ArticleThe Journal of physiology2012
A key circulatory defence against asphyxia in infancy--the heart of the matter!
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Dose-related systemic and cerebral hemodynamic effects of norepinephrine in newborn piglets with hypoxia-reoxygenation.Pediatric research · 2025Article
- A "Wear and Tear" Hypothesis to Explain Sudden Infant Death Syndrome.Frontiers in neurology · 2016Article
- Endogenous angiotensins and catecholamines do not reduce skin blood flow or prevent hypotension in preterm piglets.Physiological reports · 2014Article
- Sudden unexpected postnatal collapse of newborn infants: a review of cases, definitions, risks, and preventive measures.Translational stroke research · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A resumption of, and escalation in, breathing efforts (hyperpnoea) reflexively accelerates heart rate (HR) and may facilitate cardiac and circulatory recovery from apnoea. We analysed whether this mechanism can produce a sustained rise in HR (tachycardia) when a sleeping infant is confronted by mild, rapidly worsening asphyxia, simulating apnoea. Twenty-seven healthy term-born infants aged 1-8 days rebreathed the expired gas for 90 s during quiet sleep to stimulate breathing and heart rate. To discriminate cardio-excitatory effects of central respiratory drive, lung inflation, hypoxia, hypercapnia and asphyxia, we varied the inspired O(2) level and compared temporal changes in response profiles as respiratory sensitivity to hypoxia and asphyxia 'reset' after birth. We demonstrate that asphyxia-induced hyperpnoea and tachycardia strengthen dramatically over the first week with different time courses and via separate mechanisms. Cardiac excitation by hypercapnia improves first, followed by a slower improvement in respiratory hypoxic drive. A rise in CO(2) consequently elicits stronger, longer lasting tachycardia than moderate increases in respiratory drive or lung expansion. We suggest that without a strong facilitating action of CO(2) on the immature heart, respiratory manoeuvres may be unable to reflexively counteract strong vagal bradycardia. This may increase the vulnerability of some infants to apnoea-asphyxia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.