in both SD substrains (i.e., LTF; P < 0.05). Conversely, hypoglossal LTF was present in CRL/S but not H rats (P < 0.05 between substrains). Serotonin immunoreactivity within the hypoglossal nucleus was not different between H and CRL/S rats. We conclude that the expression of hypoglossal LTF differs between SD rat substrains, indicating a difference in their genetic predisposition to neural plasticity.

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Effects of phrenicotomy and exercise on hypoxia-induced changes in phrenic motor output

Cited by 10 publications

References 29 publications

Respiratory Motor Recovery after Unilateral Spinal Cord Injury: Eliminating Crossed Phrenic Activity Decreases Tidal Volume and Increases Contralateral Respiratory Motor Output

Respiratory Motor Recovery after Unilateral Spinal Cord Injury: Eliminating Crossed Phrenic Activity Decreases Tidal Volume and Increases Contralateral Respiratory Motor Output

Determinants of frequency long-term facilitation following acute intermittent hypoxia in vagotomized rats

Expression of hypoglossal long-term facilitation differs between substrains of Sprague-Dawley rat

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