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Mechanisms of the “Low-Flow” State during Resuscitation of the Totally Ischemic Brain

Published online by Cambridge University Press:  03 July 2018

W. A. Tweed ,
J. G. Wade  and
W. J. Davidson
W. A. Tweed*
Affiliation:
Departments of Anesthesia and Pharmacology & Therapeutics Faculty of Medicine, University of Manitoba
J. G. Wade
Affiliation:
Departments of Anesthesia and Pharmacology & Therapeutics Faculty of Medicine, University of Manitoba
W. J. Davidson
Affiliation:
Departments of Anesthesia and Pharmacology & Therapeutics Faculty of Medicine, University of Manitoba
*
Department of Anesthesia, University of Manitoba, Health Sciences Centre — General, 700 William Ave., Winnipeg, Canada. R3E 0Z3.
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Resuscitation of the brain following total circulatory arrest may be impeded by difficulty in establishing cerebral tissue perfusion, a post-ischemic “low-flow” state. We have confirmed this hypothesis in a rat model of total cerebral ischemia and have demonstrated marked improvement in post-ischemic brain tissue perfusion following epinephrine injection. This is mainly due to the systemic vascular effects of epinephrine, resulting in improved central aortic pressure and cerebral perfusion pressure. Hyperkalemic induced vasoconstriction has also been postulated as a cause of the “low-flow”. We have, therefore, investigated the in vitro effects of increasing potassium ion concentration on cerebrovascular smooth muscle strips. Large arteries constrict, while small arteries dilate in response to hyperkalemia. The net effect on cerebral blood flow remains unsettled. Our research to date suggests that resuscitation of the totally ischemic brain, in animal models at least, is enhanced by epinephrine, mainly via its effects on central aortic pressure.

Résumé

Résumé

La réactivation du cerveau après un arrêt cardiaque complet peut être entravée par la difficulté d’établir la perfusion du tissu cérébral, un état de lenteur du flot post-ischémique. Nous avons confirmé cette hypothèse dans un modèle d’ischémie cérébrale totale chez le rat et avons démontré une amélioration marquée dans la perfusion post-ischémique du tissu cérébral après une injection d’épinéphrine. Ceci est principalement dû aux effets vasculaires systémiques de l’épinéphrine, résultant en une amélioration de la pression aortique centrale et de la pression de la perfusion cérébrale. Une vasoconstriction induite par l’hyperkaliémie a également été postulée comme cause possible de ce flot lent. Nous avons donc investigué les effets in vitro de l’augmentation de la concentration de l’ion potassium sur des bandes de muscles lisses de la vasculature cérébrale. Les grandes artères rétrécissent, pendant que les petites artères se dilatent en réponse à l’hyperkaliémie. L’effet sur le débit sanguin cérébral demeure incertain. Notre recherche à date suggère que la réactivation du cerveau totalement ischémique, du moins dans certains modèles animaux, est augmentée par l’épinéphrine, principalement via ses effets sur la pression aortique centrale.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 4 , Issue 1 , February 1977 , pp. 19 - 23
Copyright
Copyright © Canadian Neurological Sciences Federation 1977

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