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Anesth Analg 2001;92:1408-1412
© 2001 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Is Endotracheal Adrenaline Deleterious Because of the Beta Adrenergic Effect?

Zvi Vaknin, MD, Yossi Manisterski, MD, Ron Ben-Abraham, MD, Ori Efrati, MD, Danny Lotan, MD, Zohar Barzilay, MD, FCCM, and Gideon Paret, MD

Department of Pediatric Intensive Care, The Chaim Sheba Medical Center, Tel Hashomer; and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

Address correspondence and reprint requests to Gideon Paret, MD, The Department of Pediatric Intensive Care, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel. Address e-mail to gparet{at}post.tau.ac.il

IV adrenaline increases coronary and cerebral perfusion pressures during cardiopulmonary resuscitation. We recently showed that endotracheal adrenaline can decrease blood pressure (BP), a detrimental effect presumably mediated by the ß2-adrenergic receptor unopposed by {alpha}-adrenergic vasoconstriction. This prospective, randomized, laboratory comparison of endotracheal adrenaline (0.05 mg/kg diluted with normal saline to 10 mL total volume) with or without nonselective ß-blocker (propranolol) pretreatment was conducted in an attempt to clarify the mechanism of this BP decrease. Five mongrel dogs were given 0.05 mg/kg endotracheal adrenaline (diluted) or 0.05 mg/kg endotracheal adrenaline followed by an IV propranolol (0.1 mg/kg) pretreatment. Each dog served as its own control (10 mL of normal saline administered endotracheally) and received each regimen at least one week apart. Endotracheal adrenaline given after the propranolol pretreatment produced an increase in systolic, diastolic, and mean arterial BPs, from 165/110 mm Hg (mean 128 mm Hg) to 177.5/125 mm Hg (mean 142.5 mm Hg), respectively, as opposed to the hypotensive effect of isolated endotracheal adrenaline (P < 0.03). Thus, endotracheal adrenaline was associated with predominantly ß-adrenergic–mediated effects, causing hypotension via peripheral vasodilatation unopposed by {alpha}-adrenergic vasoconstriction. The search for the optimal dose of endotracheal adrenaline should be aimed at achieving the higher {alpha}-adrenergic vasoconstrictive threshold.

Implications: Endotracheal adrenaline (0.05 mg/kg diluted with normal saline to 10 mL total volume) with or without nonselective ß-blocker (propranolol) pretreatment was studied to clarify the mechanism of blood pressure decrease after this anesthetic protocol in dogs. An optimal dose of endotracheal adrenaline should achieve a high {alpha}-adrenergic vasoconstrictive threshold.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2001 by the International Anesthesia Research Society.