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Dexmedetomidine blunts haemodynamic and intraocular pressure responses to tracheal intubation

Richa, Freda

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European Journal of Anaesthesiology: May 2009 - Volume 26 - Issue 5 - p 444-445
doi: 10.1097/EJA.0b013e32831bd8a1


I have read with great interest the article by Yavascaoglu et al. [1] comparing esmolol and dexmedetomidine (DEX) for attenuation of intraocular pressure (IOP) and haemodynamic responses to laryngoscopy and tracheal intubation. The authors found that DEX is more effective than esmolol in preventing the haemodynamic and IOP responses to tracheal intubation. I would like to comment on the mechanism of action of DEX in blunting haemodynamic and IOP responses to tracheal intubation.

First, DEX is a full adrenoceptor agonist with high selectivity for α2-adrenergic receptors. The α2-receptors are involved in regulating the autonomic and cardiovascular systems and are located on blood vessels, where they mediate vasoconstriction, and on sympathetic terminals, where they inhibit norepinephrine release. α2-Receptors are also located within the central nervous system, and their activation leads to a reduction of tonic levels of sympathetic outflow and an augmentation of cardiac–vagal activity. This can result in a decrease in heart rate (HR) and cardiac output [2]. Intravenous administration of an α2-adrenoceptor agonist leads to a decrease in HR and a transient increase in arterial blood pressure (BP) and systemic vascular resistance, but a decrease in cardiac output because of the activation of postjunctional vascular α2-adrenoceptors. This is followed by a long-lasting decrease in HR and BP because of a centrally mediated decrease in sympathetic tone and an increase in vagal activity [3,4]. It is believed that the vasoconstriction effect of DEX via the α2-adrenergic receptors, which are located in the smooth muscle cells of resistance vessels, might be responsible for the suppression of the decrease in BP due to anaesthetic induction. The peripheral vascular action of DEX is unmasked when sympathetic inhibition due to the central action of α2-agonists is absent [4].

Second, the effect of DEX on the IOP may be caused by a direct vasoconstrictor effect on the afferent blood vessels of the ciliary body, which results in reduction of aqueous humour production [5]. Moreover, it could increase outflow of the aqueous humour caused by a reduction of the sympathetically mediated vasomotor tone of the ocular drainage system [6]. Additionally, its associated haemodynamic response could contribute to the IOP lowering effect [7].

It would be very interesting, however, to study DEX in cardiovascular patients, especially in patients in whom hypotension during anaesthesia induction is very deleterious such as carotid endarteriectomy and coronary artery bypass surgery.


1 Yavascaoglu B, Kaya FN, Baykara M, et al. A comparison of esmolol and dexmedetomidine for attenuation of intraocular pressure and haemodynamic responses to laryngoscopy and tracheal intubation. Eur J Anaesthesiol 2008; 25:517–519.
2 Virtanen R, Savola JM, Saano V, Nyman L. Characterization of the selectivity, specificity and potency of medetomidine as an α2-adrenoceptor agonist. Eur J Pharmacol 1988; 150:9–14.
3 Yildiz M, Tavlan A, Tuncer S, et al. Effects of dexmedetomidine on haemodynamic responses to laryngoscopy and intubation: perioperative haemodynamics and anaesthetic requirements. Drugs R D 2006; 7:43–52.
4 Bloor BC, Ward DS, Belleville JP, Maze M. Effects of intravenous dexmedetomidine in humans. II. Hemodynamic changes. Anesthesiology 1992; 77:1134–1142.
5 Macri FJ, Cervario SJ. Clonidine. Arch Ophthalmol 1978; 96:2111–2113.
6 Vartiainen J, MacDonald E, Urtti A, et al. Dexmedetomidine-induced ocular hypotension in rabbits with normal or elevated intraocular pressures. Invest Ophthalmol Vis Sci 1992; 33:2019–2023.
7 Georgiou M, Parlapani A, Argiriadou H, et al. Sufentanil or clonidine for blunting the increase in intraocular pressure during rapid-sequence induction. Eur J Anaesthesiol 2002; 13:519–522.
© 2009 European Society of Anaesthesiology