Is endotracheal adrenaline deleterious because of the beta adrenergic effect?

Z. Vaknin, Y. Manisterski, R. Ben-Abraham, O. Efrati, D. Lotan, Z. Barzilay, G. Paret*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

40 Scopus citations

Abstract

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 β2-adrenergic receptor unopposed by α-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 β-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 β-adrenergic-mediated effects, causing hypotension via peripheral vasodilatation unopposed by α-adrenergic vasoconstriction. The search for the optimal dose of endotracheal adrenaline should be aimed at achieving the higher α-adrenergic vasoconstrictive threshold.

Original languageEnglish
Pages (from-to)1408-1412
Number of pages5
JournalAnesthesia and Analgesia
Volume92
Issue number6
DOIs
StatePublished - 2001
Externally publishedYes

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