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Functional characterisation of the GABAA receptors
Published in Adam Doble, Ian L Martin, David Nutt, Calming the Brain: Benzodiazepines and related drugs from laboratory to clinic, 2020
Adam Doble, Ian L Martin, David Nutt
In mice expressing α2H101R, diazepam-induced anxiolytic activity, assessed using the elevated plus maze and light-dark box selection tests (discussed further in Chapter 6), was absent but this was not the case for those mice expressing α3H101R (Low et al, 2000). Thus, targeting of agents to the α2 subunit containing receptors could be expected to provide relief from anxiety without the sedative side-effect profile that compromises the use of the currently available agents. This indeed appears to be the case (McKernan et al, 2000).
Drug-Induced Hypertension
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Rull Gurvinder, D. Lobo Melvin
Many anaesthetic agents such as propofol are potent hypotensive agents largely due to profound arterial and venous dilatation. However, a number of anaesthetic drugs can lead to temporary effects on BP regulation, leading to hypertension. Ketamine increases heart rate, systolic BP and total peripheral resistance. It also leads to increased pulmonary artery pressure and pulmonary vascular resistance (50). Desflurane also elevates heart rate and BP. BP can also be elevated by drugs if there is an underlying pheochromocytoma. This has been seen with fentanyl, opiates, neuromuscular relaxants and glucagon (51,52). Dexmedetomidine has antianxiety, sedative and analgesic effects making it useful in anaesthesia. It acts on central α2-adrenergic receptors and leads to elevated BP at high doses and reduced BP at low doses.
Emergence from anesthesia
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Manual of Neuroanesthesia, 2017
α2-agonists: α2-agonists are potent cerebral vasoconstrictors.86 Dexmedetomidine decreases Vmca in transcranial Doppler (TCD), with maximum reduction at 25% of the hypnotic doses. The CMRO2 and ICP may remain unchanged after dexmedetomidine infusion.87 The use of dexmedetomidine in a neurosurgical patient has considerably increased in the past decade. It is frequently used for awake craniotomy.
THE effect of general anesthetics on genetic absence epilepsy in WAG/Rij rats
Published in Neurological Research, 2022
Lubna Al-Gailani, Ali Al-Kaleel, Gökhan Arslan, Mustafa Ayyıldız, Erdal Ağar
In the first, second, and even third 20 min[] after the administration of dexmedetomidine, there was a significant increase in the total number of SWD and the total number of spikes when compared with other anesthetic groups, this means that the dexmedetomidine has the lowest effect on the SWD activity in the present model, which makes it the best to use during the experimental studies on absence epilepsy WAG/Rij rat model. Dexmedetomidine has decreased the number and cumulative duration of recurring seizures in a rat model of self-sustaining epilepticus with continuous amygdala stimulation and reduced the amount of glutamate in the hippocampal tissue [38]. Dexmedetomidine acts as a proconvulsant in cats during enflurane anesthesia [39] and in the pentylenetetrazol rat model [38]. The possible mechanism by which α2 agonists can act as anticonvulsants in some epileptic models, but not all, is just a great question. There is some data to suggest that norepinephrine indirectly enhances the inhibitory action of GABA [40]. These findings may indicate that by potentiating GABA, dexmedetomidine reduces epileptic activity. Dexmedetomidine is a more selective agonist of α2 than clonidine and is known to be a complete agonist [21]. α2 receptors have recently been subdivided into four subtypes, namely α2A … . α2DD [41]. The affinity of dexmedetomidine and clonidine for all these subtypes is uncertain [42]. The significant difference in the action of these drugs in various epileptic models may be explained by differences in alpha2 receptor selectivity or receptor subtype selectivity.
The state-of-the-art pharmacotherapeutic options for the treatment of chronic non-cancer pain
Published in Expert Opinion on Pharmacotherapy, 2022
Ryan S. D’Souza, Brendan Langford, Rachel E. Wilson, Yeng F. Her, Justin Schappell, Jennifer S. Eller, Timothy C. Evans, Jonathan M. Hagedorn
Alpha-2 agonists offer another unique mechanism to attenuate and modulate the transmission of pain signals. The most commonly used alpha-2-agonists in clinical practice include clonidine and dexmedetomidine. Alpha-2 agonists inhibit postsynapatic spinothalamic projection neurons, inhibit presynaptic primary nerve signals, inhibit presynaptic brainstem noradrenergic neurons, and decrease sympathetic activity [94]. The α2-A and α2-C receptors are found within the central nervous system and cause sedation, analgesia, and sympatholytic effects when activated; the α2-B receptors are found on vascular smooth muscle and are responsible for the vasopressive effects. All of the receptors have been found to inhibit cAMP, causing downstream diminution of pain nerve signals and inhibition of norepinephrine release [94]. The most common adverse effects associated with α2-agonists are sedation, hypotension, bradycardia, and dry mouth which are generally mild [94].
Effect of intrathecal dexmedetomidine on shoulder tip pain during laparoscopic ovarian cystectomy under spinal anaesthesia
Published in Egyptian Journal of Anaesthesia, 2021
Rasha Hamed, Saeid Elsawy, Abualauon Mohamed Abedalmohsen, Waleed Saleh farrag
Dexmedetomidine is a highly selective α2 adrenergic receptor agonist which is approved by the Food and Drug Administration as an intravenous sedative and general anaesthetic adjuvant. However, intrathecal use of α2-receptor agonists was found to possess antinociceptive effects on somatic and visceral pain, which are believed to be mediated by suppression of neurotransmitters released from C-fibre and post-synaptic dorsal horn neurons hyperpolarization [7]. Clinical trials revealed that dexmedetomidine decreases proinflammatory cytokines production, subsequently mitigates the systemic inflammatory response, and reduces mortality due to surgery and anaesthesia [8]. Previous studies also suggested that intrathecal use of dexmedetomidine in doses varied from 0.2 to 1 µg/kg was free of any neurotoxic manifestations [9]. Moreover, Its use in spinal cord injury revealed a neuroprotective effect resembles methylprednisolone [9,10].