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dc.contributor.authorShu Mi Chenen_US
dc.contributor.authorSuttinee Phuagkhaopongen_US
dc.contributor.authorChi Fangen_US
dc.contributor.authorJacqueline C.C. Wuen_US
dc.contributor.authorYa Hui Huangen_US
dc.contributor.authorPornpun Vivithanapornen_US
dc.contributor.authorHsun Hsun Linen_US
dc.contributor.authorChing Yi Tsaien_US
dc.contributor.otherLotung Poh-Ai Hospitalen_US
dc.contributor.otherChang Gung Memorial Hospitalen_US
dc.contributor.otherTzu Chi Universityen_US
dc.contributor.otherMahidol Universityen_US
dc.date.accessioned2020-01-27T07:56:52Z-
dc.date.available2020-01-27T07:56:52Z-
dc.date.issued2019-01-01en_US
dc.identifier.citationFrontiers in Physiology. Vol.10, No.JUN (2019)en_US
dc.identifier.issn1664042Xen_US
dc.identifier.other2-s2.0-85069753585en_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/50376-
dc.description.abstract© 2019 Chen, Phuagkhaopong, Fang, Wu, Huang, Vivithanaporn, Lin and Tsai. Whereas cadmium is a toxicant that has been shown to cause cardiovascular toxicity and mortality in mammals, few mechanistic studies address its acute circulatory actions. The present study assessed the hypothesis that cadmium effects dose-dependent acute circulatory fates via differential participation of the cardiovascular regulatory mechanisms in brain. In Sprague-Dawley rats maintained under propofol anesthesia, cadmium acetate (8 mg/kg, iv) induced significantly high mortality rate within 10 min, concomitant with progressive decline toward zero level of mean arterial pressure (MAP), heart rate (HR), baroreflex-mediated sympathetic vasomotor tone, and carotid blood flow (CBF). There were concurrent tissue anoxia, cessation of microvascular perfusion, reduction of mitochondrial membrane potential and ATP production, and necrotic cell death in the rostral ventrolateral medulla (RVLM), the brain stem site that maintains blood pressure and sympathetic vasomotor tone. On the other hand, a lower-dose of cadmium (4 mg/kg, iv) resulted in only a transient decrease in MAP that was mirrored by an increase in CBF and baroreflex-mediated sympathetic vasomotor tone, minor changes in HR, along with transient hypoxia, and apoptotic cell death in RVLM. We conclude that cadmium elicits dose-dependent acute cardiovascular effects with differential underlying biochemical and neural mechanisms. At a higher-dose, cadmium induces high mortality by effecting acute cardiovascular collapse via anoxia, diminished tissue perfusion, mitochondrial dysfunction and bioenergetics failure that echo failure of cerebral autoregulation, leading to necrosis, and loss of functionality in RVLM. On the other hand, a lower-dose of cadmium elicits low mortality, transient decrease in arterial pressure, and hypoxia and apoptosis in RVLM that reflect sustained cerebral autoregulation.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85069753585&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectMedicineen_US
dc.titleDose-dependent acute circulatory fates elicited by cadmium are mediated by differential engagements of cardiovascular regulatory mechanisms in brainen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.3389/fphys.2019.00772en_US
dc.identifier.urlhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85069753585&origin=inwarden_US
Appears in Collections:Scopus 2019

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