PubMed · 10646352
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M E Broome. "Two steps forward, one back".. https://pubmed.ncbi.nlm.nih.gov/10646352/
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Congenital central hypoventilation syndrome (CCHS) and Hirschsprung's disease (HSCR) are often classified as neurocristopathies and are thought to share a common molecular pathogenesis related to the genes that control the development of neural crest cells. We examined whether endothelin-3 (ET-3), one of the developmental regulators of neural crest cells and of which null mutation results in aganglionic megacolon in mice, fulfills the requirements for such a common molecule. To investigate the possible involvement of ET-3 in central ventilatory control, we measured ventilation in mutant mice deficient in ET-3 by whole body plethysmography. Tidal volume and breathing frequency were measured during breathing of room air, hypoxic, hyperoxic, or hypercapnic gas mixtures in awake and anesthetized mice. There were no significant differences in resting ventilation as well as ventilatory responses to hypoxia and hypercapnia between ET-3-knockout mice and wild-type mice. Our results indicate that ET-3 can not be considered as a common pathogenic mechanism for CCHS and HSCR at least in mice.
Phase synchronization between cardiac and respiratory oscillations is investigated during anesthesia in rats. Synchrograms and time evolution of synchronization indices are used to show that the system passes reversibly through a sequence of different phase-synchronized states as the anesthesia level changes, indicating that it can undergo phase transitionlike phenomena. It appears that the synchronization state may be used to characterize the depth of anesthesia.
1. Intermittent hypoxia elicits long-term facilitation (LTF) of phrenic motor output in anaesthetized rats. We tested the hypothesis that an equal cumulative duration of continuous hypoxia would not elicit phrenic LTF. 2. Integrated phrenic nerve activity was recorded in urethane-anaesthetized, vagotomized, paralysed and ventilated rats exposed to: (1) 3 X 3 min hypoxic episodes (inspired O2 fraction (FI, O2) = 0.11) separated by 5 min hyperoxia (FI,O2 = 0.5; n = 6), (2) 9 min continuous hypoxia (n = 6), or (3) 20 min continuous hypoxia (n = 7). Isocapnia was maintained throughout the protocol. 3. Consistent with previous studies, phrenic amplitude was significantly elevated for at least 1 h following intermittent hypoxia (78 +/- 15% 60 min post-hypoxia; P < 0.05) with an associated increase in burst frequency (11 +/- 2.1 bursts min-1; P < 0.05). In contrast, 9 or 20 min continuous hypoxia did not elicit LTF of either phrenic amplitude (4.7 +/- 5.1 and 10.1 +/- 10.2% 60 min post-hypoxia, respectively; P > 0.05) or frequency (4.6 +/- 1.3 and 5.1 +/- 2 bursts min-1 60 min post-hypoxia, respectively; P > 0.05). 4. The results indicate that hypoxia-induced long-term facilitation of phrenic motor output is sensitive to the pattern of hypoxic exposure in anaesthetized rats.