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“Background and Objectives: Recent research shows that locally injected dexmedetomidine enhances the local anesthetic potency of lidocaine via the alpha-2A adrenoceptor selleck chemicals llc subtype in guinea pigs. However, little is known about the effect of locally injected dexmedetomidine on the peripheral vascular response. This study aimed to evaluate the effect of locally injected dexmedetomidine on the peripheral vascular response, measuring skin blood flow in the injected area in guinea pigs. Methods: Dexmedetomidine was intracutaneously injected at a volume of

0.1 mL into the backs of guinea pigs, and further injected combined with yohimbine, a selective antagonist of alpha-2 adrenoceptors, or prazosin, a selective antagonist of alpha-1 adrenoceptors and an antagonist of both alpha-2B and alpha-2C adrenoceptor subtypes. Skin blood flow was measured until 60 minutes after injection using a laser-Doppler flowmeter. Furthermore, systemic arterial blood pressure and pulse of the guinea pigs were monitored via a catheter inserted into the carotid artery throughout every experiment. Results: Dexmedetomidine at a concentration of 1 mu M significantly decreased the skin blood flow in a dose-dependent manner with no changes in the mean blood pressure and pulse. Yohimbine completely antagonized the effect of dexmedetomidine, but prazosin did not. Conclusions: The results reveal that

locally injected dexmedetomidine at a concentration of

1 mu M induced peripheral vasoconstriction selleck compound without a systemic cardiovascular response via the peripheral alpha-2A adrenoceptor Doramapimod subtype.”
“The kinetics of the phasic synchronous and delayed asynchronous release of acetylcholine quanta was studied at the neuromuscular junctions of aging rats from infant to mature animals at various frequencies of rhythmic stimulation of the motor nerve. We found that in infants 6 (P6) and 10 (P10) days after birth a strongly asynchronous phase of quantal release was observed, along with a reduced number of quanta compared to the synapses of adults. The rise time and decay of uni-quantal end-plate currents were significantly longer in infant synapses. The presynaptic immunostaining revealed that the area of the synapses in infants was significantly (up to six times) smaller than in mature junctions. The intensity of delayed asynchronous release in infants increased with the frequency of stimulation more than in adults. A blockade of the ryanodine receptors, which can contribute to the formation of delayed asynchronous release, had no effect on the kinetics of delayed secretion in the infants unlike synapses of adults. Therefore, high degree of asynchrony of quantal release in infants is not associated with the activity of ryanodine receptors and with the liberation of calcium ions from intracellular calcium stores. (C) 2014 ISDN.