title: An Experimental Model of Vasovagal Syncope Induces Cerebral Hypoperfusion and Fainting-Like Behavior in Awake Rats.
abstract: Vasovagal syncope, a contributing factor to elderly falls, is the transient loss of consciousness caused by decreased cerebral perfusion. Vasovagal syncope is characterized by hypotension, bradycardia, and reduced cerebral blood flow, resulting in fatigue, altered coordination, and fainting. The purpose of this study is to develop an animal model which is similar to human vasovagal syncope and establish an awake animal model of vasovagal syncope. Male Sprague-Dawley rats were subjected to sinusoidal galvanic vestibular stimulation (sGVS). Blood pressure, heart rate, and cerebral blood flow were monitored before, during, and post-stimulation. sGVS resulted in hypotension, bradycardia, and decreased cerebral blood flow. One cohort of animals was subjected to sGVS while freely moving. sGVS in awake animals produced vasovagal syncope-like symptoms, including fatigue and uncoordinated movements; two animals experienced spontaneous falling. Another cohort of animals was preconditioned with isoflurane for several days before being subjected to sGVS. Isoflurane preconditioning before sGVS did not prevent sGVS-induced hypotension or bradycardia, yet isoflurane preconditioning attenuated sGVS-induced cerebral blood flow reduction. The sGVS rat model mimics elements of human vasovagal syncope pathophysiology (hypotension, bradycardia, and decreased cerebral perfusion), including behavioral symptoms such as fatigue and altered balance. This study indicates that the sGVS rat model is similar to human vasovagal syncope and that therapies directed at preventing cerebral hypoperfusion may decrease syncopal episodes and reduce injuries from syncopal falls.
authors.affiliation: Department of Physiology & Pharmacology, Loma Linda University, Loma Linda, California, United States of America.
authors.forename: Devin W
authors.initials: DW
authors.lastname: McBride
authors.affiliation: Department of Anesthesiology, Loma Linda University, Loma Linda, California, United States of America.
authors.forename: Cesar
authors.initials: C
authors.lastname: Reis
authors.affiliation: Loma Linda University School of Medicine, Loma Linda, California, United States of America.
authors.forename: Ethan
authors.initials: E
authors.lastname: Frank
authors.affiliation: Department of Physiology & Pharmacology, Loma Linda University, Loma Linda, California, United States of America.
authors.forename: Damon W
authors.initials: DW
authors.lastname: Klebe
authors.affiliation: Department of Physiology & Pharmacology, Loma Linda University, Loma Linda, California, United States of America.|Department of Neurosurgery, Loma Linda University, Loma Linda, California, United States of America.
authors.forename: John H
authors.initials: JH
authors.lastname: Zhang
authors.affiliation: Department of Anesthesiology, Loma Linda University, Loma Linda, California, United States of America.
authors.forename: Richard
authors.initials: R
authors.lastname: Applegate
authors.affiliation: Department of Physiology & Pharmacology, Loma Linda University, Loma Linda, California, United States of America.
authors.forename: Jiping
authors.identifier: http://orcid.org/0000-0002-2392-9280
authors.initials: J
authors.lastname: Tang