This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gervais, H. W. Articles by Traystman, R. J. Search for Related Content PubMed PubMed Citation Articles by Gervais, H. W. Articles by Traystman, R. J.

Stroke, Vol 22, 1554-1561, Copyright © 1991 by American Heart Association

ARTICLES

Effect of adrenergic drugs on cerebral blood flow, metabolism, and evoked potentials after delayed cardiopulmonary resuscitation in dogs

HW Gervais, CL Schleien, RC Koehler, ID Berkowitz, DH Shaffner and RJ Traystman
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, MD 21205.

BACKGROUND AND PURPOSE: Epinephrine administration during cardiopulmonary resuscitation increases cerebral blood flow by increasing arterial pressure. We tested whether potential beta- adrenergic effects of epinephrine directly influence cerebral blood flow and oxygen consumption independently of raising perfusion pressure. METHODS: Four groups of seven anesthetized dogs were subjected to 8 minutes of fibrillatory arrest followed by 6 minutes of chest compression, ventricular defibrillation, and 4 hours of spontaneous circulation. Cerebral perfusion pressure was increased to approximately equivalent ranges during resuscitation by either 1) epinephrine infusion, 2) epinephrine infusion after pretreatment with the lipophilic beta-adrenergic antagonist pindolol, 3) infusion of the alpha-adrenergic agonist phenylephrine, or 4) descending aortic balloon inflation without pressor agents. RESULTS: We found no difference in cerebral blood flow, oxygen extraction, or oxygen consumption during chest compression among groups. After ventricular defibrillation, depressed levels of cerebral blood flow, cerebral oxygen consumption, and somatosensory evoked potential amplitude were not different among groups. CONCLUSIONS: We detected no evidence that after 8 minutes of complete ischemia, epinephrine administration during resuscitation substantially influences cerebral blood flow or cerebral oxygen consumption independent of its action of raising arterial pressure or or that epinephrine has a negative impact on immediate metabolic or electrophysiological recovery attributable to its beta-adrenergic activity.

This article has been cited by other articles:

				D. H. Shaffner, S. M. Eleff, R. C. Koehler, R. J. Traystman, and J. P. Ornato Effect of the No-Flow Interval and Hypothermia on Cerebral Blood Flow and Metabolism During Cardiopulmonary Resuscitation in Dogs • Editorial Comment Stroke, December 1, 1998; 29(12): 2607 - 2615. [Abstract] [Full Text] [PDF]

				V. Wenzel, K. H. Lindner, S. Augenstein, A. W. Prengel, H. U. Strohmenger, and R. C. Koehler Vasopressin Combined With Epinephrine Decreases Cerebral Perfusion Compared With Vasopressin Alone During Cardiopulmonary Resuscitation in Pigs • Editorial Comment Stroke, July 1, 1998; 29(7): 1462 - 1468. [Abstract] [Full Text] [PDF]

				C. L. Schleien, J. W. Kuluz, and B. Gelman Hemodynamic effects of nitric oxide synthase inhibition before and after cardiac arrest in infant piglets Am J Physiol Heart Circ Physiol, April 1, 1998; 274(4): H1378 - H1385. [Abstract] [Full Text] [PDF]

				A. W. Prengel, K. H. Lindner, A. Keller, and R. C. Koehler Cerebral Oxygenation During Cardiopulmonary Resuscitation With Epinephrine and Vasopressin in Pigs Stroke, July 1, 1996; 27(7): 1241 - 1248. [Abstract] [Full Text]

				S. M. Eleff, H. Sugimoto, D. H. Shaffner, R. J. Traystman, and R. C. Koehler Acidemia and Brain pH During Prolonged Cardiopulmonary Resuscitation in Dogs Stroke, June 1, 1995; 26(6): 1028 - 1034. [Abstract] [Full Text]