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dc.contributor.authorStenslokken, Kare-Olav
dc.contributor.authorSundin, Lena
dc.contributor.authorRenshaw, Gillian
dc.contributor.authorNilsson, Goran
dc.contributor.editorDr. H Hoppler
dc.date.accessioned2017-10-23T03:58:02Z
dc.date.available2017-10-23T03:58:02Z
dc.date.issued2004
dc.date.modified2007-03-18T21:39:32Z
dc.identifier.issn00220949en_US
dc.identifier.doi10.1242/jeb.01291en_US
dc.identifier.urihttp://hdl.handle.net/10072/5508
dc.description.abstractCoral reef platforms may become hypoxic at night during low tide. One animal in that habitat, the epaulette shark (Hemiscyllium ocellatum), survives hours of severe hypoxia and at least one hour of anoxia. Here, we examine the branchial effects of severe hypoxia (<0.3 mg oxygen l–1 for 20 min in anaesthetized epaulette shark), by measuring ventral and dorsal aortic blood pressure (PVA and PDA), heart rate (fh), and observing gill microcirculation using epi-illumination microscopy. Hypoxia induced a flow of blood in two parallel blood vessels, termed longitudinal vessels, in the outer borders of the free tip of the gill filament. Hypoxia also induced significant falls in fh, PVA and PDA, and a biphasic change in ventilation frequency (increase followed by decrease). Adenosine injection (1μ mol kg–1) also initiated blood flow in the longitudinal vessels, in addition to significant drops in PVA, PDA and fh, and a biphasic response in ventilation frequency (decrease followed by increase) indicating that adenosine influences ventilation. Aminophylline (10 mg kg–1), an A1 and A2 adenosine receptor antagonist, blocked the effects of adenosine injection, and also significantly reduced blood flow in the longitudinal vessels during hypoxia. In the second part of the study, we examined the cholinergic influence on the cardiovascular circulation during severe hypoxia (<0.3 mg l–1) using antagonists against muscarinic (atropine 2 mg kg–1) and nicotinic (tubocurarine 5 mg kg–1) receptors. Injection of acetylcholine (ACh; 1μ mol kg–1) into the ventral aorta caused a marked fall in fh, a large increase in PVA, but small changes in PDA (suggesting increased Rgill). Atropine was able to inhibit the branchial vascular responses to ACh but not the hypoxic bradycardia, suggesting the presence of muscarinic receptors on the heart and gill vasculature, and that the hypoxia induced bradycardia is of non-cholinergic origin. The results suggest that adenosine mediates increases in the arterio–venous circulation in the gill during hypoxia. This may serve to increase blood supply to heart and gill tissue.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherThe Company of Biologists Ltd.en_US
dc.publisher.placeUnited Kingdomen_US
dc.relation.ispartofpagefrom4451en_US
dc.relation.ispartofpageto4461en_US
dc.relation.ispartofjournalJournal of Experimental Biologyen_US
dc.relation.ispartofvolume207en_US
dc.subject.fieldofresearchHISTORY AND ARCHAEOLOGYen_US
dc.subject.fieldofresearchcode210000en_US
dc.titleAdenosinergic and cholinergic control mechanisms during hypoxia in the epaulette shark (Hemiscyllium ocellatum), with emphasis on the branchial circulation.en_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.en_US
gro.date.issued2004
gro.hasfulltextNo Full Text


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