ArticleThe Journal of physiology2002
Hypoxic vasodilatation: is an adenosine-prostaglandins- NO signalling cascade involved?
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed, 6 citations in OpenAlex.
- The effects of pentoxifylline on skeletal muscle contractility and neuromuscular transmission during hypoxia.Indian journal of pharmacology · 2009Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During hypoxia blood vessels in various tissues including skeletal muscle, heart and brain dilate in order to increase oxygen delivery to the hypoxic organ. The mechanism has long been of interest, but is still incompletely understood. Adenosine is known to be involved; it is released from cells during hypoxia in the metabolic regulation of blood flow (Berne, 1963). There is also evidence for an involvement of endothelial prostaglandins, nitric oxide (NO) and ATP (from which adenosine can be formed following ectoenzymatic degradation), and smooth muscle K(+) channels in hypoxia-induced vasodilatation (e.g. Busse et al. 1984; Messina et al. 1992). To date there have been few attempts to reconcile these different mechanisms.
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