Show simple item record

dc.contributor.authorLall, VK
dc.contributor.authorDutschmann, M
dc.contributor.authorDeuchars, J
dc.contributor.authorDeuchars, SA
dc.date.accessioned2020-12-15T22:55:27Z
dc.date.available2020-12-15T22:55:27Z
dc.date.issued2012-12-15
dc.identifierpii: 1423-0127-19-103
dc.identifier.citationLall, V. K., Dutschmann, M., Deuchars, J. & Deuchars, S. A. (2012). The anti-malarial drug Mefloquine disrupts central autonomic and respiratory control in the working heart brainstem preparation of the rat. JOURNAL OF BIOMEDICAL SCIENCE, 19 (1), https://doi.org/10.1186/1423-0127-19-103.
dc.identifier.issn1021-7770
dc.identifier.urihttp://hdl.handle.net/11343/254320
dc.description.abstractBACKGROUND: Mefloquine is an anti-malarial drug that can have neurological side effects. This study examines how mefloquine (MF) influences central nervous control of autonomic and respiratory systems using the arterially perfused working heart brainstem preparation (WHBP) of the rat. Recordings of nerve activity were made from the thoracic sympathetic chain and phrenic nerve, while heart rate (HR) and perfusion pressure were also monitored in the arterially perfused, decerebrate, rat WHBP. MF was added to the perfusate at 1 μM to examine its effects on baseline parameters as well as baroreceptor and chemoreceptor reflexes. RESULTS: MF caused a significant, atropine resistant, bradycardia and increased phrenic nerve discharge frequency. Chemoreceptor mediated sympathoexcitation (elicited by addition of 0.1 ml of 0.03% sodium cyanide to the aortic cannula) was significantly attenuated by the application of MF to the perfusate. Furthermore MF significantly decreased rate of return to resting HR following chemoreceptor induced bradycardia. An increase in respiratory frequency and attenuated respiratory-related sympathetic nerve discharge during chemoreceptor stimulation was also elicited with MF compared to control. However, MF did not significantly alter baroreceptor reflex sensitivity. CONCLUSIONS: These studies indicate that in the WHBP, MF causes profound alterations in autonomic and respiratory control. The possibility that these effects may be mediated through actions on connexin 36 containing gap junctions in central neurones controlling sympathetic nervous outflow is discussed.
dc.languageEnglish
dc.publisherBMC
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleThe anti-malarial drug Mefloquine disrupts central autonomic and respiratory control in the working heart brainstem preparation of the rat
dc.typeJournal Article
dc.identifier.doi10.1186/1423-0127-19-103
melbourne.affiliation.departmentFlorey Department of Neuroscience and Mental Health
melbourne.source.titleJournal of Biomedical Science
melbourne.source.volume19
melbourne.source.issue1
dc.rights.licenseCC BY
melbourne.elementsid1204545
melbourne.contributor.authorDutschmann, Mathias
dc.identifier.eissn1423-0127
melbourne.accessrightsOpen Access


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record