Comparisons of two different doses of fentanyl for procedural analgesia during epidural catheter placement: a double-blind prospective, randomized, placebo-controlled study.

The purpose of this study was to investigate the effect of fentanyl on analgesic properties and respiratory responses during an epidural procedure. Sixty patients premedicated with oral brotizolam 0.25 mg were allocated to receive procedural analgesia with saline or 25 or 50 µg of fentanyl. Five minutes after administration, an epidural procedure was started. Pain assessments were made immediately after the epidural catheter placement using a visual analog scale. The lowest SpO2 levels during the procedure were recorded to evaluate respiratory depression, and cardiovascular complications were also recorded. The pain scores were significantly lower in the 25 and 50 µg fentanyl groups than in the placebo group (P < 0.01). There was no difference in pain assessment between the 25 and 50 µg fentanyl groups. The lowest SpO2 value of the 50 µg fentanyl group was significantly lower than those of the other groups (P < 0.001). Seven of 20 cases in the 50 µg fentanyl group needed oxygen administration because of a decreased SpO2 value (<94%). No cardiovascular complications were observed in any group during the entire study period. Thus, intravenous fentanyl at a dose of 25 µg provides effective procedural analgesia without the risk of hypoxemia during an epidural procedure in a patient with preanesthetic medication.

Dual alpha(2)-adrenergic agonist and alpha(1)-adrenergic antagonist actions of dexmedetomidine on human isolated endothelium-denuded gastroepiploic arteries.

UNLABELLED: The actions of dexmedetomidine (DEX) on human vascular smooth muscle are unclear. We investigated its effects on isolated, endothelium-denuded human gastroepiploic arteries in vitro and compared them with clonidine (CLO). DEX had little direct effect on resting tension, whereas CLO produced small contractile responses, an effect which is blocked by the alpha(1)-adrenergic antagonist prazosin. DEX markedly enhanced the high K(+) (40 mmol/L)-induced contraction, and this effect was reversed by the alpha(2)-adrenergic antagonists yohimbine and rauwolscine but unaffected by prazosin. However, CLO had little effect on the K(+) contractions. Interestingly, larger concentrations (>10(-7) mol/L) of both alpha(2)-adrenergic stimulants significantly inhibited the contractions elicited by the alpha(1)-adrenergic agonist phenylephrine (10(-6) mol/L) and, to a lesser extent, those elicited by the alpha(1)/alpha(2)-agonist norepinephrine (10(-6) mol/L). These results suggest the possibility that DEX and CLO each have a high affinity for alpha(1)-adrenoceptors in human isolated gastroepiploic arteries, resulting in a reduced efficacy of alpha(1)-adrenergic activation by alpha-agonists. The differing affinities of the drugs for alpha(1)- and alpha(2)-adrenoceptors may help explain their additional actions: 1) DEX enhances the high K(+)-induced contraction presumably through alpha(2)-adrenoceptor activation, and 2) CLO acts on alpha(1)-adrenoceptors as a partial agonist when present alone. IMPLICATIONS: Dexmedetomidine may not directly affect smooth muscle in human peripheral resistance vessels within the usual range of plasma concentrations (<10(-7) mol/L) achieved in clinical practice. However, in large doses, it could enhance the response to nonadrenergic vasoconstrictor agonists while antagonizing the vasoconstrictor response to alpha(1)-adrenoceptor agonists.