Clonidine in Anesthesiology: A Brief Review

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Clonidine in Anesthesiology: A Brief Review

Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2018, Vol 7, Issue 2

Abstract

Background and Aims: The alpha-2-adrenergic mechanism has been explored for a long time in anesthesiology. Clonidine belongs to this class and has some interesting characteristics for this specialty. Contents: This article illustrates pharmacological aspects, mechanisms of action and clinical use of clonidine in anesthesiology. Sedation, analgesia, lower incidence of nausea, opioid needs and adverse effects reduction are some of the beneficial effects of its use. Adverse effects are bradycardia and low blood pressure. Conclusion: Clonidine reduces post-operative needs of opioid, pain intensity and nausea incidence. However, high risk of perioperative low blood pressure and bradycardia must be taken in consideration when deciding using this drug. From cocaine to dexmedetomidine, passing through noradrenaline, the alpha-2-adrenergic mechanism for analgesia has been explored for more than one century [1]. Although it is known for long time, clonidine, an alpha-2-agonist drug, was used for the first time in human for anesthetics aims only in 1984, epidurally [2]. Since then, several clinical trials, reviews and clinical practice have demonstrated many benefits from the association of clonidine to other anesthetic drugs systemically, spinally or epidurally, with relative safety [1,3-12]. Clonidine has interesting pharmacological characteristics for anesthesia practice, including sedation, hypnosis, analgesia, opioid need reduction and anti-sympathetic response, to surgical trauma response [4]. Pharmacological Aspects: Clonidine is an imidazole compound, alpha-adrenergic agonist with selectivity for alpha-2 receptors [13]. It has fast absorption after oral intake, with great biodisponibility. The distribution volume is around 12L/kg. It is 50% metabolized by the liver into inactive compounds. The other half of the drug is eliminated with no changes by the kidney. The elimination half-life may vary when administrated by intravenously, from 6 to 23 hours, depending on kidney function. It has great lipossolubility and crosses the blood brain barrier with no difficulties [14]. The elimination half-life for the spinal administration is shorter: 1,5 hours [1]. Analgesia: There are alpha-2-agonists receptors in the terminal primary afferent (spinal and peripheral), in spinal superficial lamina neurons and in the supra-spinal nuclei (locus ceruleus) [15]. That way, clonidine and other alpha-2-agonists have analgesic actions on the three sites of sensitive afference: peripheral, spinal and brain. Although there are no such receptors on peripheral nerve axonia, clonidine may increase the effect of local anesthetics in peripheral nerve blocks, by action on C and Aδ fibers, decreasing the conduction on those fibers, because of increase of trans-membrane potassium conductance, and through vasoconstrictor effect (alpha-1-adrenergic effect), which reduces local anesthetics wash-out from perineural tissues [15-17]. When activated by an agonist agent, alpha-2 receptors inhibit the adenilciclase enzyme, reducing intracellular AMPc, leading to a hyperpolarization membrane state [18]. Inhibition of calcium voltage-dependent channels is another secondary action mechanism of clonidine [14]. Clonidine has a selective affinity to alpha-2 receptor 220 higher than its affinity to alpha-1 receptor [1]. Hemodynamics: Clonidine has central and peripheral mechanisms for cardiovascular effects. On solitary tract nuclei and on locus ceruleus, the alpha-2 receptors activation reduces the sympathetic tonus, with inhibition of noradrenaline release on the synaptic junctions, leading to bradycardia and low blood pressure effects [19]. The alpha-2 pre-synaptic receptors on peripheral nerves reduces the noradrenaline exocytosis. In the other hand, post-synaptic alpha-2 receptors stimulation, on endothelium, leads to vasoconstriction, and may cause transitory high blood pressure right after intravenous injection of clonidine [20]. As clonidine is a non-specific selective alpha-2 agonist, in high doses (450μg, spinal, for example), it may increase blood pressure. This is due to the fact that this drug, in less proportion, also is an alpha-1 agonist [21]. Respiratory system: Alpha-2 agonist do not induce deep respiratory depression, even in high doses, nor potentiate respiratory depression caused by opioids [22]. These medications can reverse the muscle stiffness induced by fentanyl, alfentanil, sufentanil and remifentanil [23].

Authors and Affiliations

Hermann S Fernandes, Shirley A Santos, Hazem A Ashmawi

Keywords

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EP ID EP585877
DOI 10.26717/BJSTR.2018.07.001481
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