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Background Recently, there have been some trials to use dexmedetomidine in the obstetric field but concerns regarding the drug include changes in uterine contractions after labor. We aimed to evaluate the effects of dexmedetomidine on the myometrial contractions of pregnant rats. Methods In a pilot study, the contraction of the myometrial strips of pregnant Sprague-Dawley rats in an organ bath with oxytocin at 1 mU/ml was assessed by adding dexmedetomidine from 10-6 to 10-2 M accumulatively every 20 min, and active tension and the number of contractions were evaluated. Then, changes in myometrial contractions were evaluated from high doses of dexmedetomidine (1.0 × 10-4 to 1.2 × 10-3 M). The effective concentrations (EC) for changes in uterine contractions were calculated using a probit model. Results Active tension and the number of contractions were significantly decreased at 10-3 M and 10-4 M dexmedetomidine, respectively (P < 0.05). A complete loss of contractions was seen at 10-2 M. Dexmedetomidine (1.0 × 10-4 to 1.2 × 10-3 M) decreased active tension and the number of contractions in a concentration-dependent manner. The EC95 of dexmedetomidine for inhibiting active tension and the number of contractions was 5.16 × 10-2 M and 2.55 × 10-5 M, respectively. Conclusions Active tension of the myometrium showed a significant decrease at concentrations of dexmedetomidine higher than 10-3 M. Thus, clinical concentrations of dexmedetomidine may inhibit uterine contractions. Further research is needed for the safe use of dexmedetomidine in the obstetrics field.

The subthalamic nucleus (STN) plays a key role in the pathophysiology of Parkinson's disease. This was demonstrated by the fact that STN neurons express more bursts in animal models of the disease and by the ability of STN inactivation to alleviate motor deficits. However, the origin of the bursts and the causal link between STN bursts and motor deficits remain unknown. The present study aimed to investigate the role of noradrenergic receptor modulation on the firing activity of STN neurons and the impact of this modulation on locomotor activity in sham and 6-hydroxydopamine-lesioned rats. Using selective agonists and antagonists of α1- and α2-adrenergic receptors (AR), we show that local infusion of clonidine, an α2-AR agonist, induced a switch from tonic to bursty pattern without changing the firing rate. This change in the pattern was prevented by the local infusion of idazoxan, an α2-AR antagonist. Furthermore, clonidine injection into the STN reduced locomotor activity in sham and 6-hydroxydopamine-lesioned rats. In contrast, local injection of phenylephrine, an α1-AR agonist, increased the firing rate of STN neurons without changing the firing pattern. In parallel, phenylephrine did not change locomotor activity. This is the first evidence showing the implication of α1-ARs in the modulation of firing rate and α2-ARs in the modulation of the firing pattern of STN neurons. Furthermore, our data provide also evidence that activation of the STN α2-ARs plays a key role in the genesis of subthalamic burst activity, which may be at the origin of motor deficits.

Because the discoordination between swallowing and respiration may cause severe respiratory disorders such as aspiration pneumonia, understanding the neuronal mechanisms underlying such coordination is important. Recently, it was reported that medullary noradrenergic neurons are involved in evoking esophageal-gastric relaxation reflex, leading to a hypothesis that such neurons are also involved in swallowing-respiration coordination. We tested this hypothesis using an in vitro brainstem preparation obtained from neonatal rats. A temporal inhibition of respiratory rhythm was consistently observed when swallowing activity was induced by electrical stimulations to the supralaryngeal nerve. We found that a broad adrenergic receptor agonist, norepinephrine, markedly blocked the swallowing-induced temporal inhibition of respiration. Further studies revealed that swallowing-induced respiratory inhibition is blocked by an α2-adrenergic receptor agonist and enhanced by an α2-adrenergic receptor antagonist, indicating an important role of α2-adrenergic receptors in regulation of the coordination between swallowing and respiration in vitro. [ABSTRACT FROM AUTHOR]