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Cardiac function and microsphere blood flow distribution in the brain-dead dog

dc.contributor.authorHuber, Thomas S.en_US
dc.contributor.authorMartin, Bradley J.en_US
dc.contributor.authorStante, Susan M.en_US
dc.contributor.authorD'Alecy, Louis G.en_US
dc.date.accessioned2006-04-10T15:10:54Z
dc.date.available2006-04-10T15:10:54Z
dc.date.issued1992-06en_US
dc.identifier.citationHuber, Thomas S., Martin, Bradlev J., Stante, Susan M., D'Alecy, Louis G. (1992/06)."Cardiac function and microsphere blood flow distribution in the brain-dead dog." Journal of Critical Care 7(2): 86-94. <http://hdl.handle.net/2027.42/29990>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B7590-4D5WXJN-4/2/30c0490ac940738abfa6d077b31632c7en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/29990
dc.description.abstractThe mechanisms for the deterioration of the brain-dead organ donor are not clearly defined. We measured myocardial blood flow and function during the 4 hours after the induction of brain death in dogs. Brain death was induced by elevating and maintaining intracranial pressure above systolic arterial pressure and effectively stopping central nervous system blood flow. Multiorgan blood flow and systemic arteriovenous shunting were measured using radioactive microspheres. The mean arterial pressure was found to decrease markedly with the induction of brain death. The initial changes in mean arterial pressure were attributed to a decrease of systemic vascular resistance, with the more terminal changes due to a decrease in cardiac index. There was a marked decrease of left ventricular dP/dt with the induction of brain death and a gradual decrease of stroke volume despite no change in pulmonary capillary wedge pressure. The microsphere calculated blood flows to the left ventricle and septum of the myocardium were significantly lower at the 1- and 4-hour time points relative to control. However, the coronary sinus oxygen extraction ratio was not statistically different from control at 4 hours. Systemic arteriovenous shunts increased after the induction of brain death but remained below 10%. We conclude that despite brain death-induced hypotension, there is little evidence to suggest that marked myocardial hypoxic ischemic changes initiated the deterioration in this model.en_US
dc.format.extent895865 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherElsevieren_US
dc.titleCardiac function and microsphere blood flow distribution in the brain-dead dogen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelSurgery and Anesthesiologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartments of Physiology and Surgery, The University of Michigan Medical School, Ann Arbor, MI, USAen_US
dc.contributor.affiliationumDepartments of Physiology and Surgery, The University of Michigan Medical School, Ann Arbor, MI, USAen_US
dc.contributor.affiliationumDepartments of Physiology and Surgery, The University of Michigan Medical School, Ann Arbor, MI, USAen_US
dc.contributor.affiliationumDepartments of Physiology and Surgery, The University of Michigan Medical School, Ann Arbor, MI, USAen_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/29990/1/0000357.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1016/0883-9441(92)90033-4en_US
dc.identifier.sourceJournal of Critical Careen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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