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DEXMEDETOMIDINE. A SUMMARY
8
Systemic effects (Figure 3)
Figure 3.
Physiology of target organs of dexmedetomidine (picture by courtesy of Ron Slagter)
Dexmedetomidine decreases tachycardic and increases bradycardic episodes in the heart, induces vasoconstriction
and vasodilatation, and has an anti-shivering and diuretic effect.
Cardiovascular
The period of hypertension, directly after the bolus administration of an α
2
-agonist, is due to
the activation of peripheral α
2B
-receptors and α
1
-receptors in the vascular wall. Subsequently,
injectionof a α
2
-agonist is followedby a longer lastingperiodof hypotension andbradycardia
- due to the central inhibition of the sympathetic activity and at the same time an increase
in parasympathetic activity. The exact mechanism behind these haemodynamic changes
is not known yet. Probably, the imidazole ring – part of both molecules, dexmedetomidine
and clonidine - is an important factor. Imidazoline receptors in the brain receive signals
from baroreceptors in the carotid artery and the aorta. Their activation causes a centrally
induced hypotension and anti-arrhythmic effect.
α
2
-agonists do not have direct myocardial effects. Due to the reduced sympathicotonus
and activation of the parasympathetic nervous system, reduction of heart rate, metabolism,
contractility, and systemic vascular resistance is induced and thus myocardial O
2
-
requirements reduced. This explains the role of clonidine in the treatment of angina pectoris.
Theoretically, activation of α
2
-receptors could induce coronary vasoconstriction, but due to